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

The medical community has not yet identified cerebrovascular pathophysiological factors that distinguish patients at high risk for stroke or aid in selecting patients for microvascular cerebral bypass. In this study, we describe the courses of 13 patients, all of whom suffered recurrent episodes of transient cerebral ischemia after previous cerebral infarction. These patients underwent regional cerebral blood flow studies using xenon inhalation with a CO2 challenge before and at various times after extracerebral-to-intracerebral microvascular anastomosis. Collateral circulation was assessed in all patients before surgery using four-vessel cerebral angiography. Patients were followed for a mean of 30 months (range, 1-7 yr) after the anastomosis. Measurements of mean cortical cerebral blood flow, as measured using the initial Slope Index, and CO2 cerebrovascular reactivity of these 13 patients were compared with those in a group of 20 patients designed as controls. Hemispheric cortical blood flow was significantly depressed in these patients before surgery compared with those in the control group (P less than 0.05). After the bypass, the mean resting Initial Slope Index in these patients increased 14% (P = 0.0005). Cerebral blood flow both before and after CO2 inhalation improved significantly in these patients after surgery (P = 0.001). Detectors bordering computed tomographic or magnetic resonance image documented infarctions, identified as peri-infarct regions, and demonstrated significant mean increases in both cerebral blood flow (38.8-43.2 ml/min/100 g, P = 0.05) and CO2 cerebrovascular reactivity in these patients after bypass (1.71 + 1.91% to 4.00 + 2.38% change Initial Slope Index/mm Hg CO2, P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved cerebral blood flow and CO2 reactivity after microvascular anastomosis in patients at high risk for recurrent stroke. 164 Nov 7

The ability of diphenylhydantoin (DPH) to protect against hypoxia-induced neuronal damage was examined using electrophysiological recordings of extracellular evoked potentials from CA1 pyramidal neurons of rat hippocampal slices in vitro. In normal medium, a 15-min hypoxic insult (95% N2/5% CO2) produced rapid and complete loss of Schaffer collateral synaptic transmission, which only recovered to 20% of pre-hypoxia values after 90 min of reoxygenation. DPH (20 microM) bath applied prior to onset of hypoxia slowed the loss of transmission during hypoxia, and led to 75% recovery of evoked potentials upon reoxygenation. Thus, DPH appears to protect against hypoxia-induced loss of synaptic transmission, and may thereby lessen neuronal damage and cognitive dysfunction associated with stroke.
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PMID:Diphenylhydantoin protects against hypoxia-induced impairment of hippocampal synaptic transmission. 164 90

The ability of diphenylhydantoin (DPH) to prevent hypoxia-induced [3H]glutamate release was examined in perfused rat hippocampal slices. Hypoxia (25 min; 95% N2/5% CO2) caused a prolonged release of [3H]glutamate, which was reduced significantly if DPH (20 microM) was present from the beginning of the perfusion. Perfusion with oxygenated medium (reoxygenation) following hypoxia also caused a pronounced release of glutamate. A therapeutic concentration of DPH, added before, during, or after hypoxia, decreased this release of glutamate. These results suggest that DPH may protect against glutamate-mediated neurotoxicity associated with stroke.
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PMID:Diphenylhydantoin attenuates hypoxia-induced release of [3H]glutamate from rat hippocampal slices. 168 11

Controversy exists as to whether plasma volume (PV) expansion has the potential to increase maximal oxygen uptake (VO2max). In the present study, VO2max and exercise time to fatigue were measured in nine untrained men when plasma volume (PV) was normal and then again on the next day following two levels of PV expansion. Resting PV was expanded (via intravenous infusion of a 6% dextran solution) by 282 +/- 16 ml (i.e., PVX-1) and then by 624 +/- 26 ml (i.e., PVX-2). PVX-1 increased stroke volume (CO2 rebreathing) during submaximal exercise by 15% (P less than 0.05) above normal levels. VO2max following PVX-1 was increased 4% (P less than 0.05; 3.78 to 3.92 l/min) despite a 4% reduction in hemoglobin concentration. Exercise time to fatigue was also increased (P less than 0.05). PVX-2 resulted in an 11% (P less than 0.05) reduction in hemoglobin concentration during maximal exercise and a return of VO2max and exercise time to normal levels. In summary, we have observed in untrained men that 200-300 ml of PV expansion increases SV, measured during submaximal exercise, yet causes only a small amount of hemodilution. As a result, VO2max is increased slightly and performance is improved. Further PV expansion to levels 500-600 ml above normal results in an excessive hemodilution and a subsequent decline in VO2max and performance to normal levels. There is an optimal PV for eliciting VO2max in untrained men which appears to be approximately 200-300 ml above their normal levels.
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PMID:Maximal oxygen uptake relative to plasma volume expansion. 169 70

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR (r = 0.69 in VMRTOT versus VMRACE and 0.79 in VMRCO2 versus VMRACE; P less than 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. 172 37

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.
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PMID:Doppler CO2-test in patients with vertebrobasilar ischemia. 179 55

While the in vitro reactivity of cerebral conducting vessels following subarachnoid hemorrhage has been extensively studied, in vivo cerebrovascular CO2 reactivity has not been systematically investigated. We tested the hypothesis that, in the canine model of subarachnoid hemorrhage, the rise in cerebral blood flow normally seen with hypercapnia is blunted during delayed vasospasm. Four groups of animals were studied: one received two 4-ml subarachnoid injections of nonheparinized arterial blood into the cisterna magna (n = 8), one received three subarachnoid injections of 5 ml blood (n = 5), one received two subarachnoid injections of 4 ml saline (n = 5), and a control group (n = 5) had no subarachnoid injections or angiography. Basilar artery diameter was measured from baseline and follow-up angiography. We determined CO2 reactivity by randomly varying the concentration of inspired CO2 and measuring regional cerebral blood flow with radiolabeled microspheres. Basilar artery diameter was not affected by saline injection and was reduced by 26 +/- 2.9% in the two-hemorrhage group and 55 +/- 1.9% in the three-hemorrhage group. Baseline cerebral blood flow and CO2 reactivity were similar in all four groups. We conclude that, in this model of delayed vasospasm, regional cerebral vascular CO2 reactivity is intact and extrapolation of in vitro data regarding basilar artery diameter and reactivity to cerebral blood flow must be done cautiously.
Stroke 1991 Mar
PMID:Cerebrovascular CO2 reactivity during delayed vasospasm in a canine model of subarachnoid hemorrhage. 190 Jun 46

To show relationship between degree of carotid arterial stenosis and cerebral blood flow reactivity (RES%) to induced hypercapnia, fluorine-18-fluoromethane and positron emission tomography (PET) was used to study 18 patients with carotid distribution transient ischaemic attacks (TIA), all free of stroke, who had angiographic-proven unilateral arterial disease. Non-involved carotid arteries were either normal or had non-stenotic plaque. Either normal arteries or nonstenotic ulcerations in the symptomatic carotid arteries were present in five of 18 (28%), ipsilateral carotid stenosis from 50-99% was present in eight of 18 (44%), and ipsilateral internal carotid occlusion was present in five of 18 (28%) patients. In comparison with 14 normal controls, all patients with symptomatic middle cerebral artery (MCA) flow territories had significantly lower mean (SEM) RES% [5.0' (0.2) vs 4.0 (0.9), p less than 0.04]. Symptomatic anterior borderzone (ABZ) RES% was also significantly lower [4.6 (0.4) vs 3.3 (0.9), p less than 0.04], than controls. In patient subgroup comparisons, the 50-99% stenosis subgroup clearly had the lowest MCA RES% [3.4 (0.2)] as well as the lowest ABZ RES% [2.8 (0.4)] on their symptomatic sides. Age, expired pCO2, mean arterial blood pressure, serum glucose, serum haematocrit and number, type and estimated duration of TIAs were not significantly different between subgroups. Linear regression showed a significant relationship between RES% and both measured percentage-stenosis (p = 0.04) and residual luminal diameter (p = 0.05) in symptomatic MCA territories. This approached significance in symptomatic ABZ regions. This preliminary data set suggests that unilateral carotid stenosis can and does result in impaired CO2 reactivity following hypercapnia. The relative normality of CO2 reactivity in those with carotid occlusion is discussed.
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PMID:Blood flow reactivity to hypercapnia in strictly unilateral carotid disease: preliminary results. 190 47

1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose-anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis. 2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2 with 5% CO2 at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2 at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air. 3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions. 4. The control animals showed a dose-dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection. 5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls. 6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role than PO2 or PCO2 abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated rats.
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PMID:Cardiovascular responses to nifedipine in anaesthetized rats with abnormal blood gas/pH levels. 190 87

We used single-photon emission computed tomography to measure cerebral blood flow, cerebral blood volume, and cerebral perfusion reserve and transcranial Doppler sonography with CO2 stimulation to assess hemispheric vasomotor reactivity in 37 patients and in normal controls. Computed tomography and magnetic resonance imaging were performed to differentiate morphologically low-flow infarcts (n = 17) from territorial infarcts (n = 20). In patients with either type of infarct, blood flow was decreased and blood volume was increased in the infarcted areas compared with the same areas in the controls. Perfusion reserve and vasomotor reactivity were significantly reduced in patients with territorial infarcts and carotid artery occlusions (n = 12) and even more reduced in patients with low-flow infarcts (p less than 0.001). Both parameters were normal in patients with cardiac embolic territorial infarcts (n = 8). In patients with territorial infarcts, blood flow and perfusion reserve changes were restricted to the infarcted areas, whereas in patients with low-flow infarcts, regions of decreased perfusion reserve considerably exceeded the area of the infarct. Low-flow infarcts are related to the hemodynamic effects of severe extracranial carotid artery disease.
Stroke 1991 Sep
PMID:Clinical and hemodynamic aspects of low-flow infarcts. 192 54


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