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)

Myocardial pH was measured continuously with a micro pH electrode inserted into the left ventricular wall in dogs. Anterior descending coronary flow was reduced to about 1/3 of the original flow by partial occlusion of the coronary artery. Myocardial pH decreased from 7.50--7.60 to 7.06--7.24 after partial occlusion. Drugs were injected intravenously during ischemia of the heart caused by partial occlusion. l-Propranolol (1 mg/kg) reduced heart rate and increased the pH from 7.06 +/- 0.04 to 7.48 +/- 0.04 (P less than 0.01). d-Propranolol (1 mg/kg) reduced heart non-significantly and increased the pH from 7.24 +/- 0.05 TO 7.56 +/- 0.05 significantly (P less than 0.05). In other studies, the effect of l- and d-propranolol on both heart rate and metabolic responses to isoproterenol (500 micrograms/kg i.p.) was studied. Isoproterenol increased heart rate and also elevated the blood levels of glucose and lactate. l-Propranolol inhibited these responses to isoproterenol. d-Propranolol did not inhibit the heart rate response but inhibited the blood lactate response to isoproterenol significantly. The blood glucose response to isoproterenol was inhibited by d-propranolol non-significantly. The action of both l- and d-propranolol on ischemic myocardial pH may be related to their action on cardiac metabolism as well as to their local anesthetic action.
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PMID:Increase of myocardial pH by 1- and d-propranolol during ischemia of the heart in dogs. 624 50

This light microscopic autoradiographic study was performed to test the hypotheses that (a) the density of beta adrenergic receptors (BAR) may differ in various components of the heart and (b) BAR in certain components of the heart may exhibit a selective response to pharmacologic and pathological stimuli. Blocks of canine left ventricle were frozen and tissue sections cut and incubated in (-)[3H]dihydroalprenolol (DHA) to label the BAR. For total and nonspecific binding, serial sections were incubated with and without 10(-5) M (+/-)propranolol. Scintillation spectrometry of sections demonstrated rapid binding, saturability, stereospecificity, a dissociation constant (KD) of 3.2 +/- 0.5 nM (SD) (n = 3), and a maximal binding of 31.3 +/- 3.1 fmol/mg of tissue protein. Isoproterenol was 12.5 times more effective than norepinephrine in displacing DHA. Sections incubated with 10(-5) - 10(-8) M metoprolol, a beta one selective antagonist, demonstrated a KD of 0.7 X 10(-6) M. For autoradiography, emulsion-coated coverslips were attached to the slides. After exposure, the slides were developed and stained, and grain density quantified. Specific BAR binding (n = 4 dogs) was 1,047 +/- 131 (SEM) grains/10(-2) mm2 for myocardial arterioles, 219 +/- 30 for myocardial arteries, 31 +/- 12 for the proximal left anterior descending coronary artery (LAD), and 231 +/- 34 for cardiac myocytes. Specific binding in the presence of 10(-5) M metoprolol was reduced approximately 75% for both arterioles and myocytes. However, at 10(-6) M metoprolol, the percent reduction in specific DHA binding was greater for myocytes (50%) than for arterioles (0%), and at 10(-7) M metoprolol, the percent reduction in specific DHA binding was 17% for myocytes with no reduction over arterioles. After 1 h of LAD occlusion, a selective increase (18%) in BAR density occurred over cardiac myocytes, but not over blood vessels in the ischemic myocardium. Thus, (a) specific BAR binding was five times greater in arterioles than in small arteries and myocardium and 34 times greater than in the proximal LAD; (b) BAR of myocytes were more sensitive than those of arterioles to displacement by the beta one selective antagonist, metoprolol; and (c) a selective increase in BAR occurs in cardiac myocytes but not in blood vessels after 1 h of ischemia in this experimental model.
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PMID:Autoradiographic characterization of beta adrenergic receptors in coronary blood vessels and myocytes in normal and ischemic myocardium of the canine heart. 632 53

The adenylate cyclase activity was determined in the left ventricles of rat hearts up to 60 min after severe ischemia and 24 hours after injection of a high dose of isoproterenol. The quantitative data show a progressive decline in the activity after 20 min of ischemia. Isoproterenol- and fluoride-stimulated activities were influenced in the same manner. The cytochemical localization showed no changes in the localization of the enzyme. But the number of cells with reaction products of the adenylate cyclase activity were decreased. The quantitative analysis of the adenylate cyclase activity in the myocardial necrosis produced by a single injection of 80 mg isoproterenol per kg body weight showed no changes in the basal activity of the enzyme however a significant reduction of the isoproterenol stimulation and a slight decrease of the fluoride-stimulated activity compared to the non-necrotic area of the same left ventricle. In cytochemical investigations no reaction of the adenylate cyclase activity was found in the centre of the necroses. But in the border zone of the basis the reaction product of the plasma membrane of the sarcolemma the main localization site of the enzyme activity was failed whereas the activity of the junctional SR was preserved. It was concluded that this activity is responsible for the unchanged basal activity in the necrotic and non-necrotic area.
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PMID:[Behavior of adenylate cyclase in ischemic and necrotic myocardial tissue]. 642 38

To assess regional ventricular wall thickening, we studied 8 open-chest dogs using digital intravenous ventriculography at a control stage, after subtotal and total coronary occlusion, and then after isoproterenol administration. In 3 dogs, 2 pairs of myocardial thickness crystals were implanted. Correlations of measures of wall thickness and percentage of wall thickening with crystal measures were excellent at the base (r greater than or equal to 0.97) and near the apex (r greater than or equal to 0.97). Four areas of the inferoapical wall muscle were measured: the base, mid-wall, distal wall, and apex. Four chamber dimensions were also examined: the long axis, base decreased with ischemia. At completion occlusion, it was -24.6 +/- 6% at the base, -27.3 +/- 5% at the mid-wall, -27.1 +/- 5% at the distal wall, and -24.7 +/- 5% at the apex. Percent thickening decreased with occlusion, although greater at the base and mid-wall than at the distal wall and apex. With isoproterenol, end-diastolic thickness increased only at the apex, with little change at the base, distal wall, and mid-wall. Percent thickening increased. In general, ischemia produced increases in end-diastolic hemichords with little change in the long axis. Isoproterenol reduced the hemichords, although the long axis did not change. We conclude the digital intravenous ventriculograms can be used to assess changes in wall thickness with high degrees of accuracy. Asymmetric thickening occurred at rest, with ischemia and with inotropic stimulation, being greatest at the apex and least at the base.
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PMID:Digital intravenous ventriculography: analysis and validation of wall thickness changes during ischemia and inotropic stimulation in dogs. 712 47

Neurologic and abdominal complications can occur in the postoperative period of aortic coarctation repair, ischemia being the pathogenic factor most likely to be involved. This study was designed to evaluate the extent of the hemodynamic changes proximal and distal to the coarctation at the time of cross-clamping, as well as the effects of pentolinium and isoproterenol upon the hemodynamic changes. Included in the study were 17 patients with adult type coarctations who had dual hemodynamic monitoring. During cross-clamping, there was an increase in the gradient between proximal and distal pressures, with severe distal hypotension (< 50 mm Hg) occurring in six patients. Isoproterenol corrected the hypotension in five patients, but the sixth required a surgical shunt. Pentolinium was effective for the treatment of proximal hypertension; however, it also decreased distal pressure. The ligation of collateral vessels was associated with a decrease in distal pressures as well. During cross-clamping, pentolinium was useful for the management of proximal hypertension and isoproterenol increased the distal pressures in some of the patients who presented distal hypotension. However, because of the difficulties in predicting the individual response, their administration would be best guided by dual pressure monitoring. It is postulated that the recognition and proper treatment of distal hypotension may be an important factor in the prophylaxis of postoperative complications.
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PMID:Technical and pharmacologic management of distal hypotension during repair of coarctation of the aorta. 740 68

The oxidation of [3-13C]pyruvate and [3-13C]propionate was studied in vivo in infused rats. The infused [3-13C]pyruvate was quickly converted to [3-13C]lactate in the blood, and the [3-13C]lactate formed was well metabolized in both normoxic and ischaemic hearts. Large differences (200-600%) in the 13C enrichment of alanine (C-3) and acetyl-CoA (C-2) compared with lactate (C-3) were found in both normoxic and ischaemic hearts, suggesting that the extracellular [3-13C]lactate preferentially entered a region of the cytoplasm which specifically transfers the labelled pyruvate (formed from [3-13C]lactate) to the mitochondria. The highly enriched mitochondrial pyruvate gave high enrichment in alanine and acetyl-CoA, which was detected by 1H- and 13C-NMR spectroscopy. Ischaemia increased 13C incorporation into the main cytoplasmic lactate pool and decreased 13C incorporation into citric acid cycle intermediates, mainly decreasing the pyruvate anaplerosis. Isoprenaline-induced ischaemia of the heart caused only a slight decrease in pyruvate oxidation. In contrast to the decreased anaplerosis of pyruvate, the anaplerosis of propionate (and propionyl-carnitine) increased significantly in ischaemic hearts, which may contribute to the protective effect of propionyl-carnitine seen in ischaemia. In addition, we found that [3-13C]propionate preferentially labelled aspartate C-3 in rat heart, suggesting incomplete randomization of label in the succinyl-CoA-malate span of the citric acid cycle. These data show that proton observed 13C edited spectroscopic methods, i.e. heteronuclear spin-echo and the one-dimensional heteronuclear multiple quantum coherence sequence, can be successfully used to study heart metabolism in vivo.
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PMID:Metabolism of [3-13C]pyruvate and [3-13C]propionate in normal and ischaemic rat heart in vivo: 1H- and 13C-NMR studies. 749 38

Effects of "ischemia" and adrenergic agonists on pacemaker current I(f) were observed in sheep cardiac Purkinje fibers. After perfusion with ischemia-mimic solution for 15, 30 and 60 min, the amplitude of I(f) current were decreased at all membrane potential levels between Ec-60 mV to -120 mV (n = 7, P < 0.05), activation time and half activation time to a steady state value of I(f) current were prolonged (n = 7, P < 0.05), activation curve of I(f) shifted to a more hyperpolarized position. Isoproterenol 1 x 10(-6) mol/L increased amplitude of I(f) current (n = 10, P < 0.05), shortened the activation time and half activation time (n = 10, P > 0.05), and shifted the activation curve to a more depolarized position; but isoproterenol of 1 x 10(-6) mol/L could not completely reverse the inhibitory effects of "ischemia" on I(f) current. In the presence of 5 x 10(-7) mol/L propranolol the effects of phenylephrine 5 x 10(-5) mol/L on I(f) current was variable; but aggravated the inhibitory effects of I(f) current due to "ischemia". The above results indicate that normal pacemaker activity of ventricular Purkinje fibers does not increase but rather decrease during myocardial ischemia-mimic condition, an observation suggesting that acute ischemic ventricular arrhythmia may not be due to abnormal strengthening of normal ventricular pacemaker activity.
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PMID:[An observation on the pacemaker current I(f) in sheep cardiac Purkinje fibers under ischemia-mimic condition]. 757 Jan 4

To determine the role of various Na+ transport systems in the edema fluid accumulation after ischemia and reperfusion in the lung, we evaluated the effect of amiloride (a Na+ channel blocker), ouabain (a Na(+)-K(+)-adenosinetriphosphatase blocker), and phloridzin (a Na(+)-glucose cotransport blocker) in isolated rat lungs. Ischemia and reperfusion (I/R) significantly increased the edema accumulation, with the wet-to-dry weight ratios increasing to 10.14 +/- 0.58 from 6.03 +/- 0.05 in control lungs (P < 0.04). Amiloride significantly augmented the amount of edema fluid (wet-to-dry weight ratio 12.26 +/- 0.77), and ouabain further increased the amount of edema (wet-to-dry weight ratio 18.58 +/- 1.00). Phloridzin did not significantly affect edema formation associated with I/R. Isoproterenol decreased the amount of edema formation in the presence and absence of amiloride. This occurred because the endothelial permeability as assessed by filtration coefficient was restored to normal values and less edema formed. The present study indicates that Na+ channels and Na(+)-K(+)-adenosinetriphosphatase, components of the active Na+ absorption transport system, are very important in opposing edema fluid accumulation in rat lungs subjected to I/R injury and operate as an edema safety factor. However, if the endothelial damage associated with I/R is allowed to persist, then the transport processes, even if operative, are insufficient to prevent continuous edema accumulation.
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PMID:Vascular permeability and epithelial transport effects on lung edema formation in ischemia and reperfusion. 783 12

Developmental differences in adrenergic responsiveness may cause age-related changes in the cellular response to ischemia. Standard microelectrode techniques were used in isolated young and adult canine Purkinje fibers to determine the effect of simulated ischemia ([K+]o = 10 mM, pH 6.7, pO2 < 25 mm Hg) alone or with adrenergic stimulation on the rhythmic activity in spontaneously beating Purkinje fibers and on transmembrane potentials and delayed afterdepolarizations in paced Purkinje fibers (basic cycle length = 800-300 ms). The adrenergic agonists used were phenylephrine (5 x 10(-8) M) and isoproterenol (1 x 10(-6) M). For all automatic fibers studied, the control maximum diastolic potential in adults (-96 +/- 1 mV, n = 37) and in the young (-98 +/- 1 mV, n = 36) went to -62 +/- 1 mV during ischemia in both groups and returned to -96 +/- 2 mV with reperfusion. The incidence of rhythmic activity (expressed as percent) during ischemia alone was similar at both ages: adults, 22%; young, 25%. The incidence of ectopic activity with phenylephrine superfusion during ischemia for adults was 63%, an effect blocked by prazosin (1 x 10(-6) M) but not by propranolol (2 x 10(-7) M); the incidence for the young was 25%. Isoproterenol caused ectopic rhythms in 86% of young fibers and 17% of adult fibers (p < 0.05 young vs. adult). During reperfusion the return to control rhythm was slower in adults after ischemia alone or ischemia + alpha-adrenergic stimulation with phenylephrine. There were no age-related differences in the transmembrane potential response of paced fibers to ischemia or reperfusion, and there were no delayed afterdepolarizations with interruption of pacing at 800, 500, or 300 ms in either group. These data suggest that age-related differences in adrenergic responses alter the cellular response to an ischemic insult. To the extent that an ectopic beat may initiate an abnormal rhythm, these differences in sensitivity to adrenergic agonists may lead to developmental differences in arrhythmogenic potential during ischemia.
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PMID:Developmental differences in the electrophysiological response of isolated canine Purkinje fibers to adrenergic stimulation during simulated ischemia. 792 67

A 21-year-old woman sustained a supracondylar crush injury of her arm. The extremity underwent severe ischemia for more than 16 hours after an unsuccessful brachial artery repair. The forearm muscles became rigid and the fingers could not be extended passively. Clinically these findings were felt to be similar to rigor mortis. Despite this dismal picture, secondary revascularization resulted in a highly functional hand with no loss of digits. Desperate attempts at revascularization in isolated extremity injury may be successful, despite prolonged warm ischemia time.
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PMID:Prolonged warm ischemia and limb survival: case report. 799 8


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