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

The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.
Stroke
PMID:The effect of a simulated subarachnoid hemorrhage on cerebral blood flow in the monkey. 0 Aug 20

The effect of blood injected into either subarachnoid space or subcortical brain tissue upon lactate and pyruvate concentrations as well as acid-base balance of cerebrospinal fluid (CSF) was studied in the anesthetized dog. CSF lactate and lactate/pyruvate ratio (L/P ratio) increased progressively following the intracranial injection of blood and reached the maximum level at six hours after injection. These changes were significantly greater in animals with intracerebral hematoma than in those with subarachnoid hemorrhage (SAH). An increase in CSF lactate and L/P ratio in hemorrhagic CSF seems to be caused by two different factors. Shed blood cells per se produce lactate and pyruvate, and blood in the subarachnoid space and intracerebral hematomas cause secondary changes in brain tissue metabolism by a probable reduction of cerebral blood flow. Therefore, an increase in CSF lactate with a concomitant rise in CSF L/P ratio is a useful indicator for brain tissue hypoxia, even when CSF is hemorrhagic. The association of an increase in CSF lactate to a disproportionate decrease in CSF HCO-3 was also observed in these animals.
Stroke
PMID:Lactate and pyruvate concentrations, and acid-base balance of cerebrospinal fluid in experimentally induced intracerebral and subarachnoid hemorrhage in dogs. 0 Aug 22

Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enchanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation. Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit. Findings from patients with cerebral infarction were compared against those of three control groups: (1)normals, (2)a stroke control group and(3)a stroke risk factor group. Plasma HMWFC findings were significantly (p less than 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p less than 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha1-antitrypsin and alpha2-macroglobulin also were significiantly higher (p less than 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p less than 0.001), and high HMWFC values were associated with poor clinical outcome. Plasma HMWFC values were significantly higher (p less than 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism. These findings docunment the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.
Stroke
PMID:Blood coagulation and plasma fibrinolytic enzyme system pathophysiology in stroke. 6 Aug 7

In order to study the effects of septic embolism on the brain, silicone rubber emboli of various types were injected into the carotid arteries of 35 dogs. Pathologic and angiographic studies were performed to assess the resultant arterial and parenchymal lesions. Pure silicone rubber emboli (14 dogs) produced occasional intra-arterial thrombosis but no arteritis. Sterile and bacterially contaminated emboli containing a lead-chromate pigment (similar to those used in previous studies of septic embolism) (11 dogs) and pure silicone rubber emboli with transversely oriented canals (10 dogs), after brief placement in a bacterial suspension, were associated with intense inflammatory arteritis. This was accompanied by focal meningitis, subarachnoid hemorrhage, thrombosis, and cerebritis of the underlying cortex. The findings resembled those found in mycotic aneurysm. Aneurysmal dilatation was observed in one postmortem angiogram. In previous models of mycotic aneurysm, the inflammation attributed to bacterial contamination was probably due to the lead-chromate pigment used.
Stroke
PMID:Cerebral arterial lesions resulting from inflammatory emboli. 10 Sep 7

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

Antecubital venous blood was sampled from stroke patients in the presence of disodium ethylenediamine tetraacetate. Plasma was analyzed for cyclic AMP applying a competitive protein binding method without any special pretreatment. In mild hemispheric infarction as manifested by moderate hemiparesis and/or dysarthria, plasma cyclic AMP remained in the normal range (8-18 picomoles/ml). In most of the cases with moderate infarction, the cyclic AMP level was distinctly below the normal range several days after the onset of symptoms. However, cyclic AMP remained in the normal range in severe infarction with signs of brain edema, and in two cases with moderately severe symptoms. One of the two cases suffered from later development of brain edema, and the other revealed a large lesion in brain scintigrams. The sizes of the lesion revealed in brain scintigrams were smaller in the moderate cases and larger in the severe cases, except in one of the cases mentioned above. It appeared that with plasma cyclic AMP levels we could predict the extent of the lesion, and perhaps the subsequent development of impending brain edema in a few days after the onset of cerebral infarction. In moderate cases of cerebral hemorrhage, judged from the consciousness, cyclic AMP decreased to a subnormal level 2-4 days after the onset. In severe cases it remained in the normal range. Subarachnoid hemorrhage showed significantly elevated cyclic AMP levels in the early stage.
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PMID:Venous plasma cyclic AMP in acute cerebrovascular disease. 18 49

Microsurgical and microscopic methods were employed in guinea pigs to expose, observe, and measure response characteristics of cerebral cortical pial microvessels and microcirculation to traumatic and nontraumatic experimental subarachnoid hemorrhage. Bleeding produced by vascular micropuncture was associated with a 44.3% arteriolar constriction. Topical application of homologous blood alone produced a 33.2% vasoconstriction. Observed microcirculatory flow characteristics subsequent to such microvascular changes were consistent with those known to be associated with cerebral cortical infarction. These changes could be prevented or reversed by topical application of the alpha adrenergic blocker, phenoxybenzamine. Topical pretreatment with the beta adrenergic blocker, propranolol, prevented blood-induced spasm, but did not reverse such spasm once it had been established. A chemo-mechanical mechanism is suggested as underlying the vasoconstriction association with rupture of pial microvessels. It is thought that consideration of such microvascular characteristics, in conjunction with those known to be associated with larger intracranial vessels, adds to current knowledge of the pathophysiology of subarachnoid hemorrhage and may be extrapolated to bear future clinical import.
Stroke
PMID:Pial microcirculation in subarachnoid hemorrhage. 23 72

Survival and factors affecting survival were studied in 1,484 new cases of acute definite stroke occurring between Jan 1, 1970, and June 30, 1971, in Manitoba. The 962 infarctions, 279 hemorrhages, and 243 unidentified strokes were ascertained from hospital claim reports. Personal, clinical, and laboratory data were collected from hospital medical records, death certificates, and autopsy reports. Cases were followed up until Dec 31, 1973, to determine survival. Survival was significantly better in infarction than in hemorrhage, in subarachnoid hemorrhage than in intracerebral hemorrhage, in men than in women, in the young than in the old, in the married than in the single, in hemorrhage cases from rural areas than from urban areas, and in those discharged home than in those transferred to long-term care hospitals. These data may help in predicting the outcome of stroke and in planning for more efficient care.
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PMID:Prognostic factors in the survival of 1,484 stroke cases observed for 30 to 48 months. I. Diagnostic types and descriptive variables. 41 5

Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.
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PMID:Prinzmetal's variant angina associated with subarachnoid hemorrhage: A case report. 43 81

Moyamoya disease is a rare but well described entity which has been found in the angiographic investigation of subarachnoid hemorrhage, its most common symptom in adults. We present 4 patients in whom moyamoya disease and an intracranial saccular aneurysm were discovered. In 2 of the 3 patients suffering a hemorrhage, the aneurysm was the source of bleeding. Three of the aneurysms were located at the basilar artery bifurcation. We recommend a careful search for a concomitant aneurysm in all patients with subarachnoid hemorrhage in whom moyamoya disease is found. We believe these patients should be treated as though the aneurysm were the source of bleeding.
Stroke
PMID:Intracranial saccular aneurysm and moyamoya disease. 44 41


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