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

A model to study pressure-induced ischemia by intravital microscopy is presented. A hamster cheek pouch is prepared to get a single layer of epithelium, together with vessels and connective tissue. Pressure, which can be varied, is transmitted to the tissue by a pressure chamber with a rubber membrane. Microcirculatory reactions may be studied while the pressure is applied, when the pressure is released and as the tissue is regaining circulation. The local environment is controlled by irrigating the test tissue with a solution approximating the composition of interstitial fluid. Local oxygen and carbon dioxide tensions are controlled. There is a marked difference in restoration of blood flow to the tissue after 2- and 4-hour ischemia. After 2-hour ischemia the tissue regained circulation rapidly. Microbleedings developed during the postpressure observation time. After 4-hour ischemia, on the other hand, the tissue regained circulation slowly and only in one third of the microvessels. Extensive white blood cells sticking to the vessel walls were seen indicating endothelial damage. In the 4-hour experiments there were very few microbleedings compared to the 2-hour experiments.
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PMID:Pressure-induced ischemia. I. An experimental model for intravital microscopic studies in hamster cheek pouch. 60 63

The effect of pulsatile cardiopulmonary bypass on intramyocardial gas tensions and regional myocardial blood flow was studied in 10 mongrel dogs. Following application of a critical stenosis to the circumflex coronary artery (CIRC), animals were placed on total bypass with vented, fibrillating hearts. During three 45 minute periods of perfusion, animals alternately received pulsatile or linear flow with perfusion pressure carefully maintained at 80 mm. Hg. In myocardium supplied by the stenosed CIRC, intramyocardial oxygen tension (PO2) rose from 13 +/- 3 to 19 +/- 5 mm. Hg when a period of linear flow was followed by a period of pulsatile flow (p less than 0.025). Similarly in the CIRC-supplied area, intramyocardial carbon dioxide (PCO2) decreased from 128 +/- 12 to 99 +/- 12 mm. Hg (p less than 0.005) with conversion from linear to pulsatile flow. Myocardial blood flow (microsphere technique) to endocardial and epicardial layers of the CIRC-supplied area was significantly greater (p less than 0.05) during pulsatile than during linear perfusion. In contrast, when periods of pulsatile bypass were followed by periods of linear perfusion, myocardial PO2 fell from 25 +/- 6 to 9 +/- 3 (less than 0.02) and myocardial PCO2 rose from 82 +/- 12 to 154 +/- 12 mm. Hg (p less than 0.001). These data suggest that (1) fibrillation-induced regional ischemia distal to a critical coronary stenosis can be reduced by pulsatile perfusion during bypass and (2) the mechanism for the reduction in regional ischemia is improved myocardial blood flow.
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PMID:Comparison of regional myocardial blood flow and metabolism distal to a critical coronary stenosis in the fibrillating heart during alternate periods of pulsatile and nonpulsatile perfusion. 62 24

The effects of whole heart ischemia on fatty acid metabolism were studied in the isolated, perfused rat heart. A reduction in coronary flow and oxygen consumption resulted in lower rates of palmitate uptake and oxidation to CO2. This decrease in metabolic rate was associated with increased tissue levels of long chain acyl coenzyme A and long chain acylcarnitine. Cellular levels of acetyl-CoA, acetylcarnitine, free CoA, and free carnitine decreased. These changes in CoA and its acyl derivatives indicate that beta oxidation became the limiting step in fatty acid metabolism. The rate of beta oxidation was probably limited by high levels of NADH and FADH2 secondary to a reduced supply of oxygen. Tissue levels of neutral lipids showed a slight increase durning ischemia, but incorporation of [U-14C]palmitate into lipid was not altered significantly. Although both substrates for lipid synthesis were present in higher concentrations during ischemia, compartmentalization of long chain acyl-CoA in the mitochondrial matrix and alpha-glycerol phosphate in the cytosol may have accounted for the relatively low rate of lipid synthesis.
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PMID:Control of fatty acid metabolism in ischemic and hypoxic hearts. 65 17

The pathological findings in four patients with courses characterized by acute coma and respiratory insufficiency occurring in obscure circumstances are presented. Carbon monoxide intoxication was excluded. After an early partial recovery from coma, the patients remained in a persistent vegetative state, with a tetrapyramidal syndrome. Pathologic changes consisted of infarction and demyelination of periventricular white matter, with associated necrotic foci in the basal ganglia in some cases. We propose that the prolonged hypoxia and ischemia produce a "no reflow" phenomenon causing brain edema (more pronounced in the white matter); this resulted in infarctions of white matter in the periventricular arterial end and border zones.
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PMID:Periventricular leukomalacia in adults. Clinicopathological study of four cases. 66 10

1. Ischaemia of a portion of the myocardium in the dog heart was produced by tying off a small branch of a coronary artery: flow in the occluded region was reduced from 5 to 82% of the initial value. 2. The effect of inhalation of 5% CO2 in air on relative tissue PO2 and perfusion in normal and partially ischaemic myocardium was determined. 3. After 10 min inhalation of 5% CO2, there was an increase in tissue perfusion as measured by hydrogen desaturation; the increase was inversely proportional to the degree of flow reduction. 4. Relative intramyocardial PO2 measured polarographically, decreased with occlusion and increased after CO2 inhalation; the changes were inversely proportional to the degree of reduction in PO2. 5. The increase in flow after CO2 inhalation suggests that partially ischaemic myocardial tissue is capable of further vasodilation.
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PMID:Blood flow and relative tissue oxygenation of normal and partially ischaemic myocardium: effect of CO2. 71 57

We sought to determine whether the pressor response to exercise-induced muscle ischemia is related to the mass of tissue rendered ischemic. Six men repeatedly exercised for 5 min at a fixed load between 75 and 150 W (bicycle ergometer). Thirty seconds before the end of exercise, circulation to one calf, two calves, one leg, and two legs was arrested with pneumatic cuffs in successive tests with 15-min recovery periods interspersed. Each occlusion was maintained until the 3rd min of exercise recovery. During postexercise occlusion we observed 1) mean arterial pressure (MAP) was elevated in proportion to the mass of ischemic muscle, 2) forearm blood flow (FBF) was elevated during the overlap of occlusion with exercise but did not show a uniform response during the following 3 min of occlusion--either vasoconstriction or vasodilation occurred, 3) heart rate (HR) was elevated only when two legs were occluded, and 4) occlusion did not affect ventilation or endtidal CO2. We conclude that the ischemic pressor response is muscle mass-dependent. Our findings suggest that the baroreflex alters peripheral vascular resistance so as to aid in the maintenance of elevated MAP.
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PMID:Cardiovascular responses to muscle ischemia in man--dependency on muscle mass. 73 May 73

A large number of clinical conditions are associated with a transient or permanent disturbance of brain function. Common to all of them is that, in some way, brain metabolism is changed from the normal. These changes cover a vast spectrum, ranging from the subtle alterations of metabolism encountered in mental disease to those underlying death and dissolution of cells in conditions of oxygen lack. This communication is concerned with brain metabolism in the critically ill with emphasis on conditions of hypoglycemia, hypoxia, and ischemia. We begin by briefly recalling the salient features of brain metabolism in the healthy individual. Since clinicians caring for critically ill patients take an interest in factors that may aggravate the primary disease and in measures that may prevent or minimize its final effect on the brain, we will also briefly consider how brain metabolism is influenced by potentially harmful factors (hyperthermia, anxiety and stress, and tissue acidosis due to CO2 retention) as well as by measures that are often instituted to ameliorate the effects of hypoxia and ischemia (hypothermia, administration of anesthetics and sedatives). We refer the reader to selected references with preference to recent articles reviewing previous literature.
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PMID:Brain metabolism in the critically ill. 80 79

Regional cerebral blood flow (rCBF) measurements with krypton-85 (100 separate determinations) were compared in squirrel monkeys anesthetized with sodium pentobarbital (a cerebral vasoconstrictor) and halothane (a cerebral vasodilator) before, during, and after middle cerebral artery (MCA) occlusion. Prior to MCA occlusion, a normal physiological response to alterations in arterial carbon dioxide tensions (Paco2) was demonstrated in both groups of monkeys; the cerebral vascular resistance was significantly lower in those anesthetized with halothane. During ischemia, there was loss of autoregulation and a failure to respond to alterations in Paco2 in both groups. Flow in the ischemic region remained uniform in the barbiturate group but decreased progressively in the halothane group, suggesting a "paradoxical response" to the dilating agent. Reactive hyperemia (luxury perfusion) was demonstrated in both groups after restoration of flow. The use of a beta-emitting isotope ensured that measurements in regions of ischemia accurately reflected rCBF and were free of the artifacts ("look through" and Compton scatter) related to use of a gamma-emitting indicator.
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PMID:Influence of cerebral vasoconstricting and vasodilating agents on blood flow in regions of focal ischemia. 81 13

Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a "critical stenosis" resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.
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PMID:Effects of atrial pacing on regional myocardial gas tensions with critical coronary stenosis. 83 20

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91


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