Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Body fluid gas pressure and electrolytes of patients with ruptured aneurysm were continuously analyzed. Intracranial pressure (ICP) was regulated at the level of 120-100 mm H2O by cerebral ventricular drainage. There was no significant change in the pH, PCO2, HCO3-, Na+, K+, Ca++ in the cerebrospinal fluid (CSF) of patients with slight or moderate disturbance of consciousness (lethargic-drowsy state). The PcsfO2 of the patients with marked disturbances of consciousness (semicoma-coma) was significantly low. PcsfO2 of the patients with cerebral vasospasm was significantly lower than for those without vasospasms. PcsfO2/PaO2 was 0.27 +/- 0.01 in the patients with vasospasm and 0.50 +/- 0.01 in those with vasospasm. PcsfO2 tended to decrease in patients with markedly bloody CSF. When the bloody CSF was cleared by ventricular drainage, PcsfO2 increased. PcsfO2 did not return to a normal value in the patients with marked disturbances of consciousness despite sufficient arterial oxygen tension. This suggests that PcsfO2 and PcsfO2/PaO2 should provide a convenient index for the prognosis of patients with ruptured aneurysm.
Stroke
PMID:Body fluid oxygen tension and prognosis in patients with ruptured aneurysm. 4 45

Cerebral arteriospasm is a common complication of subarachnoid hemorrhage and is responsible for much of the brain damage which accompanies it. No pharmacologic agent has been found which regularly alleviates arteriospasm. We have evaluated the effect of continuous intravenous nitroglycerin infusion on the diameter of the basilar artery in dogs with cerebral vasospasm experimentally induced by subarachnoid blood injection. In 6 consecutive dogs, 10 minutes after beginning intravenous nitroglycerin at 100 microgram/min and at other times during 120 minutes of infusion, the diameter of the basilar artery had increased from 75 +/- 2% of control value to 114 +/- 2% of control value (p less than 0.001). In all 6 dogs, the basilar artery diameter during infusion was greater than the control value prior to creating subarachnoid hemorrhage. Intravenous nitroglycerin caused only a moderate (8%) decrease in blood pressure. Further investigation of the effects of nitroglycerin on cerebral vasospasm is warranted.
Stroke
PMID:Intravenous nitroglycerin in experimental cerebral vasospasm. A preliminary report. 10 21

Cerebral arteries have an abundant supply of adrenergic nerve fibers which are believed to release vasoactive substances responsible for the induction of cerebral vasospasm. To assess the importance of adrenergic nerves in this phenomenon, high doses (600 microgram/ml) of 6-hydroxydopamine (6-OHDA) were used to produce in vitro chemical sympathectomy in bovine middle cerebral artery. 6-OHDA reduced catecholamine fluorescence to undectable limits. H3-norepinephrine re-uptake was reduced to 1.5% of intact controls. Arterial norepinephrine content was reduced by 92%. Contractile responses to norepinephrine, serotonin, and fresh human whole blood were modestly reduced after denervation. This reduction was probably due to alpha receptor inactivation by 6-OHDA, because after protection of the alpha receptors with phentolamine the vessel response was the same as in untreated controls. Contractions in response to aged human whole blood were not affected by denervation. The results suggest that the endogenous release of catecholamines does not play a major role in the initiation or spread of blood-induced vasospasm in large cerebral arteries.
Stroke
PMID:Role of adrenergic nerves in blood-induced cerebral vasospasm. 22 48

A method for induction of subarachnoid hemorrhage (SAH) in a rat model is described. Resolution of the hemorrhage was documented photographically and microscopically at intervals from 1 hr to 8 days. Photographs indicated that most of the hemorrhage was resorbed within 3 days, an observation confirmed microscopically by the amount of red blood cells in the subarachnoid space. Significant cerebral vasospasm was documented within the first 2 days after the induction of hemorrhage with the basilar artery returning to baseline values at an average of 3 days followed by moderate dilatation at 5 to 8 days. The suitability of the rat as an animal model for further investigation of subarachnoid hemorrhage is discussed.
Stroke
PMID:Small animal model for investigation of subarachnoid hemorrhage and cerebral vasospasm. 50 95

Uridine 5'-triphosphate (UTP) induced long-lasting contractions of isolated human brain arteries; contractions without decrement were observed for periods of up to 20-24 hours at which time the tissues were relaxed in a dose-dependent manner by theophylline. In some vessels, rhythmic oscillations accompanied the prolonged elevation in tension. In canine middle cerebral arteries, UTP produced dose related contractions within the dose range of 1.7 X 10(-6) to 1.7 X 10(-4) M; these responses were unaffected by methysergide 2.8 X 10(-7) M, phenoxybenzamine 2.9 X 10(-5) M or indomethacin 9.8 X 10(-6) M, suggesting that the UTP mechanism of action is probably independent of tryptaminergic or alpha adrenergic receptor activation, or of prostaglandin biosynthesis. The ability of UTP to produce prolonged contraction of cerebral vessels, thus, provides an in vitro preparation in which it is possible to study some of the basic mechanisms that are associated with cerebral vasospasm.
Stroke
PMID:Prolonged contraction of isolated human and canine cerebral arteries induced by uridine 5'-triphosphate. 64 5

Diazoxide failed to safely relieve cerebral vasospasm by intracisternal injections in dogs and by intracarotid injections in monkeys despite in vitro documentation of arterial relaxation with this agent. Administration of the drug frequently produced hypotension and, in the presence of vasospasm, was associated with a high mortality rate.
Stroke
PMID:Limitations of diazoxide reversal of vasospasm. 81 24

The concentration of prostaglandin F2alpha (PGF2alpha) was measured in cerebrospinal fluid (CSF) obtained by lumbar puncture in patients with subarachnoid hemorrhage and compared to control values. The level of this prostaglandin was elevated at some time in most patients during the course of their illness. However, this could not be correlated with the severity of neurological deficits observed. The possibility that the concentration of PGF2alpha in lumbar fluid may not reflect that present intracranially was tested experimentally in anesthetized dogs. In these experiments only a small fraction of the radioactive PGF2alpha injected into the cisterna magna appeared in lumbar CSF. Prostaglandin F2alpha rapidly disappeared from the cisterna magna, half time 8 minutes, and radioactivity was present in blood from the jugular vein indicating that normally this prostaglandin rapidly egresses from the CSF into blood. These findings suggest that PGF2alpha can be rapidly transported away from the brain. This could explain the low concentrations of PGF2alpha in CSF of normal individuals and in some patients who have severe cerebral vasospasm. Conversely, the elevation of PGF2alpha in lumbar CSF noted in some patients might be due, in part, to an impairment of transport caused by the size and location of the hemorrhage.
Stroke
PMID:Levels and disappearance of prostaglandin F2alpha in cerebral spinal fluid: a clinical and experimental study. 92 55

In this cooperative study among 13 institutions, 502 patients were treated with antifibrinolytic medication (epsilon-aminocaproic acid or tranexamic acid) within a 14-day period following rupture of an intracranial aneurysm. Mortality at the end of 14 days was 11.6%; proved rebleed rate was 12.7%. Patients with an internal carotid or anterior cerebral aneurysm had the highest mortality and rebleed rate. Most rebleeds occurred between the sixth and eleventh days following the initial bleed. Significantly higher mortality was reported among patients with cerebral vasospasm, yet rebleed rate was no different among those patients with or without vasospasm. The same pattern was observed among patients with a mean blood pressure value above and below 110 mm Hg. We conclude that antifibrinolytic therapy provides beneficial treatment to patients with recent onset subarachnoid hemorrhage (SAH) following rupture of an intracranial aneurysm.
Stroke
PMID:Intracranial aneurysms and subarachnoid hemorrhage. A cooperative study. Antifibrinolytic therapy in recent onset subarachnoid hemorrhage. 119 27

Longitudinal stretch of the rabbit basilar artery produces local injury followed by prolonged circular constriction. After stretching and rapid release in vitro localized constrictions promptly occurred. This could be prevented by prior treatment with cyanide or calcium-free solution. Once produced, constrictions persisted for more than 72 hours. Previously induced constriction was not reversed by treatment for two hours with cyanide or by removing calcium. Histological observation indicated that constricted areas were associated with a discrete circumferential rupture of the internal elastic lamina and disruption and thinning of the underlying media. Specific catecholamine fluorescence at the adventitio-medial junction was unchanged in constricted areas. The relationship between smooth muscle cell length and resting tension of artery segments with and without constrictions was compared. Segments with constrictions had a shorter muscle length for any given resting tension, which confirms that constriction was not due to passive collapse of the vessel wall. These findings suggest that injury of cerebrovascular smooth muscle may result in essentially irreversible vasoconstriction. Such a mechanism could contribute to the pathogenesis of prolonged cerebral vasospasm after SAH or traumatic injury to the cerebrum.
Stroke
PMID:An in vitro study of prolonged vasospasm of a rabbit cerebral artery. 126 10

31P-NMR spectroscopic studies were performed in vivo on brains of rats administered cocaine. Cocaine.HCl (1-5 mg/kg) administered systemically to lightly anesthetized rats resulted in significant and progressive deficits in whole brain intracellular free Mg ([Mg2+]i). Intracellular pH (pHi) also fell in a progressive manner but only after a significant fall in brain [Mg2+]i was noted. Both [Mg2+]i and pHi returned to normal in most rats. Brains of rats that exhibited stroke-like events, however, demonstrated continued intracellular acidosis associated with progressive loss of phosphocreatine and elevation of Pi up until death. These observations are consistent with the tenet that injection of cocaine can result in severe cerebral vasospasm, ischemia and rupture of cerebral blood vessels as a consequence of depletion of brain [Mg2+]i.
 ...
PMID:Cocaine induces intracellular free Mg deficits, ischemia and stroke as observed by in-vivo 31P-NMR of the brain. 142 Feb 62


1 2 3 4 5 6 7 8 9 10 Next >>