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 determine whether nifedipine, a calcium antagonist, protects ischemic myocardium, conscious dogs were subjected to coronary occlusion and given nifedipine by intravenous infusion beginning 30 minutes after the onset of ischemia and lasting for 24 hours while systemic arterial pressure, left atrial pressure, and cardiac output were monitored. Local myocardial perfusion at selected intervals after coronary occlusion was assessed with radioactive microspheres injected into the left atrium. In regions of myocardium exhibiting moderately depressed flow 29 minutes after occlusion in control dogs (n = 8), flow was significantly greater 3 and 23.5 hours later, reflecting increases in collateral perfusion. Corresponding zones of myocardium in treated dogs (n = 9) exhibited significantly greater increases in flow at each interval after occlusion (P less than 0.05). Furthermore, myocardial creatine kinase depletion (which correlated well with morphometric estimates of necrosis) in myocardium matched for ischemia prior to treatment was 1.5 to 3 times less in treated than in control dogs (P less than 0.05). Thus, nifedipine produced sustained increases in collateral flow and reduced myocardial ischemic injury.
Circ Res 1978 Sep
PMID:Effects of nifedipine on myocardial perfusion and ischemic injury in dogs. 67 20

Despite revascularization of the common femoral--profunda femoris system, many patients fail to obtain satisfactory relief from claudication or rest pain. Clinical observations were compared with objective physiological data in 54 technically successful aortoiliofemoral reconstructions for multilevel disease. Nine of 28 operations (32%) for claudication and five of 26 operations (19%) for ischemia at rest had poor results. While the average ankle pressure index (API = ankle blood pressure/arm blood pressure) rose from 0.52 +/- 0.03 (SEM) to 0.81 +/- 0.03 in limbs treated successfully for claudication, it changed insignificantly in those with an unsuccessful result (0.58 +/- 0.04 to 0.61 +/- 0.04). When ischemic symptoms were relieved, API rose from 0.23 +/- 0.04 to 0.55 +/- 0.03 but increased only from 0.22 +/- 0.09 to 0.40 +/- 0.02 in limbs with insufficient improvement. Preoperative thigh pressure index (TPI) in claudicating limbs with poor results (0.96 +/- 0.05) differed little from that in limbs with good results (0.92 +/- 0.05); nor was the TPI of ischemic limbs with poor results (0.83 +/- 0.13) significantly greater than that in limbs with good results (0.60 +/- 0.05). Neither the TPI nor the thigh to ankle pressure gradient was of value in predicting which extremities would respond poorly to aortoiliofemoral reconstruction.
Surgery 1978 Sep
PMID:Aortoiliac reconstruction in patients with combined iliac and superficial femoral arterial occlusion. 68 26

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.
Am J Cardiol 1978 Sep
PMID:Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion. 68 53

Ischemic rat liver tissue has been shown previously to exhibit a markedly accelerated rate of phospholipid degradation, producing a loss of almost one half the total cellular phospholipid with 3 hours of ischemia. Pretreatment of the rats with chlorpromazine completely prevented the disturbed phospholipid metabolism at the same time that it prevented the cell death associated with as much as 3 hours of ischemia. Lipid-depleted microsomal membranes were shown previously to manifest alterations in their structure and function. The present report documents that similar structural alterations are evident in ischemic liver cell plasma membranes. The technique of freeze-fracture electron microscopy was used to examine the morphology of ischemic liver cell plasma membranes. Freeze-fracture replicas of whole tissue fragments exhibited a diffuse aggregation of the intramembranous particles in the P face of the plasma membranes. The incidence of this change correlated with the duration of ischemia. Pretreatment of the rats with chlorpromazine (20 mg/kg) for 30 minutes before inducing ischemia prevented the aggregation of the membrane-associated particles. These findings establish the existence of plasma membrane alterations in ischemic liver cells. The time course of these changes, their prevention by chlorpromazine, and their similarity to the previously described structural alterations in the microsomal membranes suggest that they are related to the loss of liver cell phospholipid. The data in the present report support the hypothesis that an accelerated phospholipid degradation and its resultant membrane dysfunction are the critical alterations that produce irreversible liver cell injury and, ultimately, cell death in ischemia.
Am J Pathol 1978 Sep
PMID:Irreversible ischemic cell injury. Prevention by chlorpromazine of the aggregation of the intramembranous particles of rat liver plasma membranes. 68 54

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.
Arch Surg 1978 Sep
PMID:Enhancement of tissue Po2 of strangulated bowel by topical application of sodium nitroprusside. 68 8

A patient who had endocarditis on a prosthetic aortic valve and who had undergone two aortic valvular replacements developed classic angina pectoris. Cardiac catheterization revealed an aneurysm of the left sinus of Valsalva, which constricted a proximal segment of the left circumflex coronary artery during systole. This type of dynamic coronary arterial narrowing has not been previously described secondary to an aneurysm of a sinus of Valsalva and may be responsible for this patient's manifestations of ischemia.
Chest 1978 Sep
PMID:Aneurysm of sinus of Valsalva: cause of dynamic coronary constriction after aortic valvular replacement and bacterial endocarditis. 68 94

Lysophosphoglycerides, products of membrane phospholipid catabolism known to influence membrane function in several systems, appeared in the effluents of anoxic isolated rabbit hearts perfused at low flow and accumulated in perfused hearts and myocardium rendered ischemic in situ. Comparable concentrations of lysophosphoglycerides bound to albumin markedly and reversibly altered action potentials of isolated canine Purkinje fibers in vitro. Changes induced included diminution of the maximum diastolic potential, peak dV/dt of phase zero, amplitude, and action potential duration--alterations resembling those seen in ischemic myocardium in vivo. These electrophysiological alterations are compatible with changes implicated in predisposing to dysrhythmia dependent on reentry, a phenomenon potentiated by the presence of zones of decreased conduction. Thus, accumulation of lysophosphoglycerides induced by ischemia may contribute to the genesis of malignant dysrhythmia early after its onset.
J Clin Invest 1978 Sep
PMID:Accumulation of lysophosphoglycerides with arrhythmogenic properties in ischemic myocardium. 69 Jan 85

Under conditions of varying flow rates, total myocardial blood flow, measured by fractional uptake of rubidium-84, using a coincidence counting system, was compared with myocardial flow measured by microspheres (15 +/- 5 micrometer). The methods were compared, open-chested, in 47 dogs: 17 during control, ten following 5 min of ligation of left anterior descending coronary artery, five following i.v. isoproterenol, six following ligation and isoproterenol, and nine after ligation plus dipyridamole. Regional flows by Rb-84 and by either Ce-141 or Cr-51 microspheres were also compared for left ventricle, as well as for nonischemic posterior wall, which served as a reference area, and for anterior wall with ligation of left anterior descending artery in the same preparations. There were no significant differences in total or regional flow measured by the two methods, nor in the estimate of ischemic area size. The data indicate that measurement of myocardial blood flow by fractional uptake of a potassium analog is a reliable method in the presence of ischemia and drug intervention. It is suggested that the inequalities of extraction ratio that occur with differing flow rates do not invalidate fractional-uptake methods over the flow ranges examined.
J Nucl Med 1978 Sep
PMID:Myocardial blood flow as measured by fractional uptake of rubidium-84 and microspheres. 69 Jul 2

The effect of acute experimental heart ischemia on protein synthesis and RNA of the internal membranes of myocardial mitochondria was studied; there was a sharp increase in the protein synthesizing system activity of the internal mitochondrial membranes. The most pronounced protein and PNA exchange was noted on the 7th day of the infarction; apparently it was the most critical time in the development of the given pathological process. A study of ultrastructure of mitochondrial membranes in the course of experimental infarction development demonstrated marked changes in their ultrastructure depending on the severity of the disease.
Biull Eksp Biol Med 1978 Sep
PMID:[Effect of acute cardiac ischemia on the activity of the protein synthesizing system of the internal membranes of myocardial mitochondria]. 69 71

Epicardial ECG signs have been studied in 26 anesthetized and thoracotomized dogs in an attempt to follow the progress of tissue damage during regional myocardial ischemia. Epicardial ECG's were recorded before and during 15 min, 1 and 5 h of severe left anterior descending coronary artery narrowing. Epicardial ST segment elevation followed a complicated natural history. An analysis of variance showed the significant effects of respiration, heart rate and changes in time during myocardial ischemia. Regional epicardial R waves showed a transient increase in amplitude following coronary narrowing. There was no loss of electrically active myocardium following 15 min of ischemia. Irreversible loss of R waves were noted at between 30 and 45 min and progressed to full development within 5 h following coronary artery narrowing. The loss of electrically active myocardium (R loss plus Q waves) at 5 h was closely related to the myocardial depletion of creatine kinase activity (mu/mg DNA-1) at 24 h in each dog. The early manifestation of myocardial ischemia (ST segment elevation at 17 min) was closely related in the later evidence of cell death (R loss plus Q waves) in each dog. These relationships were less precise when the results were combined and this showed the variability between dogs in heart size and infarct size. The study suggested that the individual complete natural history of these ECG signs must be studied before they can be used to assess the extent and progress of myocardial ischemia and cell death.
Eur J Cardiol 1978 Sep
PMID:Electrocardiographic signs in experimental myocardial ischemia and infarction. 69 50


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