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

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

The major ionic conductances underlying electrical activity in cardiac tissues are described. The participation of electrogenic active transport in electrical phenomenon and the influence of metabolic inhibition on cardiac action potentials are briefly summarized. Some electrophysiological effects of lactate and acidosis, such as might be induced by ischemia, are described. In dog Purkinje fibers, lactate (20 mM pH 7.0) may induce transient periods of arrhythmias. Acidosis decreases rapid sodium conductance, slow calcium-sodium conductance, and anomalous and delayed rectifications in frog atrial fibers. CO2-induced acidosis (20% CO2, pH 6.6) may alter the repolarization phase of the action potential in dog Purkinje fibers, presumably because it decreases potassium conductance. Alterations consist of partial depolarizations (humps) that result in reexcitation of the fibers and lead to a maintained depolarization. It is proposed that acidosis induces a decrease in potassium conductance that can be responsible for ectopic foci causing arrhythmias during ischemia.
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PMID:Control of ionic permeabilities in normal and ischemic heart. 0 3

In studies in the isolated rat heart that were designed to optimize the composition of the infusion conditions for a cardioplegic protective solutuin, we have observed a complex relationship between the duration and volume of infusion and the extent of tissue protection. Our results would indicate that solutions, such as that formulated at St. Thomas' Hospital, which are based on extracellular electrolyte content, afford (after a brief equilibration period) a constant degree of protection, irrespective of infusion volume or duration. In contrast other solutions, such as the Bretschneider solution, which have extremes of electrolyre concentration, are associated with a complex dose-response relationship. In the latter instance, infusion of small volumes for short durations affords an increasing degree of protection against ischemia. Increasing the infusate volume may result in a progressive loss of protection. Excessive infusion may lead to an exacerbation of ischemia-induced damage. Our studies suggest that the relative patterns and rates of re-equilibration of various ions, especially sodium and calcium, during infusion may play a major role in determining the efficacy of the infusate.
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PMID:Protection of the ischemic myocardium. Volume-duration relationships and the efficacy of myocardial infusates. 2 95

The direct and indirect actions on left ventricular dynamics of contrast material (sodium meglumine diatrizoate) currently used for coronary arteriography, modified ionic material (sodium meglumine calcium metrizoate) and non-ionic material (metrizamide) were assessed in conscious and anesthetized dogs. In both anesthetized and conscious animals, the diatrizoate compound caused an early (3--10 sec after injection) decrease in peak dp/dt and dp/dt/LVP40, followed by late (10--20 sec after injection) increases in these variables. The predominant early and later effects of the calcium metrizoate compound were increases in parameters of LV contractile state. Metrizamide produced no significant early alterations, but later induced a small increase in these variables. The positive inotropic actions of each of the contrast materials were attenuated by beta adrenergic blockade. The early effects of the contrast materials were similar in the presence of segmental ischemia. The late positive inotropic effects in response to the diatrizoate compound and metrizamide were not observed in the ischemic state, while the positive inotropic response induced by the calcium metrizoate compound was significantly reduced. Thus intracoronary administration of sodium meglumine diatrizoate produced direct myocardial depression, followed by adrenergically mediated myocardial stimulation. Calcium metrizoate caused prominent direct and adrenergically mediated augmentation in contractile state. Metrizamide induced the least alteration in LV contractile state.
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PMID:Direct and reflex myocardial effects of intracoronary administered contrast materials in the anesthetized and conscious dog: comparison of standard and newer contrast materials. 3 Jul 33

Aggressive treatment with H(2) receptor blocking agents and/or antacids has been advocated as effective prophylaxis against and treatment for "stress ulcer," based on the logical but infrequently tested assumption that the severity of the disease is critically determined by the concentration of intraluminal acid. The present study investigated this assumption in a model which employed topical acid, topical bile acid and mucosal ischemia to induce ulcerogenesis. With vascularized, chambered ex vivo wedges of canine proximal gastric wall, groups of animals were studied during three sequential periods using topical test solutions (TS) containing either 0 mM, 100 mM or 160 mM HCI. During period 1, mucosae were exposed to TS alone; during period 2, either to TS containing 1 mM sodium taurocholate (TC) or to TS and concomitant vasopressin infusion (VP); and during period 3, to TS + TC + VP. Parameters evaluated included net H(+) flux ( big up tri, openH(+)), aminopyrine clearance (AC), a measure of mucosal blood flow, net TC flux ( big up tri, openTC) and the lesion index, graded 0-5. The data indicate that in nonischemic mucosa exposed to constant [TC], AC was significantly increased, big up tri, openH(+) ("back-diffusion") increased as a linear function of [H(+)] and no lesions were observed. Under the same circumstances in ischemic mucosa, big up tri, openH(+) increased as linear function of [H(+)]. As a consequence, lesion severity was also a linear function of [H(+)]. big up tri, openTC was enhanced at low pH but bore no relation to the degree of mucosal damage induced. Assuming applicability of the model, these studies provide support for the use of H(2) receptor blocking agents and/or antacids to prevent or ameliorate "stress ulcer" disease.
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PMID:Influence of hydrogen ion concentration on bile acid induced acute gastric mucosal ulcerogenesis. 3 49

Bilateral occlusion of common carotid arteries in Mongolian gerbils was produced for the periods (up to 15 min) which were shown to be totally reversible. There was an initial increase of cyclic AMP and GABA levels and enhanced activities of adenylate cyclase and glutamate decarboxylase, as well as the reduction of norepinephrine level and decreased activities of monoamine oxidase, GABA-transaminase and Na+-K+-ATPase. Following these changes, decreased concentration of dopamine, serotinin and glutamate were found. The activities of total protein kinase and acetylcholinesterase were found to be reduced after longer periods of short-term ischemia. The data are consistent with the concept of increased non-controled release of putative neurotransmitters in ischemia.
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PMID:Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex. 3 75

Effects of methylprednisolone were studied on isolated, blood-perfused cat hearts subjected to 1 hr of normothermic ischemic arrest. Untreated hearts sustained decreases in peak ventricular pressure pulse, dP/dt, and ventricular compliance. Ischemic hearts also became edematous, gained sodium, and lost potassium and creatine kinase enzyme activity. Steroid treatment did not significantly alter any of these ischemia-induced changes. Methylprednisolone treatment did increase resting coronary flow and also increased the hyperemic response after reperfusion. These results, in isolated hearts, provide no evidence that steroid treatment exerts a direct protective effect on the globally ischemic myocardium.
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PMID:Methylprednisolone sodium succinate treatment in global ischemia of the cat isolated heart. 9 82

A common although infrequently recognized complication associated with the use of a pneumatic tourniquet is profuse bleeding from the wound after deflation of the tourniquet. The purpose of this study was to determine whether intravascular coagulation and fibrinolysis could be induced in subhuman primates by tourniquet ischemia, and whether this phenomenon could be altered by pretreatment of the animal with heparin. It was shown that, after 2(1/2) hours of tourniquet ischemia, (400 mmHg) to one lower limb, fibrinogen levels were significantly lower (p < .005), antithrombin III levels were significantly lower (p < .05), plasminogen levels were significantly lower (p < .05), fibrin split products significantly higher (p < .025) and fibrinopeptide A levels were significantly higher (p < .02) than values measured simultaneously in the control limbs. After pre-treatment with sodium heparin, 30 units/kg, there was no change in antithrombin III levels or fibrinogen levels, but fibrin split products in the experimental limbs were significantly elevated (p < .05) when compared to control limbs. In both groups the abnormal levels returned to control levels 5-30 minutes after tourniquet deflation. We conclude that intravascular coagulation and fibrinolysis develop within ischemic subhuman primate limbs during tourniquet ischemia. Pretreatment with heparin prevents the consumption of fibrinogen and antithrombin III but does not prevent the increase in fibrin split products which was observed. It is possible that intravascular coagulation and fibrinolysis contribute to post tourniquet bleeding.
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PMID:Intravascular coagulation and fibrinolysis within primate extremities during tourniquet ischemia. 11 39

The effects of ischemia on the canine myocardial (Na+ + K+)-ATPase complex were examined in terms of alterations in cardiac glycoside binding and enzymatic activity. Ability of the myocardial cell to bind tritiated ouabain in vivo was assessed after 1, 2, and 6 h of coronary occlusion followed by 45 min of reperfusion, and correlated with measurements of in vitro (Na+ + K+)-ATPase activity and in vitro [3H]ouabain binding after similar periods of ischemia. Regional blood flow alterations during occlusion and reperfusion were simultaneously determined utilizing 15 mum radioactive microspheres to determine the degree to which altered binding of ouabain might be flow related. Anterior wall infarction was produced in 34 dogs by snaring of confluent branches of the left coronary system. Epicardial electrograms delineated ischemic and border zone areas. Coronary reperfusion after 2 and 6 h of occlusion was associated with impaired reflow of blood and markedly impaired uptake of [3H]ouabain in ischemic myocardium. In both groups, in vivo [3H]ouabain binding by ischemic tissue was reduced out of proportion to the reduction in flow. Despite near-complete restoration of flow in seven dogs occluded for 1 h and reperfused, [3H]ouabain remained significantly reduced to 58 +/- 9% of nonischemic uptake in subendocardial layers of the central zone of ischemia. Thus, when coronary flow was restored to areas of myocardium rendered acutely ischemia for 1 or more hours, ischemic zones demonstrated progressively diminished ability to bind ouabain. To determine whether ischemia-induced alteration in myocardial (Na+ + K+)-ATPase might underlie these changes, (Na+ + K+)-ATPase activity and [3H]ouabain binding were measured in microsomal fractions from ischemic myocardium after 1, 2, and 6 h of coronary occlusion. In animals occluded for 6 h, (Na+ + K+)-ATPase activity was significantly reduced by 40% in epicardial and by 35% in endocardial layers compared with nonischemic myocardium. Comparable reductions in in vitro [3H]ouabain binding were also demonstrated. Reperfusion for 45 min after occlusion for 6 h resulted in no significant restoration of enzyme activity when compared to the nonreperfused animals. In six animals occluded for 2 h, a time at which myocardial creatine phosphokinase activity remains unchanged, (Na+ + K+)-ATPase activity was reduced by 25% compared with nonischemic enzyme activity. In five dogs occluded for 1 h, (Na+ + K+)-ATPase activity in ischemic myocardium was unchanged from control levels. We conclude that reduced regional myocardial blood flow, local alterations in cellular milieu, and altered glycoside-binding properties of (Na+ + K+)-ATPase all participate in the reduction of cardiac glycoside binding observed after reperfusion of ischemic myocardium. In addition, after 2 or more hours of severe ischemia, myocardial (Na+ + K+)-ATPase catalytic activity is significantly reduced despite incubation in the presence of optimal substrate concentrations.
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PMID:Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding. 13 Mar 83

The quantitative potassium and sodium contents in the separate regions of the heart and m. rectus abdominis in cases of sudden and violent death were investigated. The disturbances of the electrolyte metabolism of potassium and sodium were established to be the earliest changes in coronary disease (acute coronary insufficiency resulting from functional disturbances of the coronary circulation and myocardial infarction). The decrease of the quantitative potassium contents and sodium increase in myocardium depend on the ischemia duration and the stage of the myocardial lesion. The highest potassium decrease was observed in the left ventricle and right auricle. Not very high but even decrease of potassium and sodium contents in the separate heart regions was observed in the deceased by electrocution and strangulation, the decrease being most negligible in the deceased by electrocution. The changes observed in potassium and sodium contents are not pathognomic signs of coronary disease. Only the sharp, focal decrease of the contents of those element is a reliable sign of myocardial infarction.
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PMID:[Quantitative K and Na levels in different parts of the heart in cases of sudden death from coronary disease, acquired heart valve defects and violent death]. 13 71


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