Effects of Diltiazem on Lactate, ATP, and Cytosolic Free Calcium Levels in Ischemic Hearts

Watts, John A.; Norris, Thomas A.; London, Robert E.; Steenbergen, Charles; Murphy, Elizabeth

doi:10.1097/00005344-199001000-00007

Cited by 30 publications

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“…DZ prevention of both hepatocyte vented both adenosine triphosphate depletion and rise of [Ca 2/ ] i in ischemic hearts. 19 The stress response to hypovo-lipid peroxidation and GSH oxidation indicated a particular role of increased Ca 2/ uptake in hepatocyte oxidant injury lemic shock releases a variety of Ca 2/ -mobilizing hormones by endocrine and proinflammatory cascades. 20 Alpha-adren-after hemorrhagic shock/resuscitation.…”

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confidence: 99%

Altered hepatocellular Ca2+ regulation during hemorrhagic shock and resuscitation

Rose¹

1997

Hepatology

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reperfusion events and septic injury altered intracellular The present study evaluated the effect of the benzothiCa 2/ homeostasis. 2 Whereas disturbance of cellular Ca 2/ regazepine Ca 2/ channel blocker diltiazem (DZ) on altered ulation is a well-studied mechanism of cellular dysfunction hepatocellular Ca 2/ regulation and oxidant injury durin excitable cells, there is growing evidence that these ing hemorrhagic shock/resuscitation. In anesthetized, changes also occur in parenchymal and endothelial cells. 3 male Sprague-Dawley rats, hemorrhagic shock was inPrevious studies showed significantly increased intracellular duced by rapid blood withdrawal and maintaining the Ca 2/ concentrations in hepatocytes isolated from rats undermean arterial blood pressure at 40 mm Hg over 60 mingoing endotoxic shock, 4 intraabdominal gram-negative seputes. Rats were then resuscitated with 60% of shed blood sis 5 or ischemia because of hemorrhage. 6 Moreover, these and and threefold the shed blood volume of Ringer's lactate.other studies also reported a protective effect by the benzothiAt the end of ischemia, and 60 or 300 minutes after resus- (Goedecke, Freiburg, Germany).Received May 29, 1996; accepted October 14, 1996. Hemorrhagic shock was induced by withdrawing 2.5 mL blood/kg as Ringer's lactate during the first 60 minutes. During the second

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confidence: 99%

Altered hepatocellular Ca2+ regulation during hemorrhagic shock and resuscitation

Rose¹

1997

Hepatology

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“…1 Our data shows that pretreatment with a calcium channel blocker protects the myocardium against mechanical dysfunction and calcium overload during ischemia, as previously reported. 2,3,7 However, our data also indicate that the protective effect of pretreatment with calcium channel blockers was blunted by compensation for their negative inotropic effects. Calcium overload during the late phase of 30-min ischemia and the early phase of reperfusion was eliminated by clentiazem, but only when the negative inotropic effects of the drug were uncompensated.…”

Section: Discussionmentioning

confidence: 49%

“…6 Considered together, it is reasonable to hypothesize that calcium channel blockers inhibit the increase in intracellular Ca 2+ concentration ([Ca 2+ ]i) during ischemia and/or reperfusion, and thereby protect myocardium against post-ischemic mechanical failure. A recent study 7 supports this hypothesis, but it remains unclear whether or not calcium channel blockers have an intrinsic benefit above and beyond that associated with the reduction of Ca 2+ entry due to pretreatment.…”

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confidence: 99%

Mechanism for the Cardioprotective Effects of the Calcium Channel Blocker Clentiazem During Ischemia and Reperfusion

et al. 1998

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“…However, the predominant evidence is that these agents significantly and consistently affect systemic haemodynamics without affecting coronary blood flow [15,28]. On the other hand, Nicorandil increases coronary blood flow and does not significantly affect systemic haemodynamics.…”

Section: Discussionmentioning

confidence: 99%

Nicorandil suppressed myocardial purine metabolism during exercise in patients with angina pectoris

Oginö

Osaki

Noguchi

et al. 1995

Eur J Clin Pharmacol

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To elucidate the effect of Nicorandil on myocardial energy metabolism and myocardial sympathetic activity, we administered Nicorandil orally to eight patients with angina pectoris prior to exercise testing. Arterial and coronary sinus levels of lactate, ammonia, hypoxanthine (HX), adrenaline and noradrenaline were measured during exercise in order to determine the irrespective myocardial extraction ratios (MER). Compared to placebo, Nicorandil increased the time to development of significant ST depression (322 vs 390 s) while decreasing the maximum amplitude of ST depression (0.244 vs 0.216 mV). Heart rate, systolic blood pressure, and the rate pressure product during exercise were not significantly affected. The MER of lactate, measured during exercise, was significantly higher after Nicorandil than placebo (13.6 vs 27.9). Similarly, the MERs of ammonia and HX were significantly higher after Nicorandil (-46.0 vs 7.4% and -47.0 vs 9.9% respectively). Nicorandil, had no apparent effect on myocardial sympathetic activity as the MERs of adrenaline and noradrenaline were essentially unaffected. We conclude that Nicorandil decreased myocardial ischaemia and suppressed myocardial accelerated purine metabolism (a marker of cellular energy metabolism) during exercise in patients with angina pectoris. This effect appears not to be related to myocardial sympathetic activity.

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Effects of Diltiazem on Lactate, ATP, and Cytosolic Free Calcium Levels in Ischemic Hearts

Cited by 30 publications

References 0 publications

Altered hepatocellular Ca2+ regulation during hemorrhagic shock and resuscitation

Altered hepatocellular Ca2+ regulation during hemorrhagic shock and resuscitation

Mechanism for the Cardioprotective Effects of the Calcium Channel Blocker Clentiazem During Ischemia and Reperfusion

Nicorandil suppressed myocardial purine metabolism during exercise in patients with angina pectoris

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