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

White and regional gray matter distributions of water, blood flow, and the protein tracer pertechnetate were measured in five normal squirrel monkeys. A second group of five monkeys, which had undergone unilateral nephrectomy six months previously, were found at the time of study to have blood pressures similar to those of the control animals but increased brain water and altered distribution of blood flow which was increased in white matter. No alteration of capillary permeability to the protein traces attended these changes, which appeared to be influenced by blood pressure. Nephrectomy without hypertension influences brain water content, perhaps because of an effect on cerebral resistance vessels. In hypertensive encephalopathy renal lesions, as well as intraluminal pressure changes, may be related to cerebral edema.
Stroke
PMID:Brain water alterations after unilateral nephrectomy. A study of regional circulatory factors in squirrel monkeys. 40 49

In the absence of universally accepted criteria for the medical treatment of stroke, we made a rigorously randomized comparative study of different treatments in 300 patients. One group of patients received only a general supportive treatment designed to ensure adequate supplies of water, electrolytes and calories, plus whatever was needed to prevent infection and correct extant associated pathology. Three other groups of patients were treated in the same way but were also given, respectively, one of the following medications: Hydergine (Sandoz) (a mixture of three ergot alkaloids), dexamethasone, and mannitol. No statistically significant difference emerged among any of the treatment groups and the reference group in terms of objective therapeutic results. The authors concluded that, at least with the dosage used in this study, none of the treatments proved more useful than conventional supportive therapy in the first 10 days after a stroke.
Stroke
PMID:Is there a real treatment for stroke? Clinical and statistical comparison of different treatments in 300 patients. 41 28

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.
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PMID:Renin-angiotensin system in stroke-prone spontaneously hypertensive rats. 42 75

Cerebral microemboli were formed in rats by injecting 4,000 carbonized microspheres, 50 +/- 10 mu in diameter, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. The microspheres were mainly distributed in the cerebral hemisphere on the side of the injection. In 61 rats this hemisphere contained 582 +/- 20 microspheres against 99 +/- 9 in the contralateral hemisphere. Brain edema was assessed by measuring brain content of water, sodium and potassium. Blood-brain barrier (BBB) permeability was determined by brain accumulation of 125I-albumin. In the ipsilateral hemisphere brain edema and an increase in BBB permeability appeared 6 hours after embolization and progressed up to 48 hours. Twenty-four hours after embolization, significant correlations were observed between the microsphere content of the cerebral hemispheres and 1) the increases in water and sodium levels, 2) the decrease in potassium level, 3) the increase in BBB permeability. The study of these correlations should make it possible to ignore the poor reproducibility of embolizations and to analyze with increased accuracy the results of various experiments.
Stroke
PMID:Brain edema and blood-brain barrier permeability following quantitative cerebral microembolism. 43 98

In experiments carried out on adult rabbit "chest-head" preparations the volume changes of the exposed brain (BrV) were determined in repeated tests during a controlled increase of the systemic venous pressure (SVP) of about 13 mm Hg. The changes of both SVP and BrV were usually parallel at the onset of the experiments, but when the brains became preedematous hysteresis appeared in the plots of their relationships. The hysteresis increased gradually (sometimes with periods of partial decrease) thus indicating a delay in the draining of blood from the brain's venous system and in the removal of excess extracellular fluid from the cebral tissue. Evidence for water filtration through the capillary walls during increase of the SVP, and, thus, of brain intravascular pressure, was obtained by detecting the dynamics of [Na+] and [K+] in the extracellular fluid of the cerebral cortex by ion-selective electrodes. This process appeared reversible in normal brains while in the preedematous ones the excessive water filtration resulted in brain edema. The preedematous state of the brain is believed to be caused by changes of the mechanical properties of brain tissue and/or by changes in osmolarity.
Stroke
PMID:Pathophysiological mechanisms of brain edema development: role of tissue factors. 43

Deaths associated with strokes from 1963 to 1975 among 36,860 adult residents of Washington County, Maryland, were studied in relation to the hardness of drinking water at home, assessed on the basis of 1,569 water samples taken during this period. There was no satisfactory evidence that water hardness was related to stroke mortality. Age was a strongly related factor. There was little or no association with sex, marital status, socio-economic status as reflected by education or housing, smoking history, or frequency of church attendance.
Stroke
PMID:Stroke-associated deaths in Washington county, Maryland, with special reference to water hardness. 44 44

The inotropic effects of albumin were studied in 94 seriously injured patients who received an average of 14.5 transfusions, 9.2 liters of crystalloid and 0.9 liters of plasma prior to end of operation; 46 patients, by random selection, received added albumin averaging 31 gm during operation, 198 gm during the early postoperative period of extravascular fluid sequestration, and 395 gm during the first 4 days of the later fluid mobilization period. Left ventricular stroke work index (LVSWI) was plotted against pulmonary wedge pressure (Ppw) in 22 patients who had indwelling thermistor pulmonary artery catheters at the time of the first study. Calculated heart work units (WU) were derived from the pulse pressure, mean arterial pressure, pulse rate, and central venous pressure (CVP) in patients without LVSWI measurements. Albumin supplementation increased serum albumin (4.2 vs. 2.9 gm%), plasma volume, CVP (15 vs. 9 cm H2O), but did not alter red cell volume (1,531 vs. 1,519 ml). The ratio of LVSWI/Ppw fell in albumin patients (1.9 +/- 1.6 vs. 4.8 +/- 1.8), and the ratio of WU/CVP was significantly depressed in albumin patients (4.9 +/- 2.3 vs. 7.3 +/- 2.1). The slopes of the LVSWI/Ppw and WU/CVP were shifted to the right in albumin patients. This negative inotropic effect was associated with impaired oxygenation, as reflected by an increased ratio of inspired oxygen per arterial oxygen tension (0.62 +/- 0.06 vs. 0.33 +/- 0.1). Finally, 24 of the 46 albumin-treated patients were digitalized for heart failure, compared to only 11 of the 48 nonalbumin patients. Pending subsequent studies, albumin should be considered a potentially negative inotropic agent.
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PMID:Negative inotropic effect of albumin resuscitation for shock. 46 73

Two experimental models were studied to determine the hemodynamic consequences of atrial volume reduction as observed after operative correction of transposition of the great arteries. The volume of the left atrium (LA) was reduced either by inflation of an intracavitary balloon (group A) or by surgical intervention (group B) to 50--60% of the control values as determined by angiography. The angiographic data correlated well with the true volumes obtained by water displacement. This major reduction of LA volume caused small but constant hemodynamic changes. Although the LA stroke volume decreased by 50% and the LA/LV volume relation was reduced by 50% (from 0.42 to 0.21), there was only a slight increase of pulmonary artery pressure (7% in group A and 14% in group B) and a slight decrease in cardiac index (13% in group A and 10% in group B) and in left ventricular end-diastolic pressure (9% in group A and 11% in group B). The reduction of atrial volume results in only minor functional alteration of the intact heart.
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PMID:Hemodynamic changes after experimental reduction of the left atrium. 49 23

Previous clinical studies establishing the efficacy of midazolam maleate (RO 21-3981), a new water-soluble benzodiazepine for induction of anesthesia, have not critically evaluated the effects of this agent on the cardiovascular system. The present study compares the cardiovascular effects of midazolam maleate and diazepam in conscious dogs. Systemic arterial, pulmonary arterial and central venous pressures, cardiac output, LVmax dP/dt, heart rate and regional coronary blood flow were measured 3 min following intravenous administration of diazepam (0.5, 1.0, and 2.5 mg/kg) or midazolam maleate (0.25, 1.0, and 10.0 mg/kg). Midazolam maleate increased heart rate 10--20 per cent with all three doses and decreased mean arterial blood pressure approximately 10--20 per cent at 1.0 and 10 mg/kg. Cardiac output was increased 10--12 per cent with all three doses of midazolam maleate, and LVmax dP/dt was decreased 13--16 per cent at the two higher doses. Diazepam at all three doses did not alter heart rate or mean arterial blood pressure. Diazepam, 1.0 and 2.5 mg/kg, produced significant (17 per cent) decreases in LVmax dP/dt, and 2.5 mg/kg produced a significant (10 per cent) increase in cardiac output. Neither drug in any dosage altered regional coronary blood flow, systemic or coronary vascular resistance, stroke volume, or stroke work. Maximum alterations in cardiovascular variables occurred with doses of midazolam maleate that are 10--15 times the recommended clinical induction dosage. It is concluded that in concentrations necessary for induction of anesthesia midazolam maleate has minimal effects on cardiovascular function.
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PMID:Cardiovascular responses to diazepam and midazolam maleate in the dog. 49 58

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
Stroke
PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96


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