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

The influences of acute cerebral ischemia on renal hemodynamics were examined in spontaneously hypertensive rats in which cerebral ischemia was induced by bilateral carotid artery occlusion. Renal and cerebral blood flow were measured with a hydrogen clearance technique. Either phenoxybenzamine (0.5 mg/kg body wt) or propranolol (2 mg/kg) was given i.v. immediately after ischemia was induced to examine the drugs' effects on cerebral and renal hemodynamics. One hour after ischemia, cerebral blood flow was markedly reduced to 5, 3, and almost 0% of the preischemic value in the untreated, phenoxybenzamine-treated, and propranolol-treated rats, respectively. In contrast, renal blood flow at that time was decreased to 65, 88, and 67%, respectively. The calculated renal vascular resistance was similarly increased to 151% in the untreated and 136% in the propranolol-treated rats, but decreased to 82% in the phenoxybenzamine-treated rats. The present results indicate that in acute cerebral ischemia renal blood flow was considerably decreased with concomitant increased renal vascular resistance, and that such reduction in renal blood flow was minimized by alpha-adrenergic blockade but not by beta-blockade. It is concluded that activation of the alpha-adrenergic system in acute cerebral ischemia causes renal vasoconstriction.
Stroke
PMID:Renal blood flow in acute cerebral ischemia in spontaneously hypertensive rats: effects of alpha- and beta-adrenergic blockade. 288 58

We looked at the relation between systemic arterial blood pressure and recovery from spinal cord injury by inducing both hypertension and hypotension in 25 rats randomly allocated to five equal groups. The rats received no injury, a mild (2.3-g), or a severe (53.0-g) spinal cord injury lasting 1 minute. We used the hydrogen clearance technique to measure spinal cord blood flow at the injury site (T1) and at an adjacent site (C6). Mean systemic arterial blood pressure was either increased with adrenaline or decreased by phlebotomy in 20-mm-Hg intervals except for the severe-injury group, in which the posttraumatic pressure could only be increased with adrenaline. Spinal cord blood flow remained constant in the no-injury group between 81 and 180 mm Hg. After a mild injury, induced moderate hypertension (121-140 mm Hg) improved spinal cord blood flow significantly, whereas hypotension decreased it in a linear fashion. Severe injury caused a marked decrease in spinal cord blood flow and mean systemic arterial blood pressure. Even extreme hypertension (161-180 mm Hg) induced by adrenaline did not significantly increase spinal cord blood flow at T1 but caused hyperemia at C6 due to loss of autoregulation. In conclusion, normotension should be attempted, irrespective of the severity of spinal cord injury. Induced hypertension after severe spinal cord injury was not beneficial in improving spinal cord blood flow at the injury site while potentially increasing hemorrhage and edema.
Stroke 1989 Mar
PMID:Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats. 292 76

The susceptibility to cerebral ischemia was studied in stroke-resistant spontaneously hypertensive rats (SHRSR) treated by a long-term antihypertensive treatment, and compared with untreated SHRSR and Wistar rats (WR). Male SHRSR, aged 8 weeks, were divided into two groups and a long-term antihypertensive treatment for 4-6 weeks was started on one group (treated SHRSR: T-SHR) while the other group was left untreated as control (untreated SHRSR: U-SHR). The changes of blood pressure were checked on these rats. The prior treatment of hypertension was achieved by administration of hydroflumethiazide (120 mg/kg/day) and captopril (15-30 mg/kg/day) orally for 4-6 weeks by mixing in drinking water. All the experiments were performed at the age of 12-16 weeks and WR of similar age served as normotensive untreated control. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and blood pressure was always checked before BLCL. The survival ratio was observed from 1 hour to 24 hours after BLCL. The regional cerebral blood flow (rCBF) were measured before and 4 hours after BLCL periodically. The brain energy metabolites were measured 4 hours after BLCL. rCBF were measured at the thalamus by the hydrogen clearance method. ATP concentrations were determined by luciferine-luciferase method, c-AMP was measured by RIA and lactate by enzymatic method. The brain water content was measured by freeze-dry method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of long-term prior antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR]. 300 93

We examined the hypothesis that oxygen radicals may mediate the vasodilator effect of VIP on cerebral arterioles in cats equipped with cranial windows. The appearance of superoxide anion radical in cerebral extracellular space during VIP application was examined by measuring the rate of superoxide dismutase (SOD)-inhibitable reduction of nitroblue tetrazolium (NBT). Although VIP (1 and 10 micrograms/ml) caused substantial reduction of NBT, the rate of the SOD-inhibitable portion was not significantly different from zero. We also examined the effect of scavenging of superoxide and hydrogen peroxide by topical application of SOD plus catalase on the vasodilator effect of VIP (0.05-1.0 microgram/ml). The dilation in response to VIP was not significantly affected in either large or small arterioles by scavenging of superoxide and hydrogen peroxide. We conclude that VIP does not cause generation of superoxide and that superoxide or other reactive oxygen species derived from it, such as hydrogen peroxide and hydroxyl radical, are not mediators of the cerebral vasodilation caused by VIP.
Stroke
PMID:Superoxide anion radical does not mediate vasodilation of cerebral arterioles by vasoactive intestinal polypeptide. 302 25

Systemic fibrinolytic therapy for acute stroke is no longer recommended because of resulting systemic fibrinolysis and the risk of intracerebral hemorrhage. Human tissue-type plasminogen activator (TPA) is a native enzyme that converts plasminogen to plasmin with subsequent clot lysis. The affinity for plasminogen is increased several-fold when the substrate is bound to fibrin. At appropriate dosage, "clot-specific" thrombolysis may be achieved at the surface of the thrombus without creating systemic fibrinolysis. The authors designed a study to evaluate the effect of intravenous TPA administered 2 hours after acute thromboembolic stroke in rats. This time course was chosen to simulate an analogous clinical situation. Middle cerebral artery embolic stroke was caused by intracarotid injection of 0.025 cc of human blood clot in 16 rats. Regional cerebral blood flow, measured by the hydrogen clearance technique, and electroencephalographic (EEG) recordings were obtained every 30 minutes for 5 hours after thromboembolism. Eight rats received a 1-hour infusion of intravenous TPA (1.5 mg/kg) 2 hours after injection of emboli. Ipsilateral blood flow increased significantly within 30 minutes after intravenous TPA and reached preembolic levels within 60 minutes. Blood flow did not improve in the eight control rats throughout the experiment. Power spectral analysis of the EEG recordings showed improvement in the treated group compared to the control group. Postmortem angiography revealed proximal middle cerebral artery occlusion in control animals and patent middle cerebral arteries in TPA-treated animals. Serum fibrinogen and fibrin split products were unchanged in both groups, indicating the absence of systemic fibrinolysis. There were no intracerebral hemorrhages. It is concluded that, in this rat model, TPA increases blood flow with subsequent improvement in the EEG recording after thromboembolic stroke without evidence of systemic fibrinolysis. Intravenous TPA may be useful in the treatment of acute stroke in man.
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PMID:Recombinant human tissue-type plasminogen activator therapy in acute thromboembolic stroke. 311 28

The primary role of the heart is to provide energy for the circulatory transport of oxygen (O2) to cells at rates commensurate with their metabolic activity. At rest, even a "sick" heart may be capable of transporting O2 adequately. But during exercise, the increase in O2 required by muscle cells demands that their blood flow be increased. The supply of O2 needed to meet the O2 requirement for muscle mitochondrial high-energy phosphate generation during exercise is a critical function of the circulation. Thus, the adequacy of cardiovascular function can be estimated, noninvasively, from the pattern of O2 uptake in response to an exercise stimulus. While arterial O2 tension (PaO2) is dependent on pulmonary function (except for intracardiac right-to-left shunt), the mass transfer of O2 (VO2) between the cells and lungs depends on pulmonary blood flow (i.e., cardiac output) and O2 concentration difference between the pulmonary arterial and pulmonary venous blood, C(a-v)O2 (Fick principle). Thus, VO2 in the first 15 seconds of exercise can be used to describe the initial increase in pulmonary blood flow and stroke volume, while the subsequent rise in VO2 results from the further increase in VO2 in response to work rate increase are used to detect circulatory disturbances. Also, the rate of CO2 output (VCO2) has been valuable in the assessment of cardiovascular function when related to VO2. Inadequate O2 availability results in anaerobic metabolism, causing increased muscle lactic acid production. At the pH of cell water, most of the hydrogen ions produced with lactate are buffered by bicarbonate. The CO2 generated by the buffering reaction (22 ml for each milliequivalent) causes a net increase in VCO2 relative to VO2 at the work rate at which buffering begins. This provides a useful estimate of the anaerobic threshold. Thus, study of the dynamic coupling of external to cellular respiration during a work rate stimulus provides valuable, direct, and noninvasive information about cardiovascular mechanisms in health and disease.
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PMID:The Dickinson W. Richards lecture. New concepts in assessing cardiovascular function. 316 85

We attempted to ameliorate postischemic edema and brain tissue injury in cats by administering aminophylline to reduce the reactive hyperemia that supposedly aggravates both these sequelae. Forty-one cats were subjected to 1 hour of middle cerebral artery occlusion and were killed after 3 hours, 3 days, or 14 days of recirculation; one half of the cats received 0.916 ml/kg of a 25 mg/ml solution of aminophylline by infusion at a constant rate via the femoral vein starting 10 minutes before release of the occlusion and continuing for 5 minutes after initiation of recirculation; the other half received saline. Regional cerebral blood flow was monitored by the hydrogen clearance method and water content was evaluated by specific gravity measurements after 3 hours of recirculation; the status of the blood-brain barrier was assessed with Evans blue tracer. Morphologic observations were carried out in cats killed after 3 or 14 days of recirculation. Aminophylline-treated cats killed after 3 hours of recirculation showed significantly reduced hyperemia and edema and no leakage of Evans blue, which was present in all untreated cats killed after 3 hours or 3 days of recirculation. Morphologic observations revealed conspicuously more severe ischemic brain tissue damage in the untreated than in the aminophylline-treated cats after 3 and 14 days of recirculation. Our studies indicate the beneficial effect of administration of aminophylline in the amelioration of postischemic edema and brain tissue injury, which is presumably achieved by reduction of reactive hyperemia.
Stroke 1988 Oct
PMID:Effect of aminophylline on postischemic edema and brain damage in cats. 317 87

Edema formation following severe permanent or temporary cerebral ischemia in gerbils with an artificially reduced platelet count was investigated. Acute focal cerebral ischemia was produced by extracranial carotid ligation, and the local cerebral blood flow was estimated using the hydrogen clearance method. Brain tissue water and sodium and potassium contents were taken as indexes of brain edema. The platelet count was reduced in some gerbils by intravenous injection of neuraminidase. After 60 minutes of ischemia, a marked increase in tissue water and sodium contents accompanied by a decrease in potassium content was observed in untreated gerbils. However, gerbils with a reduced platelet count revealed similar but significantly smaller changes in all the measured parameters. Restoration of blood flow after 60 minutes of ischemia resulted in further accumulation of water and sodium and in depletion of potassium in both groups. These changes were significantly smaller in the gerbils with a reduced platelet count. It is concluded that platelets, activated by cerebral ischemia, may be involved in the development of ischemic brain edema in gerbils.
Stroke 1988 Apr
PMID:Are blood platelets involved in the pathogenesis of ischemic brain edema in gerbils? 336 76

The effect of isovolemic hemodilution with dextran 40 on local cerebral blood flow was measured in eight cats by means of the hydrogen clearance technique. Under normotension the decrease of hematocrit from 35% to 25% causes a sudden increase of up to 30% in local cerebral blood flow. After lowering the mean arterial blood pressure from 140 to 80 mm Hg, hemodilution did not alter cerebral blood flow significantly. From this observation it is concluded that the increase of cerebral blood flow following hemodilution is caused by compensatory vasodilatation and not by reduction of blood viscosity. This could imply that hemodilution cannot improve blood flow in areas of impaired autoregulation.
Stroke 1988 May
PMID:Autoregulatory capacity and the effect of isovolemic hemodilution on local cerebral blood flow. 336 91

Participation of the autonomic nervous system in cerebellar autoregulation during supratentorial cerebral ischemia induced by bilateral carotid ligation was studied using 23 spontaneously hypertensive rats. Cerebral and cerebellar blood flows measured by a hydrogen clearance method were evaluated under stepwise hemorrhagic hypotension before and 30 minutes after ligation and after a 30-minute recirculation period following 1 hour of ligation. alpha-Adrenergic blockade with phenoxybenzamine, beta-adrenergic blockade with propranolol, and muscarinic cholinergic blockade with atropine were selectively administered before ligation for inhibition of sympathetic and parasympathetic tone. Cerebral blood flow autoregulation was severely impaired during and after cerebral ischemia in each treatment group. During cerebral ischemia, cerebellar blood flow autoregulation was also significantly impaired in both the propranolol and atropine groups although it was better preserved in the phenoxybenzamine group. After recirculation, cerebellar blood flow autoregulation recovered almost to the normal range in the phenoxybenzamine and atropine groups but remained impaired in the propranolol group. Our results suggest that impaired cerebellar blood flow autoregulation in supratentorial cerebral ischemia is partly modulated by the alpha-adrenoceptor system, which is activated by hypertensive stimuli and cerebral ischemia, leading to vasoconstriction in the cerebellum.
Stroke 1988 May
PMID:Impairment of cerebellar blood flow autoregulation during cerebral ischemia in spontaneously hypertensive rats. 336 95


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