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

The influence of isoflurane on haemodynamics and myocardial oxygen consumption was examined in seven geriatric patients under conditions of controlled ventilation and a normal arterial carbon dioxide tension. During isoflurane/nitrous oxide in oxygen anaesthesia (0.75 and 1.5 vol% inspired isoflurane) no significant changes occurred in cardiac output, stroke volume, heart rate, central venous and pulmonary artery pressure. Arterial pressure decreased, as did total peripheral resistance. A reduction in left ventricular maximum dp/dt (18-39%) was, at least in part, a result of changes in loading conditions. Total body (CaO2--CVO2) and base excess values remained within the normal range. We consider that the oxygen supply was adequate to meet the metabolic demands of the body as a whole. Myocardial oxygen consumption decreased by 25% during 0.75 vol% inspired isoflurane and by 43.5% with deepening of anaesthesia (1.5 vol% isoflurane).
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PMID:Haemodynamics and myocardial oxygen consumption during isoflurane (forane) anaesthesia in geriatric patients. 101 44

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.
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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

Effects of the drug xylazine were determined on arterial pH, arterial oxygen pressure (PaO2), arterial carbon dioxide pressure (PaCO2), aortic blood pressure, aortic flow, heart rate, pulse pressure, stroke volume, and peripheral resistance of dogs. The drug was given intravenously (IV) with and without atropine and was given intramuscularly (IM) without atropine. After IV administration of xylazine (1.1 mg/kg), arterial pH, PaO2, and PaCO2 values were not changed from control values. However, the drug did produce a statistically significant decrease in heart rate, decrease in aortic flow, initial increase in blood pressure followed by decrease, and increase in peripheral resistance. Stroke volume and pulse pressure were not significantly changed. Atropine (0.02 mg/kg, IV) did not significantly change any of the effects produced by xylazine. Intramuscular administration of xylazine (2.2 mg/kg) did not produce significant changes in arterial pH, PaO2, or PaCO2. Heart rate and aortic flow decreased significantly, but statistically significant changes did not occur in aortic blood pressure or peripheral resistance; however, the changes in these last 2 values were in the same direction and were of similar magnitude as those which occurred afger IV administration of xylazine.
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PMID:Cardiopulmonary effects of xylazine in dogs. 114 58

To evaluate the effect of different levels of arterial oxygen content on hemodynamic parameters during exercise nine subjects performed submaximal bicycle or treadmill exercise and maximal treadmill exercise under three different experimental conditions: 1) breathing room air (control); 2) breathing 50% oxygen (hyperoxia); 3) after rebreathing a carbon monoxide gas mixture (hypoxia). Maximal oxygen consumption (Vo2 max) was significantly higher in hyperoxia (4.99 1/min) and significantly lower in hypoxia (3.80 1/min) than in the control experiment (4.43 1/min). Physical performance changes in parallel with Vo2 max. Maximal cardiac output (Qmax) was similar in hyperoxia as in control but was significantly lower in hypoxia mainly due to a decreased stroke volume. A correlation was found between Vo2 max and transported oxygen, i.e., Cao2 times Amax, thus suggesting that central circulation is an important limiting factor for human maximal aerobic power. During submaximal work HR was decreased in hyperoxia and increased in hypoxia. Corresponding Q values were unchanged except for a reduction during high submaximal exercise in hyperoxia.
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PMID:Effect of changes in arterial oxygen content on circulation and physical performance. 115 May 96

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.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xe concurrently with measurements of local cerebral blood flow (LCBF) after injection of 133Xe directly into the distal stump of the occluded middle cerebral artery (MCA) by the use of the gamma camera after producing experimental ischemia in baboons by occluding the MCA. Regional MCA stump pressure (rMCAP) was also measured. Regions of ischemia assessed by intracarotid injection of 133Xe correlated well with the territory of infarct defined by injection of 133Xe into the distal MCA stump. Flow values in ischemic regions obtained by direct injection of 133Xe into the MCA were 15% to 20% lower than those obtained by intracarotid injection of 133Xe. Possible explanations for these differences are discussed. During induced hypertension autoregulation in ischemic areas was abolished and paradoxical responses of LCBF and rMCAP to changes in arterial carbon dioxide tension (PaCO2) were confirmed.
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PMID:Regional cerebral blood flow measured by the gamma camera after direct injection of 133Xe into the distal stump of the occluded middle cerebral artery. 115 74

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.
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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

Metabolic, temperature, and cardiorespiratory responses of 19 healthy males, age range 18-30 yr for one group and 40-55 yr for another, were studied during 210 minutes submaximal work at 35% Vo2 max. The subjects were exposed to four different pollutant gas mixtures at two different temperatures, 25 degrees C and 35 degrees C (relative humidity 30%). The four gas mixtures were filtered air (FA), 50 ppm carbon monoxide in filtered air (CO), 0.24 ppm peroxyacetyl nitrate in filtered air (PAN), and a combination of all three mixtures (PANCO). In the CO exposure, the heart rate was significantly greater than that observed during FA conditions (P less than 0.05). Metabolic and thermoregulatory responses to long-term work were not different in the various pollutant environments. Significant decreases in stroke volume and increases in heart rate were observed during the course of the 25 degrees C exposures with no alteration in cardiac output. Heart rates were higher during 35 degrees C exposures while cardiac output remained at the same level with a consequent further reduction in stroke output.
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PMID:Man's physiologic response to long-term work during thermal and pollutant stress. 119 54


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