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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

Cerebral autoregulation and vasomotor responsiveness to carbon dioxide were measured quantitatively in normal baboons and after intravertebral or intravenous of the beta-adrenergic blocking agent, propranolol hydrochloride (Inderal). Continuous measurements were made of cerebral blood flow (CBF: measured as bilateral internal jugular venous outflow using an electromagnetic flowmeter), cerebral perfusion pressure (CPP), arterial Po2 and Pco2 and venous Po2, cerebral arteriovenous oxygen difference and endotracheal Pco2. The autoregulation index (A.I. = deltaCBF/deltaCPP) and the chemical index (C.I.= deltaCBF/deltaPaco2), were used as quantitative measures.
Stroke
PMID:Effect of beta-adrenergic blockade with propranolol on cerebral blood flow, autoregulation and CO2 responsiveness. 81 49

Platinum microelectrodes were used to measure H2 clearance in mouse brain, and the clearance curves were used to calculate regional cerebral blood flow (rCBF). The curves were usually biexponential, whether or not electrode placement was confined to the cortex. When calculated by the height over area method, rCBF in anesthetized mice averaged 37+/-14 and 49+/-15 ml/100 gm per minute in two successive groups where cortical placement had been made. After CO2 breathing, which raised PaCO2 to 77+/-18 torr, the mean rCBF of the latter group was elevated to 70+/-36 ml/100 gm per minute. Our basal rCBF values are lower than literature values for rats or mice, when compared with data obtained by other techniques. However, our data are comparable to rat rCBF data obtainted by others using H2 electrodes and are comparable also to data for whole brain CBF obtained by a variety of methods in larger anesthetized mammals. It is possible that H2 electrodes provide low values for supposedly "cortical" rCBF in the very small mouse brain, because is such brains the electrode is usually close enough to a slow clearing compartment for the electrode reading to be influenced by that compartment. At the same time one cannot rule out the possibility that other techniques when applied to small rodents may, on occasion, produce spuriously high values for CBF. Indeed, while some studies using the latter techniques do show unusually high values for cortical flow in these animals, other studies using similar methods do not.
Stroke
PMID:Regional cerebral blood flow in the anesthetized mouse as measured by local hydrogen clearance. 83 50

The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.
Stroke
PMID:Respiratory influence on the total and regional cerebral blood flow responses to intracranial hypertension. 84 90

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

Regional cerebral blood flow (rCBF) was repeatedly measured by the hydrogen clearance method in the frontal cortex of stroke-prone spontaneously hypertensive rats (SHRSP) at the age of 50 days and thereafter. When SHRSP rats developed severe hypertension (over 200 mg Hg at the age of 60 days) rCBF began to decrease abruptly in the frontal cortex--one of the three predilection sites of stroke in these rats. In contrast, such a reduction in rCBF was not noted in either stroke-resistant spontaneously hypertensive rats (SHRSR) which developed moderate hypertension (under 200 mg Hg), or in Wistar-Kyoto rats (WK) with normal blood pressure (under 15 mm Hg). A similar marked reduction of rCBF with severe hypertension (over 200 mm Hg) was also detected in apoplectic gene-free renal infarction hypertensive rats (RHR) experimentally produced from age-matched WK animals. Blood samples were obtained through an implanted femoral artery canula without disturbing the nonanesthetized SHRSP, SHRSR and WK rats. Arterial blood gas analysis (PaCO2, PaO2 and pH) showed no significant differences at the age of 5 months in any of these rats. Chemical cerbrovascular reactivity, that is, an increase in rCBF in response to CO2 inhalation, showed no significant difference among SHRSP rats from the age of 50 days to 5 months. However, it markedly decreased in SHRSP rats at the age of 9 months and thereafter (the average age of male SHRSP rats which develop stroke is 9 months). The present study showed stroke did not occur in antihypertensive agent-treated SHRSP rats. In these SHRSP rats rCBF did not decrease as long as blood pressure was well-controlled.
Stroke
PMID:Developmental course of hypertension and regional cerebral blood flow in stroke-prone spontaneously hypertensive rats. 89 41

The effect of several agents active on autonomic nervous system functions was tested on brain oxygen autoregulation parameters. It was found that atropine, propranolol and isoproterenol had no influence in abolishing the measured parameters. Phenoxybenzamine, tolazoline and dibenamine all suppress autoregulation. In an additional experimental series, a phenoxybenzamine infusion was given during O2 breathing. The infusion induced, in most cases, an additional rise in TpO2 (tissue pressure of oxygen, which refers to the partial pressure [in mm Hg] of this gas at the measuring tip of the electrode). It is concluded that an alpha-adrenergic mechanism is part of the autoregulation process. Also, the increase in brain TpO2 induced by 59% O2-5% Co2 breathing seems to be blocked or reversed by alpha-adrenolytic drugs, thus supporting the thinking that the effect of CO2 on cerebral blood flow is at least in part mediated through an alpha-adrenergic response.
Stroke
PMID:Pharmacological control of local oxygen regulation mechanisms in brain tissue. 96 Jan 68

Cerebrovascular reactivity to CO2 inhalation and voluntary hyperventilation was studied in seven normotensive subjects and nine hypertensive patients without clinical or angiographical signs of arteriosclerosis. Cerebral blood flow (CBF) was measured by the intracarotid 133Xe clearance method and calculated as the initial slope index. Three to five CBF measurements were made in each patient in the PaCO2 range of 20 to 55 mm Hg. No difference was observed in reactivity between hypertensive and normotensive patients, either during CO2 inhalation or during hyperventilation. The shape of the CBF:PaCO2 curve suggested a decrease in reactivity below a PaCO2 of 30 to 35 mm Hg in both groups. Above a PaCO2 of 35 mm Hg, exponential regression analysis yielded a mean reactivity of 6 +/- 2%, whereas below a PaCO2 of 30 mm Hg it was about 2%. The rise in CBF during CO2 inhalation was not influenced by the intravenous infusion of a small dose of trimethaphan which blocked the concomitant rise in blood pressure.
Stroke
PMID:Cerebrovascular CO2 reactivity in normotensive and hypertensive man. 96 Jan 76

From haemodynamic and metabolic investigation of 65 comatose subjects following cranial traumatism or cerebral vascular accident, the following prognostic and therapeutic indications emerged: The isolated increase in oxygen pressure in the jugular vein to above 50 mm Hg, the simultaneous decrease in circulation of the brain to below of 30 ml/100g/min., and of the brain consumption of oxygen to below 1.5 ml/100g/min., combined with a loss of autoregulation and a decrease in carbon dioxide reactivity indicate that prognosis is very poor. Induced arterial hypertension, associated with hyperventilation, partially corrects brain hypoperfusion in coma from bulbo-pontine lesions. Sodium penthiobarbital and sodium gamma hydroxybutyrate and have the effect of reducing oxygen metabolism which might have some therapeutic value during the acute phase of coma. Clomipramine which has a stimulating effect on oxygen metabolism should be kept in reserve for the chronic phase of prolonged coma.
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PMID:[Prolonged traumatic and vascular coma: prognostic and therapeutic indications based on hemodynamic and metabolic studies]. 100 13

The local tissue PO2 in the brain cortex and in the spinal cord of rats was examined with ultramicroelectrodes. In the spinal cord the PO2 was highest in white matter, intermediate in dorsal horn gray matter, and lowest in the ventral horn gray matter. In the gray matter of the cord, as well as in the brain, the PO2 at a fixed locus was found normally to oscillate. CO2 responses were more brisk in the cord than in the brain while the responses to hypoxia were similar. Therefore, it appears that the physiological regulation of blood flow in the spinal cord is qualitatively similar to that of the brain.
Stroke
PMID:Comparison of vascular reactivity in spinal cord and brain. 100 28


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