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

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

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

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

Cerebral blood flow was measured with the 133Xenon clearance method in anesthetized cats under controlled ventilation. An acute pressure increase in the carotid system increases the cerebrovascular permeability to Evans blue, indicating damage to the blood-brain barrier. In these conditions the reactivity or cerebral blood vessels toward changes in the acid-base balance is altered: the CO2 reactivity is less pronounced, while the effect of increasing the plasma (HCO-3) is more pronounced than in normal cats. Autoregulatory capacity toward moderate alterations in arterial blood pressure or in intracranial pressure is well maintained in these conditions.
Stroke
PMID:Cerebral blood flow in cats after an acute hypertensive insult with damage to the blood-brain barrier. 112 18

Cold water is known to facilitate the drowning process. To gather information on the possible relationship between ventilation and cold stimuli, measurements of inspired and expired breath by breath ventilation and alveolar PCO2 were made on 8 male subjects suddenly immersed in both cold (11 degrees C) and warm water (28 degrees C). The mean ventilation for all subjects for the 1st three breaths following cold water immersion was 94.5, 71.3 and 94.6 L/min (BTPS) as compared to 60.0, 36.2 and 38.5 L/min (BTPS) for warm water immersion. Alveolar CO2 fell dramatically in cold water from a pre-immersion mean value of 36.4 torr to 23.9 torr, whereas there was only a change associated with the first few breaths following immersion in warm water. In prolonged cold exposure, ventilation was still markedly above that observed in warm water after 5 min. There was no relationship between skin fold thickness and ventilatory response over the period studied. A large increase in ventilations is likely to result in inefficient swim stroke mechanics. This, combined with a high probability of inspiration of water, may contribute to death as a consequence of cold water exposure.
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PMID:Sudden cold water immersion. 114 45

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
Stroke
PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Blood flow in the hemispheres of baboons three years after middle cerebral artery occlusion has been assessed by the hydrogen clearance technique. Blood flow in the infarct itself varied from very low (8 ml/100 gm per minute) to very high (89 ml/100 gm per minute) values and, averaging the values for the infarct as a whole, it was impossible to distinguish average flows in the infarct from those of the normal hemisphere. Flow values in surrounding zones of the infarct remained significantly lower than those of comparable normal hemispheres, and, excluding the infarct, the mean average hemispheral blood flow was 35.2 ml/100 gm per minute. This indicates a significant reduction in flow in the cortex, subsequently shown histologically to be normal, compared with normal blood flow values for the baboon hemisphere. Autoregulation was lost in the infarct and impaired in surrounding tissue. CO2 reactivity was grossly reduced in the hemisphere as a whole but was present in all areas, even occasionally in electrode placements within the infarct itself. After perfusion fixation of the head, pathological study of the area of infarction showed a fairly consistent distribution, the infarct itself consisting of many dilated blood vessels of non-capillary nature scattered among fibrous tissue in what was virtually a glial scar.
Stroke
PMID:Local cerebral blood flow and vascular reactivity in a chronic stable stroke in baboons. 117 54

The time courses of ventilation (VE), O2 uptake (VO2), CO2 elimination (VCO2), respiratory exchange ratio (R), end-tidal PO2 and PCO2 and heart rate (HR) were studied in seven subjects performing light dynamic leg exercise in the supine position. Individual and group mean time courses in response to step changes in work load were computed and displayed graphically. A computer-based method was also used to fit mono- or bi-exponential mathematical functions to the recorded responses. The over-all rate of HR change in response to the transition from 0-load pedalling to exercise (on-response) was faster (mean response time, MRT = 31 s) than the corresponding VO2 response (MRT = 45 s) while VE responded considerably slower (MRT = 86 s). During the reverse transition (off-response), VO2 and VE changed with the same rate as in the on-response, while the HR-change was slower than during the on-response (MRT = 50 s). During the initial 15-sec period, VO2 changed only slightly, which contrasts to previous results in the sitting position, where 50% of the final change in VO2 has been reported to occur within the first 15-sec period, and where changes in blood distribution and stroke volume are known to be more pronounced than in the supine position. Our results emphasize the importance of central circulatory changes for the time course of VO2 at the start and end of exercise.
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PMID:Time courses of pulmonary gas exchange and heart rate changes in supine exercise. 118 40


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