Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether coronary occlusion causing transmural ischemia was accurately reflected by ST-segment elevation on routine electrocardiograms, intracoronary and surface electrocardiograms were simultaneously recorded during percutaneous transluminal coronary angioplasty (PTCA). The study group consisted of 54 patients who had intracoronary ST-segment elevation during transient coronary occlusion (left anterior descending [LAD]: 25 patients, left circumflex [LC]: 19 patients, right coronary artery: 12 patients). Elevation of the ST segment on the surface electrocardiogram (greater than or equal to 0.1 mV) was recorded in 84% of patients during LAD dilatation, in 32% of patients during LC dilatation (p less than 0.01 vs LAD and right), and in 92% of patients during right coronary dilatation (not significant vs LAD). The magnitude of intracoronary ST elevation was 1.10 +/- 0.8, 1.68 +/- 1.2 and 0.8 +/- 0.6 mV for the LAD, LC and right occlusions, respectively (not significant). Thus, despite the comparable magnitude of intracoronary ST elevation, LC occlusion resulted in ST-segment elevation on the surface electrocardiogram in significantly fewer patients than did LAD or right occlusion. During LC occlusion, 9 patients had no electrocardiographic changes and 4 had only precordial ST depression. Thus, in patients with transmural ischemia during right or LAD occlusions, concordant ST elevation on the surface electrocardiogram is common. In contrast, ST-segment elevation is an insensitive marker of LC occlusion. In patients with ongoing ischemic symptoms and isolated precordial ST depression or no repolarization abnormalities, LC occlusion should be considered in the differential diagnosis.
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PMID:Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion. 252 Nov 94

In dogs anesthetized with pentobarbital, the anterior descending coronary artery (LAD) was partially occluded to reduce LAD flow to about half of the original flow (partial occlusion). Myocardial pH (MpH) was measured by the use of a micro glass pH electrode. MpH decreased from 7.5-7.63 to 6.82-6.86 30 min after partial occlusion of the LAD. Nipradilol (0.3 mg/kg) was injected intravenously 30 min after partial occlusion, which continued for a further 60 min after nipradilol injection. Nipradilol decreased blood pressure and heart rate, and significantly increased myocardial pH which had been decreased by partial occlusion, within 60 min after injection. Nipradilol-induced restoration of the myocardial [H+] (calculated from the pH data), that had been increased by partial occlusion, was 48.5%. Bradycardia induced by nipradilol was not a determinant factor in the pH effect of nipradilol, because even in the paced heart, nipradilol restored the myocardial [H+] that had been increased by partial occlusion. These results indicate that nipradilol attenuates ischemia-induced myocardial acidosis, suggesting the favorable effect of nipradilol on ischemic myocardium. The favorable effect of nipradilol may be due to the beta-adrenoceptor antagonistic effect rather than the vasodilating effect.
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PMID:Nipradilol, a beta-adrenoceptor antagonist having a vasodilatory action, attenuates myocardial acidosis induced by coronary artery occlusion in dogs. 256 18

The effects of carvedilol, a new vasodilating beta-blocking drug, were studied in experimental pigs during short-term acute myocardial ischemia. In 21 anesthetized pigs 0.01, 0.03, and 0.1 mg/kg b.w. carvedilol was studied during repeated 2-min distal LAD-occlusions and a 60-min-period of ischemia. Left ventricular volume was continuously measured by the impedance catheter method. Intravenous administration of 0.01 mg/kg carvedilol resulted in a significant decrease of heart rate (-13%), dp/dtmax (-32%), and ejection fraction (-9%), slight changes of systolic pressure (-3%), and an increase of vascular resistance (+24%), indicating a beta-blocker effect without vasodilation-while the first vasodilatory effect was found at a dose of 0.1 mg/kg. During ischemia carvedilol had no influence on the time-course or the extent of systolic bulging of the ischemic myocardium, but the ischemia-induced decrease of left ventricular ejection fraction was diminished. Both during short-term ischemia, as well as during the 60-min-ischemia-period carvedilol significantly reduced ventricular premature beats. During the 60-min-ischemia-period activation delay measured from local DC-electrograms of the ischemic myocardium, as well as the occurrence of activation block were not altered by carvedilol, as was the incidence of ventricular fibrillation (69%). We conclude that at low dosages the beta-blocking effect of carvedilol exceeds the vasodilating properties. This may also hold true in patients with cardiac failure; they are more sensitive to beta-blocking drugs. During ischemia carvedilol slightly reduces the ischemia-dependent decrease of global ventricular function and it has an antiarrhythmic effect. Therefore, it may be protective in patients with acute myocardial infarction.
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PMID:Effects of carvedilol on left ventricular function and arrhythmias during repeated short-time myocardial ischemia in experimental pigs. 257 14

Eighteen patients with a first AMI, who during the acute ischemic phase did not develop ST segment elevation, but only positive or peaked T waves, are described. Patients who do not develop ST segment elevation during evolving anterior AMI represent a subgroup with a high probability of total obstruction of the LAD artery with retrograde filling via collateral vessels and a small degree of left ventricular dysfunction. We assume that during the period of total obstruction there was preexisting adequate collateral circulation in order to prevent transmural ischemia, which explains the absence of ST segment elevation.
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PMID:Acute anterior wall myocardial infarction presenting with positive T waves and without ST segment shift. Electrocardiographic features and angiographic correlation. 272 Dec 54

The effect of inhibition of glycolysis with sodium iodoacetate (IAA) on the changes induced by total ischemia was studied in canine left ventricle. Hearts were excised from phenobarbital anesthetized dogs and the circumflex (LCC) and anterior descending (LAD) branches of the left coronary artery were perfused in order to expose the LCC region to 48 mumol of IAA (about 1.5 mumol/g wet wt). The LAD regions of the same hearts served as untreated control myocardium. Hearts then were subjected to total ischemia in vitro at 37 degrees C. Metabolites, ultrastructure, and the capacity of thin incubated slices of heart to maintain volume and ion gradients were studied in the control and IAA-treated regions. Depletion of ATP to levels of 3-4% of control occurred in only 4-5 min of ischemia in the IAA-treated myocardium, but similar depletion required 90 min of total ischemia in untreated myocardium. These low levels of ATP were associated with marked contracture-rigor. Depletion of ATP in the IAA treated region was accompanied by a marked increase in adenosine levels in the tissue at the onset of rigor (approximately 5 min); at this time, as much as 50% of the adenine nucleotide pool (sigma Ad) was in the form of adenosine. In contrast, inosine was the predominant catabolite at 5 min in control myocardium, and only composed 16% of the sigma Ad pool. Thus, pretreatment with IAA produced an enormous acceleration in the rate at which the sigma Ad pool was consumed in totally ischemic myocardium. Lactate, the principal glycolytic intermediate which accumulates in totally ischemic tissue, was not formed in the IAA-treated heart. Moreover, IAA treatment did not accelerate the rate at which ultrastructural evidence of lethal injury developed in the poisoned myocytes. Thus, in a setting in which lactate accumulation did not occur, totally ischemic myocytes tolerated a very low level of high energy phosphate for a longer period of time than did untreated tissue before ultrastructural signs of cell death developed. The results indicate that marked ATP depletion, pe se, does not necessarily cause prompt sarcolemmal disruption.
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PMID:Total ischemia III: Effect of inhibition of anaerobic glycolysis. 273 29

Potassium loss from the myocardium during brief ischemic periods is well documented, but whether intrinsic myocardial mechanisms restore this loss during reperfusion is unclear. To address this question, we established a shunt from the coronary sinus to the right atrium in seven open-chest pigs. Shunt flow and arterial and coronary sinus potassium concentrations were measured continuously in order to determine myocardial potassium balance. Thirty, 60 and 120 s occlusions of the mid-LAD coronary artery were repeated four times each at 10 min intervals with reproducible metabolic and hemodynamic responses. A myocardial K+ reuptake amounting to 51 to 77% of K+ release during ischemia occurred between 20 and 140 s of reperfusion. The maximal rate of K+ reuptake was 1.4 (0.7 to 3.6), (median and 95% confidence interval), 4.3 (2.5 to 9.6) and 7.3 (4.9 to 13.4) mumol/100 g min after occlusion periods of 30, 60 and 120 s, respectively. Concomitant with the K+ reuptake a progressive rise in LV dP/dt occurred. Adrenoceptor stimulation could not explain these findings since catecholamine release declined during occlusion and reperfusion. We suggest that increased intracellular Na+ concentration in early reperfusion stimulates the Na,K-pump and favours Ca++ entry through Na+/Ca++ exchange, thereby mediating K+ reuptake and the rise in contractility.
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PMID:Myocardial K+ repletion and rise in contractility after brief ischemic periods in the pig. 279 61

We studied the efficacy of coronary angioplasty (PTCA) of the infarct-related artery in 29 patients with prior myocardial infarction by stress thallium scan. Twenty-seven patients had anterior myocardial infarction (single LAD disease), one had inferior (single RCA disease) and one had posterior (single LCX disease). According to the stress-redistribution thallium scintigraphic finding before PTCA, the patients were classified in 4 groups; (A): three patients with complete redistribution. (B): fourteen patients with incomplete redistribution. (C): seven patients with partial redistribution. (D): five patients with no redistribution. After PTCA, the parameters of residual ischemia in the infarct area (% RD and Thallium ischemic score = TIS) were improved significantly but those of infarct size (RD% uptake and Defect Score = DS) were improved slightly in group A. In group B and C, % RD, TIS, RD% uptake and DS were all improved significantly. In group D, TIS was improved slightly and DS was improved slowly 3 months after PTCA. Group A had high probability of viable muscle and group D had high probability of scar at the infarct zone. Group B and C showed intermediate type between group A and D. The change of infarct area after PTCA was variable in 4 groups but both residual ischemia and infarct size decreased in all groups. Thus, PTCA of infarct-related coronary artery is useful even in the patients with prior myocardial infarction.
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PMID:[Usefulness of coronary angioplasty (PTCA) of the infarct-related artery in patients with prior myocardial infarction--follow up of infarct zone pre- and post-angioplasty by stress thallium scan]. 281 Sep 2

The effect of beta-adrenoceptor blockade and activation on ischemic regional and microregional myocardial O2 supply/consumption parameters was assessed in 28 open chest, anesthetized dogs. Ten minutes after LAD occlusion, dogs were given i.v. saline, 2 mg/kg propranolol, 0.2 mg/kg pindolol, or 1 microgram/kg per min isoproterenol. Coronary blood flow was determined using radioactive microspheres before and 2 h after LAD occlusion while O2 supply/consumption parameters were determined using microspectrophotometry. Ischemia resulted in a 66% reduction in subendocardial flow in controls in the ischemic zone and no experimental treatment significantly altered this flow. Pindolol resulted in a significant improvement in the ischemic regional subendocardial/subepicardial flow ratio (from 0.69 in the control ischemic region to 0.88 during pindolol treatment). O2 extractions were significantly increased and O2 consumptions were significantly depressed in the ischemic regions of all groups. O2 extractions were increased to a lesser degree in the ischemic region with the use of pindolol and propranolol. Propranolol and pindolol both significantly decreased the proportion of veins with low (0-20%) O2 saturations in the ischemic region indicating an improved microregional distribution of blood flow and/or O2 consumption within the ischemic region.
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PMID:Beta-adrenoceptor stimulation and blockade during myocardial ischemia in dogs: effect on cardiac O2 supply and consumption. 289 41

Hypoxia in isolated myocytes results in accumulation of long-chain acylcarnitines (LCA) in sarcolemma. Inhibition of carnitine acyltransferase I (CAT-I) with sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA) prevents both the accumulation of LCA in the sarcolemma and the initial electrophysiologic derangements associated with hypoxia. Another amphiphilic metabolite, lysophosphatidylcholine (LPC), accumulates in the ischemic heart in vivo, in part because of inhibition of its catabolism by accumulating LCA. It induces electrophysiologic alterations in vitro analogous to early changes induced by ischemia in vivo. The present study was performed to determine whether POCA could prevent accumulation of both LCA and LPC induced by ischemia in vivo and if so, whether attenuation of early arrhythmogenesis would result. LAD coronary artery occlusions were induced for 5 min in chloralose-anesthetized cats. Coronary occlusion in untreated control animals elicited prompt, threefold increases of LCA (73 +/- 8 to 286 +/- 60 pmol/mg protein) and twofold increase of LPC (3.3 +/- 0.4 to 7.5 +/- 0.9 nmol/mg protein) selectively in the ischemic zone, associated with ventricular tachycardia (VT) or ventricular fibrillation (VF) occurring within the 5-min interval before acquisition of myocardial samples in 64% of the animals. POCA prevented the increase of both LCA and LPC. It also prevented the early occurrence of VT or VF (within 5 min of occlusion) in all animals studied. The antiarrhythmic effect of POCA was not attributable to favorable hemodynamic changes or to changes in myocardial perfusion measured with radiolabeled microspheres. Thus, inhibition of CAT-I effectively reduced the incidence of lethal arrhythmias induced early after the onset of ischemia. Accordingly, pharmacologic inhibition of this enzyme provides a promising approach for prophylaxis of sudden cardiac death, that typically occurs very soon after the onset of acute ischemia, in man.
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PMID:Prophylaxis of early ventricular fibrillation by inhibition of acylcarnitine accumulation. 292 26

Fourteen mongrel dogs were anesthetized and instrumented to measure arterial pressure (AP), left ventricular pressure (LVP), aortic blood flow, and heart rate (HR). Hydraulic occluders were placed around the left anterior descending (LAD, n = 9) and left circumflex (LCC, n = 14) coronary arteries. A bilateral carotid occlusion (BCO) was made before and during either anterior (LAD occlusion) or posterior (LCC occlusion) ischemia. Posterior ischemia significantly (P less than 0.01) reduced the BCO-induced increases in mean AP (by 44.3 +/- 7.3%), systolic LVP (by 65.5 +/- 6.9%), first derivative of LVP (dLVP/dt, by 95.7 +/- 44.3%), and aortic resistance (by 117.7 +/- 26.9%). In contrast, anterior ischemia failed to alter significantly the hemodynamic response to BCO. Bilateral vagotomy attenuated or eliminated many of the effects of posterior ischemia on the BCO response. In fact, the change in aortic resistance was no longer affected by the ischemia and increased to the same extent, as noted during the control BCO. However, mean AP (38.7 +/- 6.8%), systolic LVP (40.3 +/- 8.7%), and dLVP/dt (62.4 +/- 11.0%) remained significantly reduced when compared with the control (no coronary occlusion) response. These data suggest that 1) posterior ischemia elicits a greater reduction in the BCO response than anterior ischemia, and 2) vagal afferents as well as depression of contractile function may both contribute to the BCO response inhibition noted during posterior ischemia.
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PMID:Effect of myocardial ischemia on hemodynamic response to carotid occlusion. 292 33


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