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Journal articles on the topic 'Isradipine and Quality Control'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Chrysant, Steven G., and Michael Cohen. "Sustained Blood Pressure Control with Controlled-Release Isradipine (Isradipine-CR)." Journal of Clinical Pharmacology 35, no. 3 (March 1995): 239–43. http://dx.doi.org/10.1002/j.1552-4604.1995.tb04053.x.

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2

CHRYSANT, S., and M. COHEN. "Sustained blood pressure control with controlled-release isradipine." American Journal of Hypertension 8, no. 1 (January 1995): 87–89. http://dx.doi.org/10.1016/0895-7061(94)00158-8.

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3

Johnson, Cary E., Pamala A. Jacobson, and Min H. Song. "Isradipine Therapy in Hypertensive Pediatric Patients." Annals of Pharmacotherapy 31, no. 6 (June 1997): 704–7. http://dx.doi.org/10.1177/106002809703100606.

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OBJECTIVE: To evaluate the dosage and effectiveness of isradipine to control acute or chronic hypertension in pediatric patients. DESIGN: Retrospective medical record review. SETTING: University teaching hospital. PARTICIPANTS: Hospitalized pediatric patients aged 1 day to 16 years with hypertension treated with isradipine between January 1994 and March 1996. MEASURES: Patient age, gender, weight, disease states, current medications, isradipine dosage and formulation, pre- and postsystolic, and pre- and postdiastolic blood pressure measurements with each dose of isradipine. RESULTS: Fifty-three patients with a mean age of 5.8 ± 4.0 years were evaluated. A mean change in the blood pressure measurements taken before the first dose of isradipine compared with the values recorded after the last dose or at discharge for all patients was −11.8% ± 12.5% and −17.4% ± 19.6%, respectively, for systolic and diastolic pressure. The mean dosage of isradipine in 46 patients who received regularly scheduled doses was 0.38 ± 0.22 mg/kg/d. Patients who demonstrated a response received a mean dosage of 0.40 ± 0.20 mg/kg/d. The total daily dosage was administered in one dose for 1 patient, two doses for 15 patients, three doses for 27 patients, and four doses for 3 patients. CONCLUSIONS: Isradipine was an effective antihypertensive agent to reduce the systolic and/or diastolic blood pressure 10% or more compared with pretreatment measurements in 43 (81 %) of 53 pediatric patients. The mean dosage was 0.38 ± 0.22 mg/kg/d, most frequently administered in two or three equally divided doses, which is higher than the normal recommended dosage for adults.

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4

KANTOLA, I. "Subjective sleep quality during two different antihypertensive medications: isradipine vs metoprolol." American Journal of Hypertension 12, no. 4 (April 1999): 117. http://dx.doi.org/10.1016/s0895-7061(99)80408-7.

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5

Jacques, Danielle, Ghassan Bkaily, Gaétan Jasmin, Pedro D'Orléans-Juste, and Mirna Chahine. "Isradipine prevents the development of spontaneously occurring cardiac necrosis in cardiomyopathic hamster." Canadian Journal of Physiology and Pharmacology 81, no. 2 (February 1, 2003): 120–24. http://dx.doi.org/10.1139/y03-021.

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Recent studies on the heart necrotizing process at the early stages of hamster polymyopathy have led us to believe that this hereditary disease derives from an anomalous transmembrane ion flux due to the presence of slow Na+ channels that contribute to intracellular Na+ accumulation which promote intracellular Ca2+ overload via the Ca2+ influx through the Na+Ca2+ exchanger. In the present study, we investigated the potential beneficial effect of chronic treatment with a dual L-type Ca2+ and slow Na+ channel blockers isradipine, on the development of necrosis in myopathic hamster hearts. Young cardiomyopathic (CM) hamsters (CMH) were treated with isradipine (0.1 mg·kg1·day1) and nifedipine (1 mg·kg1·day1) for 4 consecutive weeks. Microscopic assessments were carried out in staged serial paraffin sections of heart ventricles from tissues freshly dissected at autopsy. In comparison with control nontreated hearts, which exhibited numerous necrotic calcific foci, myolytic lesions, and dilated right ventricle, isradipine treatment prevented, in a significant manner, all the above spontaneous pathological changes, while nifedipine had no effect. Our present observations provide evidence for the first time that in vivo treatment with a DHP Ca+ channel blocker, isradipine, is cardioprotective against the development of necrosis in hereditary cardiomyopathy in the hamster. It is possible that the protective effect of isradipine in CMH could be largely due to the indirect blockade of Ca2+ influx through the Na+Ca2+ exchanger as well as to possible direct blockade of Ca2+ influx through the T-type Ca2+ channel.Key words: isradipine, cardioprotection, hamster cardiomyopathy, slow Na+ channel.

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6

Pǐtre, Maryse, Nathalie Gaudreault, Marta Santuré, André Nadeau, and Hélène Bachelard. "Isradipine and insulin sensitivity in hypertensive rats." American Journal of Physiology-Endocrinology and Metabolism 276, no. 6 (June 1, 1999): E1038—E1048. http://dx.doi.org/10.1152/ajpendo.1999.276.6.e1038.

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The present study was designed to investigate the effect of a reduction in blood pressure, by using the calcium channel antagonist isradipine, on insulin sensitivity and vascular responses to insulin in conscious spontaneously hypertensive male rats (SHR). The rats were instrumented with intravascular catheters and pulsed Doppler flow probes to measure blood pressure, heart rate, and blood flows. Insulin sensitivity was assessed by the euglycemic-hyperinsulinemic clamp technique. Two groups of rats received isradipine at a dose of 0.05 or 0.15 mg ⋅ kg−1 ⋅ h−1, whereas a third group received a continuous infusion of vehicle (15% DMSO). Both doses of isradipine were found to decrease mean blood pressure (−25 ± 4 mmHg at the dose of 0.05 mg ⋅ kg−1 ⋅ h−1and −20 ± 2 mmHg at the dose of 0.15 mg ⋅ kg−1 ⋅ h−1) and to improve insulin sensitivity. Moreover, in the rats treated with the low dose of isradipine, we observed vasodilations in renal, superior mesenteric, and hindquarter vascular beds. In the untreated group, the euglycemic infusion of insulin (4 mU ⋅ kg−1 ⋅ min−1) was found to cause vasoconstrictions in superior mesenteric and hindquarter vascular beds, but no changes in mean blood pressure, heart rate, or renal vascular conductance were found. In contrast, in the isradipine-treated groups, the same dose of insulin was found to produce vasodilations in the renal vascular bed and to abolish the vasoconstrictor responses previously observed. We concluded that short-term treatment with isradipine in SHR can lower blood pressure and improve insulin sensitivity, mainly through hemodynamic factors, as supported by experiments with hydralazine as a positive vasodilator control.

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7

&NA;. "Isradipine does not affect platelet aggregation or metabolic control in NIDDM." Inpharma Weekly &NA;, no. 742 (June 1990): 17. http://dx.doi.org/10.2165/00128413-199007420-00043.

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8

Wegener, Jörg W., Matthias Lee, and Franz Hofmann. "Hypothyroidism does not affect the dihydropyridine sensitivity of precontracted murine uterus." Canadian Journal of Physiology and Pharmacology 81, no. 9 (September 1, 2003): 890–93. http://dx.doi.org/10.1139/y03-090.

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Thyroid hormones are known to influence various processes of cell differentiation. Recently, it was reported that hypothyroidism reduces the sensitivity to Ca2+-channel antagonists in the rat uterus. We examined the sensitivity to dihydropyridines of the uterus from mice that had reduced thyroid hormone levels. Isradipine relaxed with the same potency precontracted uterine muscle strips from control and hypothyroid mice, independently from a pseudo-pregnant state. These results demonstrate that hypothyroidism does not change dihydropyridine sensitivity (i.e., the pattern of Ca2+-channel expression) in the murine uterus.Key words: uterus, smooth muscle, Ca2+ channel, isradipine.

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9

Darcie, Silvana, Cléa R. Leone, Valdenise M. L. T. Calil, Elizete P. Prescinotti, Soubhi Kahhale, and Marcelo Zugaib. "Glycemia in newborns of hypertensive mothers according to maternal treatment." Revista do Hospital das Clínicas 59, no. 5 (2004): 244–50. http://dx.doi.org/10.1590/s0041-87812004000500004.

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PURPOSE: To evaluate the evolution of glycemic levels in newborns of hypertensive mothers according to maternal treatment. METHODS: Prospective randomized study, including 93 newborns of mothers treated with isradipine (n = 39), atenolol (n = 40), or low sodium diet (control group - n=14). Glycemia was determined at birth (mother and newborn by the oxidase glucose method) and in the 1st, 3rd, 6th, 12th, and 24th hours after birth (newborn by a test strip method). The evolution of glycemia was analyzed in each group (Friedman test). The groups were compared regarding glycemia (Kruskall-Wallis test), and linear regression models were constructed for the analyses (independent variable = maternal glycemia; dependent variables = umbilical cord, 3rd, and 6th hour glycemia). RESULTS: There were no statistically significant differences among the mean blood glucose levels of the 3 groups in any of the assessments. There was a correlation between maternal and umbilical cord blood glucose in the isradipine (r = 0.61; P <.05) and control (r = 0.84; P <.05) groups. Regarding glycemia levels of the mothers and newborns in the third and sixthhours postpartum, this correlation was present only in the control group (maternal x third hour: r = 0.65; P <.05; maternal x sixth hour: r = 0.68; P <.05). There were no correlations in the atenolol group. Hypoglycemia was detected in 51.3% of the isradipine group, 60% of the atenolol group, and 35.7% of the control group, and it was more frequent in the first hour postpartum in all groups. CONCLUSIONS: The results suggest a similar effect of the 3 types of treatment upon newborn glycemia. The correlation analysis suggests that isradipine could have effects upon newborn glycemia only after birth (correlation only in umbilical cord blood), whereas atenolol could act earlier (there was no correlation at any moment). The results also point to the need for glycemic control from the first hour postpartum of newborns of hypertensive mothers whether they have or have not undergone treatment with antihypertensive drugs.

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10

Viskoper, J. R., A. Laszt, and D. Faraggi. "Twenty-Four-Hour Blood Pressure Control With Isradipine in Mild Essential Hypertension." American Journal of Hypertension 4, no. 2_Pt_2 (February 1991): 161S—162S. http://dx.doi.org/10.1093/ajh/4.2.161s.

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11

Frithz, Göran, Brage åström, Björn Dahlöf, Lennart Hansson, Claes Tollin, Pertti Himanen, and Carl-David Sundstedt. "Improved blood pressure control with isradipine in hypertensive patients treated with pindolol." American Journal of Medicine 86, no. 4 (April 1989): 115–18. http://dx.doi.org/10.1016/0002-9343(89)90204-0.

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12

Lawrence, C. J., A. Lestrade, and S. de Lange. "Isradipine, a Calcium Antagonist, in the Control of Hypertension Following Coronary Artery-Bypass Surgery." American Journal of Hypertension 4, no. 2_Pt_2 (February 1991): 207S—209S. http://dx.doi.org/10.1093/ajh/4.2.207s.

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13

Nitert, Marloes Dekker, Cecilia L. F. Nagorny, Anna Wendt, Lena Eliasson, and Hindrik Mulder. "CaV1.2 rather than CaV1.3 is coupled to glucose-stimulated insulin secretion in INS-1 832/13 cells." Journal of Molecular Endocrinology 41, no. 1 (April 9, 2008): 1–11. http://dx.doi.org/10.1677/jme-07-0133.

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In clonal β-cell lines and islets from different species, a variety of calcium channels are coupled to glucose-stimulated insulin secretion. The aim of this study was to identify the voltage-gated calcium channels that control insulin secretion in insulinoma (INS)-1 832/13 cells. The mRNA level of CaV1.2 exceeded that of CaV1.3 and CaV2.3 two-fold. Insulin secretion, which rose tenfold in response to 16.7 mM glucose, was completely abolished by 5 μM isradipine that blocks CaV1.2 and CaV1.3. Similarly, the increase in intracellular calcium in response to 15 mM glucose was decreased in the presence of 5 μM isradipine, and the frequency of calcium spikes was decreased to the level seen at 2.8 mM glucose. By contrast, inhibition of CaV2.3 with 100 nM SNX-482 did not significantly affect insulin secretion or intracellular calcium. Using RNA interference, CaV1.2 mRNA and protein levels were knocked down by ∼65% and ∼34% respectively, which reduced insulin secretion in response to 16.7 mM glucose by 50%. Similar reductions in calcium currents and cell capacitance were seen in standard whole-cell patch-clamp experiments. The remaining secretion of insulin could be reduced to the basal level by 5 μM isradipine. Calcium influx underlying this residual insulin secretion could result from persisting CaV1.2 expression in transfected cells since knock-down of CaV1.3 did not affect glucose-stimulated insulin secretion. In summary, our results suggest that CaV1.2 is critical for insulin secretion in INS-1 832/13 cells.

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14

Cléroux, Jean, NʼGuessan Kouamé, Christopher Yardley, Adele Marshall, and Yves Lacourcière. "Postexercise Reflex Control of Forearm Vascular Resistance During Calcium Antagonism with Slow-Release Oral Isradipine." Journal of Cardiovascular Pharmacology 19, Supplement (1992): 66–69. http://dx.doi.org/10.1097/00005344-199200001-00016.

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15

Cléroux, Jean, NʼGuessan Kouamé, Christopher Yardley, Adele Marshall, and Yves Lacourcière. "Postexercise Reflex Control of Forearm Vascular Resistance During Calcium Antagonism with Slow-Release Oral Isradipine." Journal of Cardiovascular Pharmacology 19 (1992): 66–69. http://dx.doi.org/10.1097/00005344-199200193-00016.

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16

Ebsworth, Patricia. "Quality control." Nursing Standard 16, no. 15 (December 12, 2001): 24. http://dx.doi.org/10.7748/ns.16.15.24.s35.

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17

Davey, Ronald W. "Quality control." British Homeopathic Journal 82, no. 01 (January 1993): 79. http://dx.doi.org/10.1016/s0007-0785(05)80983-4.

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18

Baum, Michael. "Quality control." Lancet 357, no. 9261 (March 2001): 1007. http://dx.doi.org/10.1016/s0140-6736(00)04247-1.

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19

Sutton, George W. "Quality Control." AIAA Journal 30, no. 1 (January 1992): 1–2. http://dx.doi.org/10.2514/3.59973.

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20

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 1 (January 1998): 59–61. http://dx.doi.org/10.1016/s0026-0576(97)80247-4.

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21

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 10 (October 1997): 52–55. http://dx.doi.org/10.1016/s0026-0576(97)80703-9.

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22

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 11 (November 1997): 65–68. http://dx.doi.org/10.1016/s0026-0576(97)81453-5.

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23

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 2 (February 1997): 76–78. http://dx.doi.org/10.1016/s0026-0576(97)81819-3.

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24

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 8 (August 1997): 58–61. http://dx.doi.org/10.1016/s0026-0576(97)82267-2.

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25

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 5 (May 1997): 65–68. http://dx.doi.org/10.1016/s0026-0576(97)82547-0.

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26

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 12 (December 1997): 45–48. http://dx.doi.org/10.1016/s0026-0576(97)82648-7.

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27

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 9 (September 1997): 84–87. http://dx.doi.org/10.1016/s0026-0576(97)85867-9.

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28

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 4 (April 1997): 65–69. http://dx.doi.org/10.1016/s0026-0576(97)86066-7.

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29

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 4 (April 1998): 62–65. http://dx.doi.org/10.1016/s0026-0576(97)86648-2.

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30

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 7 (July 1997): 42–45. http://dx.doi.org/10.1016/s0026-0576(97)87998-6.

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31

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 6 (June 1997): 121–24. http://dx.doi.org/10.1016/s0026-0576(97)88990-8.

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32

Trammell, Susan. "Quality Control." CFA Institute Magazine 25, no. 2 (March 2014): 29–33. http://dx.doi.org/10.2469/cfm.v25.n2.10.

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33

Flott, Leslie W. "Quality control." Metal Finishing 94, no. 5 (May 1996): 50–54. http://dx.doi.org/10.1016/s0026-0576(96)80028-6.

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34

Flott, Leslie W. "Quality control." Metal Finishing 94, no. 12 (December 1996): 52–55. http://dx.doi.org/10.1016/s0026-0576(96)80096-1.

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35

ROCKOFF, ALAN. "Quality Control." Skin & Allergy News 43, no. 6 (June 2012): 10. http://dx.doi.org/10.1016/s0037-6337(12)70224-3.

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36

McComb, Mark Anthony. "Quality Control." Technometrics 33, no. 4 (November 1991): 473–74. http://dx.doi.org/10.1080/00401706.1991.10484877.

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37

Doucet, Mia. "Quality Control." Mechanical Engineering 131, no. 03 (March 1, 2009): 32–33. http://dx.doi.org/10.1115/1.2009-mar-2.

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This review emphasizes on the importance of communication between business performing parties. According to a survey, many business owners who work with mainland Chinese suppliers report that consistent quality is their biggest challenge. The biggest challenge in doing business in China is quality, reliability, and delivery. The survey shows that though the cost is quite low, but that is part of the problem. Companies are constantly being disappointed by their Chinese suppliers because they are taking shortcuts that have not been approved to save money. This has resulted in product yield loss and reliability problems. According to an application engineer, most Westerners think that most Asians speak English, which is a big misunderstanding. The person who works in overseas marketing does, but the engineers and quality control people do not. Westerners make their presentations, unaware they are not being understood 100%. Asians have a lot of ideas, but it is hard to explain over the language barrier.

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38

Flott, Leslie W. "Quality control." Metal Finishing 94, no. 7 (July 1996): 37–40. http://dx.doi.org/10.1016/0026-0576(96)81358-4.

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39

Flott, Leslie W. "Quality control." Metal Finishing 94, no. 9 (September 1996): 76–122. http://dx.doi.org/10.1016/0026-0576(96)82108-8.

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40

Flott, Leslie W. "Quality control." Metal Finishing 94, no. 4 (April 1996): 66–68. http://dx.doi.org/10.1016/0026-0576(96)81270-0.

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41

Flott, Leslie W. "Quality control." Metal Finishing 95, no. 1 (January 1997): 68–71. http://dx.doi.org/10.1016/s0026-0576(97)94630-4.

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42

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 7 (July 1998): 40–44. http://dx.doi.org/10.1016/s0026-0576(98)80048-2.

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43

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 6 (June 1998): 129–31. http://dx.doi.org/10.1016/s0026-0576(98)80271-7.

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44

Flott, Leslie W. "Quality Control." Metal Finishing 96, no. 8 (August 1998): 47–50. http://dx.doi.org/10.1016/s0026-0576(98)80593-x.

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45

Flott, Leslie W. "Quality Control." Metal Finishing 96, no. 10 (October 1998): 53–55. http://dx.doi.org/10.1016/s0026-0576(98)80754-x.

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46

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 11 (November 1998): 60–63. http://dx.doi.org/10.1016/s0026-0576(98)80874-x.

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47

Flott, Leslie W. "Quality control." Metal Finishing 96, no. 12 (December 1998): 44–46. http://dx.doi.org/10.1016/s0026-0576(98)81278-6.

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48

Flott, Leslie W. "Quality Control." Metal Finishing 96, no. 9 (September 1998): 66–69. http://dx.doi.org/10.1016/s0026-0576(98)81483-9.

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49

Guajardo-Bernal, German. "Quality control." British Homeopathic Journal 83, no. 02 (April 1994): 127–28. http://dx.doi.org/10.1016/s0007-0785(94)80072-3.

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50

AVALLONE, E. M. "QUALITY CONTROL." Journal of the American Society for Naval Engineers 73, no. 1 (March 18, 2009): 115–20. http://dx.doi.org/10.1111/j.1559-3584.1961.tb02424.x.

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