Journal articles: 'Heart of a dog'

1

Shapiro, Alan. "Dog Heart." Hopkins Review 7, no. 4 (2014): 463–64. http://dx.doi.org/10.1353/thr.2014.0097.

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Rouslin, W., and C. W. Broge. "Mechanisms of ATP conservation during ischemia in slow and fast heart rate hearts." American Journal of Physiology-Cell Physiology 264, no. 1 (1993): C209—C216. http://dx.doi.org/10.1152/ajpcell.1993.264.1.c209.

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In the present study we compared the quantitatively most important, Pi-activated mechanisms for conserving ATP during ischemia in dog and rat cardiac muscle. Earlier studies by ourselves showed that dog heart, like all slow heart rate mammalian hearts examined, possesses the ability to inhibit its mitochondrial ATPase by binding IF1, the ATPase inhibitor protein, during ischemia. Rat heart, like other fast heart rate mammalian hearts studied, does not. The present study demonstrated that this IF1-mediated ATPase inhibition in ischemic dog heart, as in other slow heart rate hearts, appears to depend on matrix space acidification mediated largely by Pi-H+ symport via the mitochondrial Pi carrier. The present study further confirmed that maximal glycolytic flux rates are five- to sixfold greater in ischemic rat than in ischemic dog heart. Both of these systems are activated by increasing Pi concentration ([Pi]) during ischemia, and both appear to be regulated somewhat differently in dog than in rat heart. Thus intact dog heart mitochondria exhibited a [Pi]-dependent ATPase inhibition at low external pH, whereas rat heart mitochondria did not. The [Pi] required for maximal ATPase inhibition in dog heart mitochondria was approximately 6 mM. Although both dog and rat heart phosphofructokinase were stimulated by Pi, the enzyme in dog heart was maximally activated by approximately 6 mM Pi, whereas the rat heart enzyme required only approximately 3 mM Pi for its maximal stimulation under otherwise identical conditions. The most active nonmitochondrial ATPase in ischemic dog and rat cardiac muscle, the Ca(2+)-activated actomyosin ATPase, accounted for approximately one-half of the total nonmitochondrial ATPase activity in each species.(ABSTRACT TRUNCATED AT 250 WORDS)

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Anninskii, Lev. "Heart of a Dog?" Soviet Studies in Literature 27, no. 4 (1991): 44–61. http://dx.doi.org/10.2753/rsl1061-1975270444.

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Toerien, Barend J., and Breyten Breytenbach. "Dog Heart (A Travel Memoir)." World Literature Today 73, no. 3 (1999): 583. http://dx.doi.org/10.2307/40155021.

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Balcells, Eduardo, Qing C. Meng, Walter H. Johnson, Suzanne Oparil, and Louis J. Dell’Italia. "Angiotensin II formation from ACE and chymase in human and animal hearts: methods and species considerations." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (1997): H1769—H1774. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h1769.

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The current study examined the contributions of angiotensin-converting enzyme (ACE) vs. chymase to angiotensin II (ANG II) generation in membrane preparations from left ventricles of humans, dogs, rabbits, and rats and from total heart of mice. ACE and chymase activity were measured in membrane preparations extracted with low or high detergent (LD and HD, respectively) concentrations. We hypothesized that ACE, which is membrane bound in vivo, would be preferentially localized to the HD preparation, whereas chymase, which is localized to the cytoplasm and cardiac interstitium, would be localized to the LD preparation. In human heart, ACE activity was 16-fold higher in the HD than in the LD preparation, whereas chymase activity was 15-fold higher in the LD than in the HD preparation. Total ANG II formation was greater in human heart [15.8 ± 3.4 (SE) μmol ANG II ⋅ g−1 ⋅ min−1] than in dog, rat, rabbit, and mouse hearts (3.90 ± 0.35, 0.41 ± 0.02, 0.61 ± 0.07, and 1.16 ± 0.08 μmol ANG II ⋅ g−1 ⋅ min−1, respectively, P < 0.05, by analysis of variance). ANG II formation from ACE was higher in mouse heart (1.09 ± 0.05 μmol ANG II ⋅ g−1 ⋅ min−1, P < 0.001) than in rabbit, human, dog, and rat hearts (0.55 ± 0.06, 0.34 ± 0.01, 0.32 ± 0.06, and 0.31 ± 0.02 μmol ANG II ⋅ g−1 ⋅ min−1, respectively). In contrast, chymase activity was higher in human heart (15.3 ± 3.4 μmol ANG II ⋅ g−1 ⋅ min−1) than in dog, rat, rabbit, and mouse hearts (3.59 ± 0.29, 0.10 ± 0.01, 0.06 ± 0.01, and 0.07 ± 0.01 μmol ANG II ⋅ g−1 ⋅ min−1, respectively). Our results demonstrate important species differences in the pathways of intracardiac ANG II generation. Chymase predominated over ACE activity in human heart, accounting for extremely high total ANG II formation in human heart compared with dog, rat, rabbit, and mouse hearts.

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Griffiths, E. J., and A. P. Halestrap. "Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion." Biochemical Journal 307, no. 1 (1995): 93–98. http://dx.doi.org/10.1042/bj3070093.

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1. The yield of mitochondria isolated from perfused hearts subjected to 30 min ischaemia followed by 15 min reperfusion was significantly less than that for control hearts, and this was associated with a decrease in the rates of ADP-stimulated respiration. 2. The presence of 0.2 microM cyclosporin A (CsA) in the perfusion medium during ischaemia and reperfusion caused mitochondrial recovery to return to control values, but did not reverse the inhibition of respiration. 3. A technique has been devised to investigate whether the Ca(2+)-induced non-specific pore of the mitochondrial inner membrane opens during ischaemia and/or reperfusion of the isolated rat heart. The protocol involved loading the heart with 2-deoxy[3H]glucose ([3H]DOG), which will only enter mitochondria when the pore opens. Subsequent isolation of mitochondria demonstrated that [3H]DOG did not enter mitochondria during global isothermic ischaemia, but did enter during the reperfusion period. 4. The amount of [3H]DOG that entered mitochondria increased with the time of ischaemia, and reached a maximal value after 30-40 min of ischaemia. 5. CsA at 0.2 microM did not prevent [3H]DOG becoming associated with the mitochondria, but rather increased it; this was despite CsA having a protective effect on heart function similar to that shown previously [Griffiths and Halestrap (1993) J. Mol. Cell. Cardiol. 25, 1461-1469]. 6. The non-immunosuppressive CsA analogue [MeAla6]cyclosporin was shown to have a similar Ki to CsA on purified mitochondrial peptidyl-prolyl cis-trans-isomerase and mitochondrial pore opening, and also to have a similar protective effect against reperfusion injury. 7. Using isolated heart mitochondria, it was demonstrated that pore opening could become CsA-insensitive under conditions of adenine nucleotide depletion and high matrix [Ca2+] such as may occur during the initial phase of reperfusion. The apparent increase in mitochondrial [3H]DOG in the CsA-perfused hearts is explained by the ability of the drug to stabilize pore closure and so decrease the loss of [3H]DOG from the mitochondria during their preparation.

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Van Winkle, D. M., A. N. Swafford, and J. M. Downey. "Subendocardial coronary compression in beating dog hearts is independent of pressure in the ventricular lumen." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 2 (1991): H500—H505. http://dx.doi.org/10.1152/ajpheart.1991.261.2.h500.

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Ventricular decompression has been shown to have little effect on either the magnitude or transmural distribution of the extravascular resistance in the small hearts of the cat or rabbit. This study tests whether that independence from ventricular pressure also occurs in the large heart of the dog, which should be more representative of the human. We measured regional myocardial flow in each in situ dog heart during three conditions: normally beating, vented beating, and arrest. Hearts were perfused at constant pressure and maximally dilated with 0.4-1.0 mg/min ic adenosine. Total coronary blood flow was measured with an electromagnetic flowmeter, and regional flow was assessed with radiolabeled microspheres. Although arrest resulted in more than a doubling of flow to the inner layer, greatly reducing ventricular pressure by venting had no significant effect on subendocardial flow. Subepicardial flow was minimally affected by either venting or arrest. We conclude that both the magnitude and the transmural distribution of extravascular resistance in the large heart of the dog is unrelated to the pressure in the ventricular lumen.

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Rouslin, W., C. W. Broge, and I. L. Grupp. "ATP depletion and mitochondrial functional loss during ischemia in slow and fast heart-rate hearts." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 6 (1990): H1759—H1766. http://dx.doi.org/10.1152/ajpheart.1990.259.6.h1759.

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In the present study, isolated dog and rat hearts were perfused in the Langendorff mode with Krebs bicarbonate buffer in the absence and presence of 10(-5) M oligomycin. The perfusion protocols employed allowed tissue pH to drop during subsequent ischemic incubations essentially as it would in blood-perfused hearts. Tissue pH, ATP, lactate, and mitochondrial respiratory function were measured during the course of subsequent zero-flow ischemic incubations. The adenosinetriphosphatase (ATPase) activities attributable to both mitochondrial and nonmitochondrial ATPases in sonicated heart homogenates and the actomyosin ATPase in isolated cardiac myofibrils were measured in both species. Consistent with earlier results with a different model in which tissue pH was buffered during the ischemic incubations [W. Rouslin, J. L. Erickson, and R. J. Solaro. Am. J. Physiol. 250 (Heart Circ. Physiol. 19): H503-H508, 1986], the inhibition of the mitochondrial ATPase in situ by oligomycin markedly slowed both tissue ATP depletion and the loss of mitochondrial function during ischemia in the dog. However, oligomycin had only a very small and transient effect on ATP depletion and mitochondrial function in the rat. This was apparently so because of the fivefold higher rate of glycolytic ATP production as well as the nearly threefold higher total nonmitochondrial ATPase activity of ischemic rat compared with ischemic dog heart. These results suggest that although the inhibition of the mitochondrial ATPase makes a major contribution to ATP conservation in ischemic dog heart, it makes only a very small contribution in rat.

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9

Patterson, D. F. "CONGENITAL HEART DISEASE IN THE DOG*." Annals of the New York Academy of Sciences 127, no. 1 (2006): 541–69. http://dx.doi.org/10.1111/j.1749-6632.1965.tb49423.x.

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10

MATIC, S. E. "Congenital heart disease in the dog." Journal of Small Animal Practice 29, no. 12 (1988): 743–59. http://dx.doi.org/10.1111/j.1748-5827.1988.tb01900.x.

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NILSSON, TORSTEN. "HEART-BASE TUMOURS IN THE DOG." Acta Pathologica Microbiologica Scandinavica 37, no. 5 (2009): 385–97. http://dx.doi.org/10.1111/j.1699-0463.1955.tb00961.x.

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12

Barron, B. "Screening for opioids in dog heart." Journal of Molecular and Cellular Cardiology 24, no. 1 (1992): 67–77. http://dx.doi.org/10.1016/0022-2828(92)91160-7.

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13

KANEMOTO, Isamu, Shinzi SHIBATA, Haruhiko NOGUCHI, et al. "Autotransplantation of the heart in a dog." Japanese Journal of Veterinary Anesthesia & Surgery 20, no. 3 (1989): 79–83. http://dx.doi.org/10.2327/jvas.20.79.

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14

Wallace, Charles R. "SPONTANEOUS CONGESTIVE HEART FAILURE IN THE DOG." Annals of the New York Academy of Sciences 127, no. 1 (2006): 570–80. http://dx.doi.org/10.1111/j.1749-6632.1965.tb49424.x.

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15

Chastulik, Perri. "“Recognize This”: Anderson’s Heart of a Dog." Film Matters 8, no. 3 (2017): 53–54. http://dx.doi.org/10.1386/fm.8.3.53_1.

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16

SWINNEY, GR, and R. MALIK. "Intermittent heart block in a lethargic dog." Australian Veterinary Journal 76, no. 10 (1998): 663–64. http://dx.doi.org/10.1111/j.1751-0813.1998.tb12277.x.

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17

Kraetschmer, S., K. Ludwig, F. Meneses, I. Nolte, and D. Simon. "Vertebral heart scale in the beagle dog." Journal of Small Animal Practice 49, no. 5 (2008): 240–43. http://dx.doi.org/10.1111/j.1748-5827.2007.00531.x.

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18

Jepsen-Grant, K., R. E. Pollard, and L. R. Johnson. "VERTEBRAL HEART SCORES IN EIGHT DOG BREEDS." Veterinary Radiology & Ultrasound 54, no. 1 (2012): 3–8. http://dx.doi.org/10.1111/j.1740-8261.2012.01976.x.

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19

Kettunen, Raimo, Jouni Timisjärvi, Eero Kouvalainen, Pauliina Anttila, and Leo Hirvonen. "Electromechanical delay in the intact dog heart." International Journal of Cardiology 9, no. 2 (1985): 161–71. http://dx.doi.org/10.1016/0167-5273(85)90195-0.

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20

Noordin, Norhidayah, Kuan Hua Khor, Kuan Siew Khor, Yi Jun Lim, and Yong Chong Lee. "Dog Owners’ Perspectives on Canine Heart Disease in Klang Valley, Malaysia." Animals 12, no. 8 (2022): 985. http://dx.doi.org/10.3390/ani12080985.

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Canine heart disease often requires long-term treatment, which involves a continuous commitment from the dog owners. In addition to investigating their awareness and knowledge, the Theory of Planned Behavior was applied to also analyze attitude, subjective norm, and perceived behavioral control (PBC) of the dog owners, with empathic concern as a moderator in predicting intention to treat canine heart disease. Through a convenience sampling approach, 261 respondents, who were clients of University Veterinary Hospital, Universiti Putra Malaysia (UVH-UPM), with experience in owning or caring for dogs, were recruited. While the majority of the respondents (83.5%) claimed that they were aware of canine heart disease, most respondents (45.6%) could only identify 5 to 8 (Fair) out of 12 of the salient clinical signs. Most dog owners (92.3%) were willing to seek treatment if the pet dogs were affected, although the intent is deterred by cost (39.5%). In this study, attitude, subjective norms, and perceived behavioral control were significant predictors for the intention to treat. Dog owners with low empathic concern can be motivated to treat affected dogs by cultivating perceived behavioral control. Therefore, continual education may improve dog owners’ preconceived ability to provide care, and veterinarians may play an important role to encourage treatment in dogs diagnosed with heart disease.

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Prosdocimi, M., M. Finesso, N. Banzatto, A. Zanetti, G. de Gaetano, and E. Dejana. "Prostacyclin Release in the Coronary Circulation During Sustained Stimulation in In Vitro and in In Vivo Experimental Systems." Thrombosis and Haemostasis 59, no. 02 (1988): 180–85. http://dx.doi.org/10.1055/s-0038-1642750.

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SummaryProstacyclin release from rat isolated perfused hearts and from dog coronary circulation was studied by measuring immunoreac- tive 6-keto-PGFlalpha (6-keto-PGFla) in heart perfusate and in plasma obtained from the great cardiac vein respectively.

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Williams, Terrie M., Penni Bengtson, Diana L. Steller, Donald A. Croll, and Randall W. Davis. "The Healthy Heart: Lessons from Nature's Elite Athletes." Physiology 30, no. 5 (2015): 349–57. http://dx.doi.org/10.1152/physiol.00017.2015.

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The incidence of cardiovascular disease in humans is more than three times that of many wild and domestic mammals despite nearly identical heart morphologies and responses to exercise. A survey of mammalian species from 0.002-kg shrews to 43,000-kg whales shows that the human heart is more dog-like than cat-like and that neither body size nor longevity accounts for the relative vulnerability to cardiovascular disease. Rather, a major difference is daily activity patterns, which may underlie the comparatively healthy hearts of wild mammals.

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Cole, Kathie M., Anna Gawlinski, Neil Steers, and Jenny Kotlerman. "Animal-Assisted Therapy in Patients Hospitalized With Heart Failure." American Journal of Critical Care 16, no. 6 (2007): 575–85. http://dx.doi.org/10.4037/ajcc2007.16.6.575.

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Background Animal-assisted therapy improves physiological and psychosocial variables in healthy and hypertensive patients. Objectives To determine whether a 12-minute hospital visit with a therapy dog improves hemodynamic measures, lowers neurohormone levels, and decreases state anxiety in patients with advanced heart failure. Methods A 3-group randomized repeated-measures experimental design was used in 76 adults. Longitudinal analysis was used to model differences among the 3 groups at 3 times. One group received a 12-minute visit from a volunteer with a therapy dog; another group, a 12-minute visit from a volunteer; and the control group, usual care. Data were collected at baseline, at 8 minutes, and at 16 minutes. Results Compared with controls, the volunteer-dog group had significantly greater decreases in systolic pulmonary artery pressure during (−4.32 mm Hg, P = .03) and after (−5.78 mm Hg, P = .001) and in pulmonary capillary wedge pressure during (−2.74 mm Hg, P = .01) and after (−4.31 mm Hg, P = .001) the intervention. Compared with the volunteer-only group, the volunteer-dog group had significantly greater decreases in epinephrine levels during (−15.86 pg/mL, P = .04) and after (−17.54 pg/mL, P = .04) and in norepinephrine levels during (−232.36 pg/mL, P = .02) and after (−240.14 pg/mL, P = .02) the intervention. After the intervention, the volunteer-dog group had the greatest decrease from baseline in state anxiety sum score compared with the volunteer-only (−6.65 units, P =.002) and the control groups (−9.13 units, P &lt; .001). Conclusions Animal-assisted therapy improves cardiopulmonary pressures, neurohormone levels, and anxiety in patients hospitalized with heart failure.

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Sahashi, Yu, Miwako Sahashi, and Yoshiaki Hikasa. "Effect of Pravastatin as an Adjunctive Therapeutic for Mitral Insufficiency with Hyperlipidemia in a Dog." Case Reports in Veterinary Medicine 2021 (September 3, 2021): 1–5. http://dx.doi.org/10.1155/2021/6054125.

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Pravastatin (PS) has been found to increase left ventricle (LV) expansion capacity and decrease LV constriction and left atrial pressure in healthy dogs. To date, there are no available reports on the effects of PS in dogs with hypercholesterolemia with chronic heart failure (CHF). This case report demonstrates a successful long-term treatment plan using PS in a dog suffering from mitral insufficiency with hyperlipidemia. A 12-year-old, castrated male Chihuahua dog had mitral insufficiency with hyperlipidemia. The dog presented with symptoms of chronic coughing. PS was orally administered (1 mg/kg, SID) in addition to general treatment for mitral insufficiency. The follow-up period was 375 days. PS administration decreased the heart rate (HR), vertebral heart size (VHS), and N-terminal probrain natriuretic peptide (NT-proBNP) concentration of the dog. In addition, PS administration also improved chronic cardiac failure induced by mitral insufficiency and hyperlipidemia. This report suggests that PS can be useful as an adjunctive therapeutic for dogs with hypercholesterolemia with mitral insufficiency.

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Keenan, Charlotte M., and Justin D. Vidal. "Standard Morphologic Evaluation of the Heart in the Laboratory Dog and Monkey." Toxicologic Pathology 34, no. 1 (2006): 67–74. http://dx.doi.org/10.1080/01926230500369915.

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The nonrodent species most commonly utilized in preclinical safety studies are the purpose-bred beagle dog and cynomolgus macaque ( Macaca fascicularis). Potential effects of a new chemical entity (NCE) on the heart pose serious concerns; consequently in vivo testing is focused on detection of functional alterations as well as morphological changes. Macroscopic and microscopic evaluation of the heart is based on a standard survey of key structures to properly assess presence of spontaneous and potential drug-induced lesions. Evaluation of historical controls to determine type and frequency of background change is valuable, as studies with non-rodent species generally have a small sample size. Archived control dog and monkey data were retrospectively reviewed, including terminal body weight (BW), heart weight (HW), and archival glass slides of heart. Control dogs had minimal background changes that included myxomatous or cartilagenous change in the cardiac skeleton and a variable degree of vacuolation in Purkinje fibers. Control monkey hearts commonly contained inflammatory cell infiltrates, myocyte anisokaryosis, and handling artifacts, while myocyte degeneration, squamous plaques, pigment, and intimal plaques were occasionally observed. These findings highlight the utility of consistently recorded and readily accessible archived control data when attempting to discern background spontaneous changes and artifacts from test-article induced changes.

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Chen, Weina, Wayne Glasgow, Elizabeth Murphy, and Charles Steenbergen. "Lipoxygenase metabolism of arachidonic acid in ischemic preconditioning and PKC-induced protection in heart." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (1999): H2094—H2101. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h2094.

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We tested the hypothesis that activation of the 12-lipoxygenase (12-LO) pathway of arachidonic acid metabolism contributes to the protective effect of protein kinase C (PKC) activation and ischemic preconditioning (PC), and we report, in perfused rat heart, that both PC and the PKC activator 1,2-dioctanoyl- sn-glycerol (DOG) confer a similar protective effect and stimulate a comparable accumulation of 12-LO metabolites. The 12-LO product, 12( S)-hydroxyeicosatetraenoic acid [12( S)-HETE], was increased in DOG-treated (22.8 ± 4.4 ng/g wet wt) and PC hearts (26.8 ± 5.5 ng/g wet wt) compared with control (13.8 ± 2.1 ng/g wet wt, P < 0.05), and this increase was blocked by 12-LO or PKC inhibitors. Both DOG pretreatment and PC improved recovery of left ventricular developed pressure (LVDP) nearly twofold after 20 min of ischemia; this improvement was blocked by 12-LO inhibitors and was mimicked by infusion of 12-hydroperoxyeicosatetraenoic acid [12( S)-HpETE; 67 ± 6% recovery of LVDP vs. 35 ± 3% for untreated hearts]. Also, the protection afforded by 12( S)-HpETE, as well as by PC, was attenuated by the K+-channel blocker 5-hydroxydecanoate, suggesting that the downstream mechanisms of 12( S)-HpETE-mediated protection are similar to PC. Furthermore, PC stimulates 12-LO metabolism in perfused rabbit heart, and 12-LO inhibition blocks PC-induced cardioprotection. Thus the data suggest that 12-LO metabolism plays an important role in cardioprotection.

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KANEMOTO, Isamu. "Hypothermia and Open-heart Surgery in the Dog." Japanese Journal of Veterinary Anesthesia & Surgery 36, no. 1 (2005): 1–9. http://dx.doi.org/10.2327/jvas.36.1.

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van der Vusse, G. "Metabolic alterations in the chronically denervated dog heart." Cardiovascular Research 37, no. 1 (1998): 160–70. http://dx.doi.org/10.1016/s0008-6363(97)00220-4.

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Kawaguchi, Akira, Paul D. Hirsh, Timothy C. Wolfgang, A. Scott Mills, and Richard R. Lower. "Heart and unilateral lung transplantation in the dog." Journal of Thoracic and Cardiovascular Surgery 91, no. 4 (1986): 485–89. http://dx.doi.org/10.1016/s0022-5223(19)36015-5.

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Schäfers, H. J., and T. Wahlers. "Heart and unilateral lung transplantation in the dog." Journal of Thoracic and Cardiovascular Surgery 93, no. 1 (1987): 149. http://dx.doi.org/10.1016/s0022-5223(19)36491-8.

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Larosa, G., P. W. Armstrong, P. Seeman, and C. Forster. "Adrenoceptor recovery after heart failure in the dog." Cardiovascular Research 27, no. 3 (1993): 489–93. http://dx.doi.org/10.1093/cvr/27.3.489.

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Luciani, Marilia Gabriela, Jéssica Aline Withoeft, Helena Mondardo Cardoso Pissetti, et al. "Vertebral heart size in healthy Australian cattle dog." Anatomia, Histologia, Embryologia 48, no. 3 (2019): 264–67. http://dx.doi.org/10.1111/ahe.12434.

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Yamaguchi, Masuhiro, Tomio Ando, Tsuneaki Goto, et al. "Stimulation of Dog Heart by Pulsed Magnetic Fields." Japanese Journal of Applied Physics 30, Part 2, No. 11A (1991): L1905—L1906. http://dx.doi.org/10.1143/jjap.30.l1905.

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Pace, Charlotte. "Recognising heart failure in the dog and cat." Veterinary Nursing Journal 25, no. 2 (2010): 14–17. http://dx.doi.org/10.1111/j.2045-0648.2010.tb00012.x.

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Kobayashi, Kazuo, and Seiki Yamakawa. "Fibrosarcoma of the heart in a beagle dog." Journal of Toxicologic Pathology 7, no. 3 (1994): 413–16. http://dx.doi.org/10.1293/tox.7.413.

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Reddy, Padala V., and Harald H. O. Schmid. "Acylation of dog heart lysophosphatidylserine by transacylase activity." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 922, no. 3 (1987): 379–85. http://dx.doi.org/10.1016/0005-2760(87)90062-2.

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TANAKA, Nobuaki, Takashi NOZAWA, Yoshio YASUMURA, Shiho FUTAKI, Katsuhiko HIRAMORI, and Hiroyuki SUGA. "Heart-rate-proportional oxygen consumption for constant cardiac work in dog heart." Japanese Journal of Physiology 40, no. 4 (1990): 503–21. http://dx.doi.org/10.2170/jjphysiol.40.503.

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YAKU, Hitoshi, Yoichi GOTO, Shiho FUTAKI, et al. "Equivalent Heart Rate during Ventricular Fibrillation in the Dog Heart: Mechanoenergetic Analysis." Japanese Journal of Physiology 41, no. 6 (1991): 945–59. http://dx.doi.org/10.2170/jjphysiol.41.945.

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Laughlin, Maren R., Joni Taylor, A. Scott Chesnick, and Robert S. Balaban. "Nonglucose substrates increase glycogen synthesis in vivo in dog heart." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (1994): H217—H223. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h217.

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The effects of circulating nonglucose substrates on insulin-stimulated cardiac glycogen synthesis were studied in the dog heart in vivo using13 C-nuclear magnetic resonance (-NMR) and arteriovenous difference techniques. [1-13C]glycogen was monitored in hearts during an intravenous infusion of 20 mU/min insulin and glucose while [1-13C]glucose (10 mg/min) was infused into the left anterior descending coronary artery. When 1 mmol/min of lactate, pyruvate, or beta-hydroxybutyrate was added to the venous infusion, the measured rate of glycogen synthesis was increased, on average, sixfold. It was not increased further after a subsequent 10-min infusion of 5 μg/min epinephrine. Lactate extraction increased from 0.18 ± 0.05 to 0.62 ± 0.11 μmol·min-1·g wet wt-1 during lactate infusion, whereas glucose extraction did not change significantly (0.15 ± 0.05 μmol·min-1·g wet wt-1 at 45 min of insulin and glucose infusion to 0.09 ± 0.02 μmol·min-1·g wet wt-1 at 45 min of the lactate infusion). Therefore, the uptake and oxidation of circulating nonglucose substrates redirects the fate of extracted glucose from glycolysis to glycogen synthesis in the dog heart in vivo. carbon-13-nuclear magnetic resonance; lactate; pyruvate; β-hydroxybutyrate Submitted on October 19, 1993 Accepted on February 3, 1994

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Glyantsev, S. P., E. S. Maksimov, and M. V. Gordeeva. "PHENOMENON OF DEMIKHOV. At N.V. Sklifosovsky Institute (1960–1986). Grishka the dog lived with a second, additional heart and transplanted lung without immunosuppression for 142 days (1962)." Transplantologiya. The Russian Journal of Transplantation 14, no. 1 (2022): 98–114. http://dx.doi.org/10.23873/2074-0506-2022-14-1-98-114.

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On June 20, 1962, at the N.V. Sklifosovsky Research Institute for Emergency Medicine in Moscow, V.P. Demikhov, a biologist, physiologist, and experimental surgeon transplanted a second, additional heart together with the lung through the left thoracotomy access in the fourth intercostal space into the place of the removed two upper lobes of the left lung into the chest to the dog named Grishka. The second heart was implanted in such a way that arterial blood circulated in it and in the transplanted lung. The donor and recipient were selected according to the blood group match. The immediate postoperative period was uneventful. On day 4, the dog became active. On day 12, the sutures were removed from the skin wound. On day 15, antibiotics (penicillin and streptomycin) were discontinued. During the daily examination, general condition and physical activity were noted, rectal temperature, respiratory rate and contractions of one's own and transplanted heart were measured; electrocardiograms were taken from both hearts. On day 13, Grishka gnawed through the electrode, which helped taking the electrocardiograms from the transplanted heart during the first 2 weeks. As a result, in place of the electrode remaining in the chest, the animal developed a fistula with purulent discharge. For this reason, as well as for coughing and wheezing in the lungs on the left, Grishka was periodically administered antibiotics. After the operation and before the withdrawal from the experiment, the dog was injected with heparin. No other pharmaceuticals were given. The dog led an active lifestyle, ate well, and displayed interest in female dogs. The second heart ceased beating 142 days after the operation, on November 8, 1962. Resuscitation measures were unsuccessful. At autopsy, in the right atrial auricle of the transplanted heart, diffuse transmural hemorrhage and a thrombus from the endocardium were revealed, which blocked the blood flow to the heart. The lower lobe of Grishka's lung was in a state of hepatization. Signs of edema and inflammation were observed in the transplanted lung. There were no blood clots at the sites of vascular anastomoses. There were no visual signs of rejection. The results of histological studies are not known. This article for the first time introduced into scientific circulation an operation protocol, a diary of postoperative management and an autopsy protocol for an animal that had lived with a second, additional heart and a transplanted lung without immunosuppression for 142 days, which has been a unique observation in world transplantology. Despite the long-term survival of the animal, nursing the recipient dog in the postoperative period did not meet the complexity of the operation performed, which allows us to conclude that it was impossible at that time to implement the results obtained in the experiment into clinical heart transplantation in humans.

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41

DeFrancesco, TC, CE Atkins, and BW Keene. "Myocardial infarction complicating management of congestive heart failure in a dog." Journal of the American Animal Hospital Association 32, no. 1 (1996): 68–72. http://dx.doi.org/10.5326/15473317-32-1-68.

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A 7.5-kg, 10-year-old, spayed female, mixed-breed dog was evaluated for sudden onset of weakness, tachypnea, and an irregular cardiac rhythm. Congestive heart failure secondary to mitral valve regurgitation had been diagnosed six weeks earlier. The dog was stable on furosemide, enalapril, and hydralazine. Complex ventricular tachycardia, altered QRS conformation of sinus complexes, echocardiographic evidence of a hypokinetic left-ventricular free wall, and elevated creatine kinase suggested a diagnosis of myocardial infarction. Despite antiarrhythmic therapy, the dog developed ventricular fibrillation and died 36 hours after admission. Postmortem examination confirmed the myocardial infarction. Although a rare diagnosis in the veterinary patient, myocardial infarction must be considered in the differential diagnosis for sudden onset of weakness, tachypnea, and ventricular tachycardia.

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42

Filipejova, Z., CF Agudelo, B. Koskova, et al. "Neuroendocrine carcinoma of the heart base in a dog: A case report." Veterinární Medicína 67, No. 5 (2022): 257–62. http://dx.doi.org/10.17221/17/2021-vetmed.

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A case of a nine-year-old, intact female, American Bulldog with a heart mass is described. Echocardiography was used to identify this pathological lesion. Part of the mass and pericardial sac were surgically removed for histopathological examination. A final diagnosis of neuroendocrine carcinoma was diagnosed by necropsy and histopathology. To the author’s knowledge, there is very limited information in the literature about this pathology.

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Mootha, V. K., A. E. Arai, and R. S. Balaban. "Maximum oxidative phosphorylation capacity of the mammalian heart." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (1997): H769—H775. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h769.

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It is difficult to estimate the maximum in vivo aerobic ATP production rate of the intact heart independent of limitations imposed by blood flow, oxygen delivery, and maximum mechanical power. This value is critical for establishing the kinetic parameters that control oxidative phosphorylation, as well as for providing insights into the limits of myocardial performance. In this study, the maximum ADP-P(i)-driven heart mitochondrial respiratory rate (MV(O2 mito)) was determined with saturating levels of oxygen, substrates, and cofactors at 37 degrees C. These rates were normalized to cytochrome alpha1 alpha3 (cytochrome oxidase; Cyt a) content. To extrapolate this rate to the intact heart, the Cyt a content of the myocardium (nmol Cyt a/g wet wt myocardium) was determined in the same hearts. The maximum ADP-P(i)-driven mitochondrial respiratory rates were 676 +/- 31 and 665 +/- 65 nmol O2 x min(-1) x nmol Cyt a(-1) in the dog and pig, respectively. The Cyt a content in the two species was 43.6 +/- 2.4 and 36.6 +/- 3.1 nmol Cyt a/g wet wt, respectively. With these values, the MV(O2 mito) was calculated to be 29.5 (dog) and 24.3 (pig) micromol O2 x min(-1) x g wet wt myocardium(-1). Comparison with in vivo studies shows that the exercising heart can utilize 80-90% of its maximum oxidative capacity, implying there is little aerobic ATP production reserve in the mammalian heart.

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McCulloch, A. D., B. H. Smaill, and P. J. Hunter. "Left ventricular epicardial deformation in isolated arrested dog heart." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 1 (1987): H233—H241. http://dx.doi.org/10.1152/ajpheart.1987.252.1.h233.

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We have developed a method for measuring epicardial deformation in the isolated arrested dog heart. A biplane video system was used to record the motion of discrete epicardial markers at midanterior sites (n = 4 hearts) and midposterior sites (n = 1) during quasi-static left ventricular (LV) filling. Experimental procedures, performed at room temperature, were completed within 20 min, and LV pressure-volume curves were repeatable and within the range of data presented by other authors. To obtain a complete description of local deformation, epicardial displacements derived from the video record were analyzed using homogeneous strain theory. Local epicardial strain was nonuniform; the mean ranges of midanterior major and minor extensions were 0–13.9 and 0-7.2%, respectively, for LV filling pressures of 0–20 mmHg. For the midanterior wall, the mean orientation of the major extension was 28–35 degrees below the LV circumference, compared with an orientation of approximately 62 degrees at the midposterior site. The results demonstrate the value of this preparation for studying passive ventricular mechanics and are not consistent with the predictions of mathematical models of ventricular stress and strain, in which it has been assumed that the material properties of the passive myocardium are isotropic.

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Viott, Aline, Mayane Faccin, Mônica Matos, João Cavasin, Ana Bochi, and Mariana Pavelski. "Bilateral auricular aneurysm with intact pericardial sac in a dog." Brazilian Journal of Veterinary Pathology 14, no. 1 (2021): 46–49. http://dx.doi.org/10.24070/bjvp.1983-0246.v14i1p46-49.

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A nine-year-old, male, Pekingese dog was presented with a history of dyspnea, lethargy, syncope, polyuria, polydipsia, and selective appetite over two years. When the clinical signs first began, a radiographic exam revealed a radiopaque mass in the cranial mediastinum. An adequate treatment was not performed and the dog was presented to the hospital with severe tachycardia, dyspnea, and tachypnea, and died during physical examination. On necropsy, the heart presented bilateral auricular aneurysms. The pericardial sac was intact, and no other defects were found within the heart. Microscopically, the cardiomyocytes were marked degenerated and proliferation of connective tissue. This is the first case report of a bilateral auricular aneurysm with intact pericardial sac in a dog.

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Guevara, Jose L., Elaine S. Holmes, Jennifer Reetz, and David E. Holt. "Porcupine Quill Migration in the Thoracic Cavity of a German Shorthaired Pointer." Journal of the American Animal Hospital Association 51, no. 2 (2015): 101–6. http://dx.doi.org/10.5326/jaaha-ms-6093.

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A 7 yr old German shorthaired pointer presented with progressive respiratory distress and lethargy. Two weeks prior to presentation, the dog had porcupine quills removed from the left forepaw, muzzle, and sternal area. At the time of presentation, the dog had bounding pulses and friction rubs in the right dorsal lung field. Harsh lung sounds and decreased lung sounds were ausculted in multiple lung fields. Radiographs revealed a pneumothorax and rounding of the cardiac silhouette suggestive of pericardial effusion. Computed tomographic imaging was performed and revealed multiple porcupine quills in the thoracic cavity. Surgery was performed and quills were found in multiple lung lobes and the heart. Following surgery the dog remained hypotensive. A post-operative echocardiogram revealed multiple curvilinear soft-tissue opacities in the heart. Given the grave prognosis the dog was subsequently euthanized and a postmortem examination was performed. A single porcupine quill was discovered in the left atrium above the mitral valve annulus. The quill extended across the aortic root, impinging on the coronary artery below the level of the aortic valve. To the authors' knowledge, this is the first known report of porcupine quill migration through the heart.

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Ortmeyer, Heidi K., and Leslie I. Katzel. "Effects of Proximity between Companion Dogs and Their Caregivers on Heart Rate Variability Measures in Older Adults: A Pilot Study." International Journal of Environmental Research and Public Health 17, no. 8 (2020): 2674. http://dx.doi.org/10.3390/ijerph17082674.

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Heart rate variability (HRV) is a noninvasive tool used to evaluate autonomic nervous system function and is affected by age, stress, postural changes, and physical activity. Dog ownership has been associated with higher 24-hr HRV and increased physical activity compared to nonowners. The current pilot study was designed to evaluate the effects of proximity to a dog in real time (minute-by-minute) on older dog caregivers’ HRV measures and stress index during normal daily life over a 24-hr period. Eleven caregivers (56–83 years of age) wore ActiGraph GT9X Link accelerometers and camntech electrocardiogram monitors, and 11 dogs wore PetPace Collars and ActiGraph monitors to determine (a) proximity (absence or presence of Received Signal Strength Indicator, RSSI), (b) heart rate and HRV measures, (c) position (lying vs. sitting vs. standing), and (d) physical activity in the 11 dyads. Twenty-four hour HRV (SDNN index) and physical activity in the caregivers and dogs were related. Stress index was lower, and HRV parameters (SDNN, rMSDD, high frequency power (HF)) were higher when an RSSI signal was detected (presence of dog) compared to no RSSI signal (absence of dog) in the caregivers while inactive (lying + sitting + standing combined). HRV parameters (rMSDD and HF) were lower in the caregivers while standing and sitting compared to lying. The results from this pilot study support the hypothesis that spending time in the presence of a companion dog increases caregivers’ HRV throughout the day and suggest that proximity to a dog may contribute to overall improvements in 24-hr HRV and cardiac health in dog caregivers.

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Stancu, Adrian, Alina Ghise, Marius Pentea, et al. "Chylothorax Consecutive Heartworm Disease in Dog." Materiale Plastice 54, no. 4 (2017): 785–87. http://dx.doi.org/10.37358/mp.17.4.4946.

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Chylothorax was diagnosed in a Afghan dog 3 year old, that presented in the necropsy a accumulation of lymphatic fluid in the chest cavity. Also to examine the right heart was observed to this heartworms - Dirophylaria immitis.

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Bode, Elizabeth. "Pericardial disease in the dog and cat." Companion Animal 24, no. 5 (2019): 262–70. http://dx.doi.org/10.12968/coan.2019.24.5.262.

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The pericardium is a double-walled sac that surrounds the heart and the roots of the great vessels. Although survival is possible without a pericardium, it does serve several functions: balancing right and left ventricular cardiac output; acting as a barrier for infection; and fixing the position of the heart within the thorax. Pericardial diseases can have profound effects on the cardiovascular system and can lead to circulatory collapse, therefore they need to be identified promptly. This article briefly reviews normal pericardial anatomy and physiology, and addresses congenital and acquired pericardial disease processes together with their diagnosis and management.

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Kawaguchi, Akira, and Richard R. Lower. "Heart and unilateral lung transplantation in the dog: Reply." Journal of Thoracic and Cardiovascular Surgery 93, no. 1 (1987): 149–50. http://dx.doi.org/10.1016/s0022-5223(19)36492-x.

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Journal articles on the topic 'Heart of a dog'

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