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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
Stroke
PMID:Influence of cerebral vasoconstricting and vasodilating agents on blood flow in regions of focal ischemia. 81 13

The autoregulatory capacity of areas of the cerebral circulation subjected to ischemia by acute middle cerebral occlusion has been assessed in experimental primates. Autoregulation was tested to a rise in blood pressure induced by aramine, and to a fall in blood pressure induced by exsanguination. Whole hemisphere autoregulation was substantially disturbed due to both increased blood pressure and lowered blood pressure, but fractionation of this response indicated that autoregulation to increased blood pressure was preserved in the parasagittal and intermediate zones of the hemisphere, and totally lost in the region of the sylvian opercula where middle cerebral occlusion had produced the most dense ischemia. In relation to reduced perfusion pressure, autoregulation was again widely impaired and assessment of the degree of impairment by areas indicated no significant difference between the areas of the sylvian opercula and the remainder of the lateral aspect of the hemisphere studied. Where the degree of ischemia in each individual electrode was assessed, however, it appeared that the degree of auto-regulatory loss to decreased perfusion pressure was dependent upon the intensity of ischemia, and autoregulation was partially preserved in electrodes whose immediate post-occulsion flow values were greater than 40% of basal flow. Retransfusion following exsanguination in animals with acute middle cerebral occlusion indicated that there was a linear relationship between the degreee of reperfusion achieved by retransfusion and the intensity of ischemia induced by exsanguination following middle cerebral occlusion. Thus there was some support for the no-reflow phenomenon in intensely ischemic areas.
Stroke
PMID:Autoregulation in acute focal ischemia. An experimental study. 82 33

Electron and light microscopic studies were performed on rabbit brain to re-examine the structural changes of endothelial cells and perivascular glia following ischemia. Although swelling of perivascular glia occurred, earlier findings of extreme perivascular glial swelling and bleb formation leading to luminal collapse and plugging could not be confirmed. Ischemic brains, however, had a higher proportion of small-diameter capillaries than controls. It is felt that structural changes in ischemic capillary walls in themselves are not sufficient to explain failed cerebral reperfusion, or the no-reflow phenomenon.
Stroke
PMID:Reassessment of cerebral capillary changes in acute global ischemia and their relationship to the "no-reflow phenomenon". 83 56

In normothermic anesthetized cats cerebral blood flow was interrupted completely for one hour by arterial clamping and induced hypotension. The effect of ischemia on the ionic gradients of the cerebral cortex was assayed by determining total cortical electrolytes and by recording the activities of extracellular potassium ([K+i1e) and subarachnoid sodium ions ([Na+])s) with ion-sensitive electrodes. During ischemia [K+]e increased from 3.3+/-0.3 to 56+/-5.4 mEq per liter (means+/-SE) and [Na+]s decreased from 133+/-3.8 to 53+/-5.8 mEq per liter. When the brains were recirculated with blood after one hour's ischemia, [K+]e and [Na+]a gradually returned to normal within 45 minutes. The calculated intracellular uptake of sodium during ischemia amounted to 139 mEq per kilogram dry weight, whereas the intracellular release of potassium was only 64 mEq per kilogram. The increase in intracellular cation was accompanied by a movement of water from the extracellular into the intracellular compartment, causing a reversible shrinkage of the extracellular space from 18.9 to 8.5 vol %. The changes in ionic gradients were related to the development and resolution of ischemic brain swelling, and to the elctrophysiological events during and after ischemia.
Stroke
PMID:Cation activities in reversible ischemia of the cat brain. 83 60

A technique is described for reliably producing quantifiable impairment of microvascular reperfusion of the brain after ischemia in dogs. The technique is derived from an analysis of the cerebrospinal fluid compression ischemia model as a Starling resistor. It is proposed that this model would be useful in systematic study of post-ischemic impairment of reperfusion.
Stroke
PMID:Experimental model for systematic study of impaired microvascular reperfusion. 84 89

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.
Stroke
PMID:Coagulopathy following experimental cerebral ischemia. 84 91

To determine the sequence of changes in segmental myocardial function, regional lactate metabolism and global left ventricular function induced by mild regional ischemia, blood flow in the left anterior descending coronary artery of 10 dogs was reduced by 10 percent decrements with use of a screw clamp. At each level of flow, segmental mechanical function and regional metabolism were assessed, the former with use of a mercury-in-Silastic length gauge and the latter with transmyocardial lactate balance measurements obtained with sampling from the anterior interventricular vein. Coronary arterial flow at the onset of regional lactate production was 48 +/- 4 percent (mean +/- standard error of the mean) of the control value. The onset of segmental mechanical dysfunction coincided with the onset of lactate production. Epicardial S-T segment abnormalities over the ischemic zone usually could not be detected until coronary flow was further reduced. After the onset of regional ischemia there was a linear correlation between coronary arterial flow and regional lactate production. At the onset of mild regional ischemia, defined as the onset of regional lactate production, no significant or directionally consistent changes were noted in standard measurements of global left ventricular performance, including heart rate, mean aortic pressure, left ventricular end-diastolic pressure, cardiac output, stroke volume, stroke work and peak positive dP/dt (maximal rate of rise of pressure). However, peak negative dP/dt (maximal rate of pressure decrease) decreased from 99 +/- 2 to 89 +/- 3 percent of the control value (P less than 0.0005) coincident with the onset of ischemia. It is hypothesized that dyssynchronous wall motion in the ischemic zone during isometric relaxation accounts for this decrease in peak negative dP/dt.
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PMID:Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. 84 38

Records of 248 patients undergoing aortoiliac reconstruction for occlusive disease between 1957 and 1975 were reviewed. Carotid bruits were ausculted in 35 patients (14%). Five of the patients with bruits also were thought to have symptoms of transient ischemia. Strokes occurred after operation in four of the 248 patients (1.6%). No patient with a previously noted bruit developed postoperative stroke. Two patients with transient cerebral ischemia and no confirmed bruit before operation did develop postoperative strokes. Cerebral angiography was performed in 18 of the patients with carotid bruits. Two of these patients underwent carotid endarterectomy prior to aortoiliac reconstruction. None of these 18 patients developed strokes following their carotid surgery of aortoiliac reconstruction. A third patient with no bruit but with retinal cholesterol emboli also underwent arteriography and endarterectomy without complication. The results suggest that the asymptomatic carotid bruit alone does not indicate an increased risk of stroke during aortoiliac reconstruction. The authors conclude that their experience does not support prophylactic carotid endarterectomy in the asymptomatic patient prior to aortoiliac reconstruction.
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PMID:Carotid bruit as a risk factor in aortoiliac reconstruction. 85 Aug 72

To examine the influence of preexistent diabetes mellitus on left ventricular performance and coronary blood flow responses to acute ischemia, mild normoglycemic diabetes was induced in nine mongrel dogs after three doses of alloxan, (20 mg/kg, iv), at monthly intervals. Hemodynamic measurements and coronary blood flow (85Kr clearance) were obtained before and after the onset of ischemia. This was produced by occlusion of the proximal left anterior descending coronary artery via a balloon-type catheter in nine intact anesthetized diabetic dogs and 10 nondiabetic dogs. During the 1st hour of ischemia in the diabetic group, the end-diastolic pressure rose from 7 +/- 1.1 (mean +/- SE) mm Hg to 23.8 +/- 2.3 without a significant increase of end-diastolic volume. In controls end-diastolic pressure rose from 8.6 +/- 1.1 mm Hg to 15.3 +/- 1.4, and end-diastolic volume was significantly increased, so that the ratio of end-diastolic pressure and volume was significantly higher in the diabetic group (P less than 0.005). Although indices of contractility did not differ, stroke volume and work reductions were significantly greater in diabetics, despite the fact that coronary blood flow was reduced to a similar extent. Size of the ischemic areas appeared comparable as judged by distribution of dye injected distal to the occlusion. Since potassium loss and sodium gain in the inner and outer layers of ischemic tissue did not differ between the two groups, the intensity of ischemia seemed similar. Glycogenolysis was unimpaired in the diabetic ischemic muscle but triglyceride levels remained elevated. Morphologically the diabetic myocardium was characterized by a diffuse accumulation of periodic acid-Schiff-positive glycoprotein in the interstitium, which was thought to limit diastolic filling of the ischemic ventricle and to contribute to the substantial reduction of ventricular performance.
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PMID:Myocardial function and coronary blood flow response to acute ischemia in chronic canine diabetes. 87 Feb 38

Four patients with symptoms and signs of brain stem ischemia due to occlusive disease of the vertebrobasilar system and one patient with similar cerebrovascular disease who was thought to be prone to brain stem stroke underwent a microvascular anastomosis between the occipital artery and the caudal loop of the posterior inferior cerebellar artery. There was no morbidity of mortality and neurologically all patients improved. Post-operative angiograms showed patent anastomosis in all the patients and improved circulation in three. This new operation may prove beneficial in a selected group of stroke patients who suffer from vertebrobasilar insufficiency and cannot be treated with gross surgical techniques.
Stroke
PMID:Possible prevention of brain stem stroke by microvascular anastomosis in the vertebrobasilar system. 87 Oct 22


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