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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The threshold of the initiation of myocardial ischemia was determined for conscious rabbits with the help of a special preliminary implanted appliance, which made it possible to perform the occlusion and reperfusion of the coronary artery. Nitroglycerin and propranolol were shown to increase the threshold of the initiation of ischemia, while dipyridamole was discovered to reduce it. The method described is offered for evaluation of the drug antianginal effect, since it is adequate and easily reproduced.
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PMID:[Evaluation of the antianginal action of pharmacological substances by the change in the initiation threshold for myocardial ischemia in conscious rabbits]. 643 58

The effects of intravenous dipyridamole (20 mg) and sublingual nitroglycerin (0.6 mg) were compared at rest and during rapid atrial pacing in patients with significant coronary obstruction. Dipyridamole, which had no significant effect on resting systolic blood pressure, caused a significant increase in coronary sinus flow (CSF) and reduction of coronary vascular resistance (CVR) and arterial-coronary sinus oxygen difference (AO2CSO2 delta), whereas nitroglycerin reduced resting systolic pressure but had no significant effect on CSF, CVR, or AO2-CSO2 delta. Although theses effects of dipyridamole and nitroglycerin on resting systolic pressure, CSF, CVR, and AO2-CSO2 delta were qualitatively similar during rapid atrial pacing, the onset of chest pain and ischemic ECG changes occurred at a lower heart rate following dipyridamole (136 +/- 5 beats/min) than following nitroglycerin (149 +/- 6 beats/min, p less than 0.01). However, maximal double product and myocardial oxygen consumption achieved during pacing were similar following both dipyridamole and nitroglycerin and were less than control pacing values. Coronary dilatation following dipyridamole appears to reduce tolerance to pacing-induced ischemia probably by maldistribution of coronary flow away from ischemic myocardium. Nitroglycerin differs from dipyridamole by improving tolerance to pacing; however, this difference appears to be due to systemic vasodilator effects of nitroglycerin rather than to enhancement of flow to ischemic myocardium.
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PMID:Comparative effect of intravenous dipyridamole and sublingual nitroglycerin on coronary hemodynamics and myocardial metabolism at rest and during atrial pacing in patients with coronary artery disease. 678 Feb 57

The present study was performed to compare hemodynamic effect of intravenous Nitroglycerin (TNT i.v.) in 14 patients developing acute hypertension (Group I) and in 7 non hypertensives after open heart surgery (Group II). In all patients, m.a. 56.6 yrs, (10 mitral and/or aortic prosthetic valve replacements, 9 aorto-coronary bypass, 1 open mitral commissurotomy, 1 closure of atrial septal defect) TNT was infused at doses of 0.5, 1, 2 microgram X kg X min. and subsequently at 2 microgram X kg X min. after volume administration (2 + V.A.) to maintain right and left atrial pressure the same as control (P = N.S.). Mean arterial, right and left atrial pressures (MAP, RAP, LAP), cardiac frequency and index (CF, CI and systemic vascular resistance index (SVRI) were monitorized. TNT i.v. resulted in hypertensive patients (Group I) in reduction vs. control of: a) RAP (--20.17%) and LAP (--20.58%) at 0.5 microgram X kg X min. b) RAP (--26.13%), LAP (--27.50%), MAP (--19.94%) and CI (--12.98%) at 1 microgram X kg X X min. c) RAP (--22.47%), LAP (--26.89%), MAP (--24.68%), CI (--12.6%) and SVRI (--17.34%) at 2 microgram X kg X min. When RAP and LAP was maintained by volume administration TNT i.v. (2 microgram X kg X min.) resulted in an even greater increase in CI and a greater decrease in MAP and SVRI ((--22.04% and --24.88% respectively). No significant hemodynamic modification (P less than or equal to 0.05) were observed in non hypertensive patients (Group II) at all doses of TNT i.v. The results confirm a predominant venodilator effect of TNT at low doses and a good effect on arterial resistances at high doses in hypertensive patients. In view of previous reports of differing effects on ischemia TNT i.v. may be preferable to other vasodilator drugs for control of acute post-ECG hypertension, only on condition to maintain an adequate left ventricular filling pressure to prevent a fall of cardiac index. Moreover the absence of significant (P less than or equal to 0.05) hemodynamic modifications in non hypertensive patients may be a further advantage in the treatment of myocardial ischemia with i.v. TNT.
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PMID:[Effect of intravenous nytroglicerin in hypertensive patients during and after open heart surgery (author's transl)]. 678 Apr 1

In acute experiments on open-chest dogs nitroglycerin (5 microgram/kg, i.v.) was injected 1 minute before a 60-second occlusion of the descending branch of the left coronary artery. At the height of ischemia nitroglycerin increased oxygen tension and produced a lowering of contractility of the deep and superficial layers of the myocardium adjacent to the zone of ischemia, this lowering was less as compared to that seen in control occlusions. Nitroglycerin did not produce marked or significant changes in oxygen tension and myocardial contractility in the central ischemic or distant areas. No significant changes in the hemodynamics were recorded either.
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PMID:[Effect of nitroglycerin on myocardial function in short-term ischemia]. 681 64

It has been established that malonate-like action of isoquinoline derivatives (papaverine and nospan) on respiratory function of myocardial mitochondria leads to inhibition of the accumulation rate of Ca2+ by these organelles on the use of glutamate and alpha-ketoglutarate as substrates. A greater inhibition of Ca2+ transport rate in the mitochondria is observed in the presence of glutamate. It has been validated theoretically that the decreased intensity of Ca2+ accumulation is aimed at protecting the mitochondria from irreversible lesions in ischemia. Nitroglycerin and sodium nitrite do not affect Ca2+ exchange in the mitochondria.
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PMID:[Protection of myocardial mitochondria from penetration by calcium ions using isoquinoline and phenothiazine derivatives]. 726 1

It is known that intravenous administration of dipyridamole can induce chest pain and ECG signs of ischemia in patients with coronary artery disease. In the present study we evaluated ECG and hemodynamic changes in response to dipyridamole (0.56 mg/kg in 10 min) under basal conditions and 3 hours after administration of nitroglycerin (10 mg/24 h patch) in 14 patients with coronary artery disease. The effects of nitroglycerin were also compared to those induced by the same drug on a bicycle stress test in the same patients. Exercise stress test induced specific ST changes in all patients when performed off-drug. Nitroglycerin administration completely prevented exercise-induced ischemia in 2 patients, and significantly prolonged exercise time in the remaining patients (p < 0.01). This effect was accompanied by a significant increase in heart rate (HR) and rate-pressure product at the threshold of ischemia (HRBP, p < 0.01); furthermore we observed a significant increase in HR at the maximal work load (p < 0.05). In the absence of treatment, dipyridamole infusion induced ST segment changes and/or typical chest pain in 12/14 patients. Moreover we observed a significant increase (p < 0.05) in HR, BP and HRBP during the test with respect to basal conditions. Following nitroglycerin administration, dipyridamole infusion failed to induce ischemia in 4 patients, and the time to ST depression in the remaining 8 patients (459 +/- 69 vs 610 +/- 127 s; p < 0.05) was significantly prolonged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ECG-dipyridamole and ECG-exercise test in the assessment of ischemic cardiopathy: effects of the acute administration of nitroglycerin]. 755 92

To determine the role of the vasoconstrictor peptide endothelin-1 in cardiopulmonary bypass in neonates, we measured plasma endothelin-1 concentrations in infants before and after cardiopulmonary bypass for arterial switch procedures and studied the effects of endothelin-1 on coronary tone and contractility in normal and reperfused neonatal pig hearts. Endothelin-1 blood concentrations (picograms per milliliter, mean +/- standard error) were significantly higher in neonates with arterial transposition and in umbilical venous blood (22.9 +/- 2.3 and 19.2 +/- 2.9, respectively) than in older children with atrial septal defects (13.2 +/- 1.6) or in healthy adults (10.7 +/- 2.5). After cardiopulmonary bypass, endothelin-1 concentrations increased 29% in neonates undergoing arterial switch procedure and 28% in children undergoing atrial septal defect repair (p < 0.05 versus before bypass). In isolated, blood-perfused neonatal pig hearts, endothelin-1 had dose-related coronary constrictor and inotropic effects between 25 and 100 pmol. Endothelin-1 concentrations that did not increase coronary perfusion pressure (5 to 10 pmol) caused significant coronary constriction in the presence of norepinephrine (10 nmol/L). During reperfusion after 30 minutes of global normothermic ischemia, the coronary vasoconstrictor effects of both endothelin-1 alone and endothelin-1 plus norepinephrine were significantly enhanced. Nitroglycerin reversed vasoconstriction produced by endothelin-1 and endothelin-1 plus norepinephrine both before and after ischemia-reperfusion. We conclude that endothelin-1 concentrations are significantly elevated in neonates and are further increased after cardiopulmonary bypass. Coronary vasoconstriction caused by endothelin-1 is enhanced by ischemia-reperfusion and by norepinephrine present in concentrations typically observed after neonatal cardiopulmonary bypass. Nitroglycerin reverses coronary vasoconstriction induced by endothelin-1 and may therefore be beneficial in the postoperative management of neonates after cardiac operations.
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PMID:Coronary vasoconstriction mediated by endothelin-1 in neonates. Reversal by nitroglycerin. 781 11

Nitroglycerin (NTG) spray and sublingual tablets rapidly relieve an established attack of angina, and their infrequent use is not associated with the development of tolerance. Although, following a suitable nitrate-free interval, the first dose of oral, long-acting nitrates produces significant hemodynamic effects, increases angina free walking, and decreases exercise-induced ischemia, during continued long-term therapy tolerance limits their usefulness. Appropriate dosing regimens of controlled-release formulations of isosorbide dinitrate (ISDN) and controlled-release NTG during long-term therapy have not been established. Use of immediate-release formulation of 15-120 mg of ISDN in a qid regimen lead to a marked reduction in the size and duration of antianginal effects compared to the initial dose. Asymmetric tid therapy with 30 mg of ISDN (7 a.m., 1 p.m., and 6 p.m.) is also associated with the development of partial tolerance and appears to provide antianginal prophylaxis for only a period of 6 hours each day. Asymmetric bid therapy with ISDN at 7 a.m. and noon may give sustained effect but is supported by only a single, small study that did not examine effectiveness after the noon dose in long-term use. Isosorbide-5-mononitrate (IS-5-MN) has been the subject of more recent studies than other nitrates because of attempts to bring a number of products into the U.S. market. IS-5-MN in qid, tid, and standard bid (8 a.m. and 8 p.m.) dosing regimens produce tolerance. Asymmetric regimens of immediate-release IS-5-MN (10 and 20 mg) given bid (once in the morning and again 7 hours later) decrease the development of tolerance compared to symmetric regimens and produce an increased exercise duration after each dose of the day; the 20 mg bid dosing is more effective. Similarly, once-daily 120 and 240 mg controlled-release IS-5-MN does not produce tolerance and gives a sustained increase in daytime exercise duration. Both asymmetric bid immediate-release and once-daily controlled-release IS-5-MN preparations do not produce deterioration in exercise performance prior to the administration of the medication in the morning (i.e., no zero-hour effect). Further studies are needed to establish useful dosing regimens for ISDN, for controlled-release ISDN, and for controlled-release nitroglycerin. None of the dosing regimens of any oral, long-acting nitrate (including IS-5-MN) provide 24 hour antianginal and antiischemic effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Short and long-acting oral nitrates for stable angina pectoris. 784 96

We studied 30 patients with cirrhosis to determine the effect of nitroglycerin on portal and gastric mucosal hemodynamics. Systemic hemodynamics, portal venous pressure (PVP), the hemoglobin index (IHB), and the oxygen saturation index (ISO2) of the gastric mucosa were measured before and after a continuous infusion of nitroglycerin. The patients were divided into two groups according to the presence or absence of major portal-systemic collateral routes on portograms. Nitroglycerin caused a reduction in PVP in all patients. Although there was no significant difference in systemic hemodynamic changes between the two groups, the reduction in PVP in patients with major portal-systemic collaterals was significantly higher than in those without major collaterals. A nitroglycerin infusion, at a dose of 1.0 micrograms/kg per min for 10 min, produced a reduction in both IHB (-16%, P < 0.001) and ISO2 (-13%, P < 0.001) in the gastric mucosa, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. These findings suggest that the continuous infusion of nitroglycerin reduces PVP in cirrhotic patients, particularly in those with major portal-systemic collaterals, and reduces the congestion of the gastric mucosa in patients with portal hypertension.
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PMID:Influence of nitroglycerin on portal pressure and gastric mucosal hemodynamics in patients with cirrhosis. 801 7

It has recently been shown that ischemia in collateral-dependent myocardium may develop at a very variable threshold in anginal patients; accordingly, the aim of this study was to assess whether nifedipine and diltiazem can increase blood flow to collateralized myocardium in man. Nine patients with complete coronary occlusion filled by collaterals, with no other coronary stenosis, normal left ventricular function, and reproducibly positive exercise tests were studied. They underwent exercise tests off therapy and after acute randomized administration of nifedipine (10 mg sublingually), diltiazem (120 mg orally), and nitroglycerin (0.5 mg sublingually), the latter a drug known to increase blood flow to collateralized myocardium. Following nifedipine, time to 1 mm ST segment depression increased significantly (from 430 +/- 176 to 576 +/- 205 seconds, p < 0.01), while heart rate and rate-pressure product remained unchanged (115 +/- 16 vs 121 +/- 17 beats/min and 199 +/- 29 vs 204 +/- 44 beats/min.mm Hg.10(2), respectively, p = NS for both). Similarly, diltiazem significantly increased time to ischemic threshold from baseline to 638 +/- 125 seconds (p < 0.01), but did not change heart rate and rate-pressure product at 1 mm ST segment depression. Submaximal rate-pressure products were significantly lowered by both nifedipine and diltiazem. Nitroglycerin not only significantly improved time to ischemic threshold (from baseline to 666 +/- 76 seconds, p < 0.01), but also increased heart rate (from baseline to 137 +/- 16 beats/min, p < 0.01) and rate-pressure product (from baseline to 242 +/- 48 beats/min.mm Hg.10(2), p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemia in collateral-dependent myocardium: effects of nifedipine and diltiazem in man. 832 95


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