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

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

Sodium meglumine calcium metrizoate was injected into isolated blood-perfused canine hearts to evaluate the effect of contrast agents containing calcium on normal and ischemic myocardium. Under normal perfusion pressure and mild ischemia, this contrast agent produced a positive inotropic effect, but during profound ischemia, this positive effect was followed by a period of myocardial depression. These findings indicate that the addition of an inotropic agent to contrast medium can produce a paradoxical depressant effect which can be deleterious to the ischemic myocardium.
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PMID:Differential effects of sodium meglumine calcium metrizoate on the inotropic state of normal and ischemic myocardium. 66 67

The effect of long-term tourniquet ischemia on electrolyte levels in muscle tissue and plasma during and after occlusion was investigated in man. Muscle tissue electrolytes were studied in nine patients using a percutaneous muscle biopsy technique. The estimation of the intra- and extracellular electrolyte content was based on the determination of the chloride space. In another similar group of patients (n=11) plasma electrolytes were investigated by taking blood samples from fine plastic catheters inserted into both femoral veins and one radial artery. Capillary blood flow was measured using the 133Xenon-clearance technique. During occlusion there were no significant changes in muscle tissue or plasma electrolytes. After release of the tourniquet an increase in plasma potassium of the operated leg and arterial plasma were observed. Maximal muscle blood flow and maximal potassium values occurred at the same time giving a pronounced potassium release from the operated leg. The osmol release from the occluded leg showed a maximum 1 min after tourniquet release. The total and intracellular content of potassium and sodium in the muscle tissue did not significantly alter after release of the occlusion. A moderate increase in extracellular water was found after tourniquet release.
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PMID:Electrolyte changes in muscle tissue and plasma in tourniquet-ischemia. 66 4

Rats were subjected to 25 min of unilateral renal artery occlusion and were studied at 5, 15, and 30 min and at 1, 2, 4, 8, 16, 24, and 48 hr following ischemia. The patterns of epithelial injury and repair in proximal tubule (PT) segments S1, S2, and S3 were followed, and associated changes in renal function were determined. We found that S1 and S2 cells alike are only reversibly injured and recover completely to normalcy within 4 hr, whereas S3 cells selectively undergo progressive cell injury and death and are exfoliated into tubular lumina. The necrotic S3 cells are replaced by mitotic division of survivor cells 24 to 48 hr following the ischemic insult. In addition, there was selective damage within tubular cells. Wiithin 5 min of blood reflow following ischemia, the majority of brush border microvilli (MV) in all three PT segments underwent coalescence by membrane fusion and thus were interiorized into the cytoplasm of PT cells. A minority of MV fragmented and were shed into PT lumina, but nephron obstruction by shed membranes was only mild and transient, unlike in the 1-hr ischemia model. Loss of MV reached a maximum of 15 min. By 30 min, MV began to reappear; by 2 hr, large numbers of MV had been regenerated; and by 4 hr, S1 and S2 cells appeared normal. The regenerative process included the luminal repositioning of previously interiorized MV membrane. MV regeneration occurred in S3 segments also, but before the process was complete, the cells developed features of irreversible cellular injury. Glomerular filtration rate (GFR) was 22% of control at 30 min of reflow, rose progressively to 55% of normal by 7 to 8 hr, and was normal at 24 hr. Single nephron filtration rate (SNGFR) was not significantly different from normal throughout. Proximal tubular sodium reabsorption was depressed and urinary sodium excretion increased at 30 min and at 2 to 3 hr, i.e., at times when MV alterations were prominent, but both were normal by 7 to 8 hr when MV in S1 and S2 cells had been fully reconstituted. Our major conclusions are: 1) There is differential susceptibility by cell type to ischemic injury in rat PT. 2) A rapid brush border loss/regeneration cycle occurs after ischemic injury. 3) Intact brush border may be required for normal sodium reabsorption by PT. Reasons for the GFR/SNGFR discrepancy are unclear, but tubular malfunction may partly explain the phenomenon.
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PMID:Ischemic damage and repair in the rat proximal tubule: differences among the S1, S2, and S3 segments. 68 23

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.
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PMID:Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion. 68 53

Intracellular acidosis may depress myocardial function and metabolism during ischemia. In the present study, the function and metabolism of a globally ischemic, isovolumic cat left ventricle preparation, perfused with oxygenated Krebs-Ringer biocarbonate solution, was examined. Addition of tris(hydroxymethyl)-aminomethane (Tris) (15 mM) to the perfusate at physiologic pH and PCO2 increased performance during ischemia to a greater extent and for a longer period than low PCO2 )15 mmHg), alkalotic (pH, 7.8) perfusate and a control sucrose perfusate. Under nonischemic conditions the inotropic effect of Tris was only briefly greater than sucrose perfusate. The inotropic effect of Tris during ischemia did not appear to depend on changes in coronary flow, oxygen consumption, sodium concentration, perfusate osmolality, or catecholamine release. During ischemia, lactate production was unchanged with Tris, but increased with low PCO2-alkalosis. Tissue levels of ATP and creatine phosphate for control ischemic hearts did not differ from Tris-perfused or low PCO2-alkalosis hearts. Thus, Tris appears to exert an inotropic effect that is more prominent in ischemic than nonischemic myocardium. The results are consistent with the possibility that Tris acts as an intracellular buffer to increase the efficiency of energy production and/or utilization during ischemia.
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PMID:Effect of tris(hydroxymethyl)aminomethane on ischemic myocardium. 68 84

The Po2 was measured in the tissue of the ileal wall of dogs before, during, and up to one hour after reversible occlusion of segmental arteries. The occlusion was then released and the reoxygenation of the bowel wall was observed. Sodium nitroprusside (50 mg in 100 ml of solution) applied topically to the ischemic segment enhanced reoxygenation as compared to control animals. Nitroprusside absorbed into the portal system did not cause hypotension, as is usual with systemic administration, because nitroprusside is inactivated by passage through the liver. Topically applied sodium nitroprusside alleviates intestinal ischemia by direct local vasodilatation and relaxation of smooth muscle spasm in the ischemic bowel wall. The intraperitoneal use of sodium nitroprusside should be clinically evaluated in situations where visceral perfusion is impaired.
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PMID:Enhancement of tissue Po2 of strangulated bowel by topical application of sodium nitroprusside. 68 8

Serial 72-point precordial mapping of ECG has been recorded to describe the natural history of changes in the precordial areas of ST segment elevation and the development of Q waves in 51 patients with acute uncomplicated anterior myocardial infarction. Eight patients have been studied in the same way but received 25 mg/kg of methylprednisolone sodium succinate as a single intravenous injection within 6 hours from the onset of chest pain. There was a linear relationship between the stable precordial area of Q waves at 24 hours and the rapidly changing precordial areas of ST segment elevation at 2--3 hours, 5--6 hours and 12 hours after the onset of pain in the untreated patients. When methylprednisolone was given, the treated patients developed a smaller precordial area of Q waves at 24 hours than was predicted from the precordial area of ST elevation recorded before the drug was given. This study has introduced a technique that can provide a qualitative assessment of the relationship between ECG evidence of ischemia and infarction in each patient.
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PMID:Electrocardiographic precordial mapping in anterior myocardial infarction. The critical period for interventions as exemplified by methylprednisolone. 69 56

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

It is not known whether ventricular relaxation can be altered by ischemia independent of associated hemodynamic changes. The effect of acute myocardial ischemia on diastolic relaxation was studied under controlled hemodynamic conditions in 16 anesthetized dogs on right-heart bypass. In nine dogs, left ventricular end-diastolic pressure was maintained constant throughout the experiments. Ischemia produced a significant prolongation of the isovolumetric relaxation period (IVRP) from 29 +/- 3 (SE) to 88 +/- 7 ms (P less than 0.01). Ischemia, per se, the associated decrease in contractility, or the fall in peak left ventricular pressure (LVP) may have contributed to the increase in IVRP. The latter was not the only mechanism involved, because in seven dogs studied with constant peak LVP, IVRP again was prolonged from 64 +/- 8 to 95 +/- 8 ms (P less than 0.01). Moreover, in five nonischemic hearts in which peak LVP was maintained constant, contractility was decreased by sodium pentobarbital to the same extent as with ischemia; IVRP did not change. Thus, the additional prolongation of the IVRP in the ischemia experiments is secondary to a direct effect of ischemia on the relaxation process of the myocardium.
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PMID:Effects of acute global ischemia on diastolic relaxation in canine hearts. 73 60


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