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

The use of vasodilators represents a new approach in the treatment of heart failure. These drugs have the property of causing vasodilatation of either arterial or venous predominance or balanced between these two vascular beds. Arterio-dilators (phentolamine, hydralazine) increase stroke volume and cardiac output by decreasing ventricular afterload. Veno-dilators (nitroglycerine) have little effect on cardiac output but decrease ventricular filling pressure, thereby relieving pulmonary venous hypertension. Mixed vasodilators (Sodium nitroprussideate, trimetaphan) combine these two groups of properties in various degrees. The majority of these drugs can only be administered intravenously, with careful haemodynamic surveillance.
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PMID:[The treatment of congestive heart failure by using vasodilators. I. Physiological basis. Different vasodilators (author's transl)]. 9 22

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

The author determined the phasic structure of the systole of the left ventricle by the method of polycardiography and hemodynamics in 20 patients suffering from hypothyrodism. Blood plasma and erythrocyte electrolytes were examined at the same time. Patients with hypothyroidism displayed a phasic syndrome of hypodynamia and a marked correlation between the phase of the synchronous contraction, the period of ejection, the strength of contraction of the left ventricle and the electrolyte content. Sodium and magnesium produced the greatest influence on the phasic structure of the systole; potassium and calcium had a lesser effect. The heart stroke volume diminished; as to the cardiac index, expenditure of the energy of cardiac contractions directed to the maintenance of movement of 1 litre of the minute blood volume; the external work, and the peripheral vascular resistance displayed no significant change.
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PMID:[Myocardial contractility and hemodynamics in hypothyroidism]. 84 74

From haemodynamic and metabolic investigation of 65 comatose subjects following cranial traumatism or cerebral vascular accident, the following prognostic and therapeutic indications emerged: The isolated increase in oxygen pressure in the jugular vein to above 50 mm Hg, the simultaneous decrease in circulation of the brain to below of 30 ml/100g/min., and of the brain consumption of oxygen to below 1.5 ml/100g/min., combined with a loss of autoregulation and a decrease in carbon dioxide reactivity indicate that prognosis is very poor. Induced arterial hypertension, associated with hyperventilation, partially corrects brain hypoperfusion in coma from bulbo-pontine lesions. Sodium penthiobarbital and sodium gamma hydroxybutyrate and have the effect of reducing oxygen metabolism which might have some therapeutic value during the acute phase of coma. Clomipramine which has a stimulating effect on oxygen metabolism should be kept in reserve for the chronic phase of prolonged coma.
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PMID:[Prolonged traumatic and vascular coma: prognostic and therapeutic indications based on hemodynamic and metabolic studies]. 100 13

We evaluated the effects of beraprost Na (Sodium (+-)-(1R*,2R*, 3aS*,8bS*)-2,3,3a,8b-tetrahydro-2-hydroxy-1-[(E)-(3S*)-3- hyd roxy-4-methyl-1- octen-6-ynyl]-1H-cyclopenta[b]benzofuran-5-butylate, beraprost), a stable and orally active prostacyclin (PGI2) analog with potent antiplatelet and vasodilating properties, on two stroke models, namely sudden death induced by arachidonate (AA) in rabbits and spontaneous stroke in stroke-prone spontaneously hypertensive rats (SHRSP). In the AA-induced sudden death model, 30 min after beraprost administration (1 or 3 mg/kg, po), AA was injected into the rabbit internal carotid artery, and incidence of convulsion and sudden death were assessed. Beraprost decreased both incidence of convulsion and mortality of rabbits. In SHRSP, orally administered beraprost (100 micrograms/kg, twice a day from 56-385 d of age) improved survival rate and decreased incidence of stroke. Preventive effects of beraprost on the two stroke models may have been caused mainly by the improvement of cerebral circulation. These results indicate that beraprost may have potential in the treatment and/or prevention of the cerebral circulatory disorders.
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PMID:The effects of beraprost Na, a stable prostacyclin analog, on animal models of stroke. 138 52

Sodium restriction by 50 to 100 mmol/day in populations with intakes averaging 150 to 180 mmol/day would likely lead to a reduction of population mean blood pressures, and less of a tendency for blood pressures to rise with age. Fewer people would require antihypertensive drug therapy, and those who did would require less drugs. The extent of any blood pressure fall would be greatest in the elderly or those with established hypertension. A corresponding reduction in stroke incidence might be anticipated, with less certain effects on coronary deaths and diseases. Other factors, such as weight control, alcohol moderation and increased physical activity, may be of greater importance in preventing hypertension in many populations, while cessation of smoking, control of obesity, increased physical fitness and reduction in dietary saturated fat consumption should probably receive the highest priority in terms of overall reduction in the risk of atheromatous cardiovascular disease. In countries such as Japan, which has a relatively high incidence of stroke and a low incidence of coronary disease, a high sodium intake assumes relatively greater importance, in conjunction with obesity and alcohol, as a risk factor for cerebrovascular disease.
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PMID:Dietary salt and risk factors for cardiovascular disease. 163 79

The effects of sodium nitroprusside on the proliferation of cultured vascular smooth muscle cells (SMC) from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY) were examined. Sodium-nitroprusside (SNP, 1mM) inhibited DNA synthesis by SMC from SHRSP and WKY by 90% and 95%, respectively. SNP also decreased cell proliferation. However, SNP was inactive when SMC were pretreated 6 and 12 hrs before growth stimulation by FCS. On the other hand, the inhibitory action of SNP decreased with time (posttreatment) in SHRSP SMC (42% inhibition at 12 hr post addition). However, in WKY SMC, the decrease of inhibitory action was very slight and SNP still inhibited 73% of DNA synthesis at 12 hr post treatment. SNP inhibited RNA synthesis for 3-6 hr and 6-9 hr after FCS stimulation, however no difference was noted between SHRSP and WKY. Protein synthesis was inhibited more strongly by SNP (9-12 hr after FCS stimulation) in WKY SMC than SHRSP SMC. It is probable that the specific protein(S) whose synthesis is inhibited by SNP is/are responsible for the differences in cell proliferation rate between SHRSP and WKY SMC.
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PMID:Differences in response between SHRSP and WKY vascular smooth muscle cells to inhibition of cell proliferation by sodium nitroprusside. 177 10

Epidemiological evidence suggests that low potassium intake is associated with the probability of occurrence of hypertension and stroke. The short-term response to increased potassium intake is increased sodium excretion as well as increased potassium excretion; the short-term response to increased sodium intake is increased potassium excretion as well as increased sodium excretion. In some experimental studies, increased amounts of potassium have been able to block the noxious influences of sodium. Sodium and potassium must be concomitantly considered in the investigation of the association of either of these cations with hypertension and cardiovascular disease. The chloride ion is also important for sodium's effects; its importance in potassium's effects has not been extensively explored.
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PMID:Sodium-potassium interaction in hypertension and hypertensive cardiovascular disease. 198 94

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.
Stroke 1991 Feb
PMID:Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum. 200 87

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.
Stroke 1989 Sep
PMID:Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils. 277 85


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