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

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

In 64 patients with ischemic strokes that occurred on the background of atherosclerosis (33) and a combination of atherosclerosis with arterial hypertension (31) using the dilution method of Evans's blue the authors studied indices of general hemodynamics compared to rheoencephalographic data. Twenty similar patients without signs of brain circulation disturbances and 20 healthy persons were taken as control groups. In 69% of the patients with ischemic strokes deep disturbances of general hemodynamics were observed. An increase of tonus, a decrease of elasticity of cerebral vessels and deficit of pulse blood repletion were determined rheoencephalographically. Insufficiency of general hemodynamics in conditions of changed autoregulation of brain circulation promotes development of ischemic disorders of brain circulation and unfavourably influences the course and outcome of the stroke.
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PMID:[State of general and cerebral hemodynamics in patients with ischemic strokes]. 42 64

Conscious rats and rats under nitrous oxide anesthesia were subjected to blood pressure elevations by injection of epinephrine, bicuculline and amphetamine. Mean arterial pressure was measured from a chronic indwelling cannula in the aorta in awake rats. The protein leakage in the brains was studied using Evans blue and 125IHSA. Conscious animals developed less blood-brain barrier dysfunction than anesthetized ones. The largest difference was obtained with amphetamine and the smallest with epinephrine. Possible explanations to the results are discussed.
Stroke
PMID:Effect of an acute increase of the intravascular pressure on the blood-brain barrier: a comparison between conscious and anesthetized rats. 74 92

Total mortality showed no association with heavy coffee consumption in the four race-sex groups of Evans County. Deaths from coronary heart disease in WM, WF and BM showed no statistically significant differences between the two coffee consuming groups. Sex differences in cerebrovascular death rates, consistent in both races, suggest the possibility for a female excess of stroke deaths among coffee drinkers, and a "protective" effect of coffee drinking among males. Thus, in an area of the United States which has been designated the "Stroke Belt", neither the cardiovascular nor the cerebrovascular death rates seem strongly nor consistently related to coffee drinking habits. Although the number of deaths (339) is fairly large, representing a 13% mortality in this community over a four and one-half year observation period, the classification in four race-sex groups with further division into the groups with different coffee drinking habits limits each stratum to rather small numbers. In addition, 86 cases of CHD and CVD were diagnosed during lifetime already and, therefore, were excluded from the prospective mortality study. Confidently to refute or confirm the allegations of a detrimental influence of high coffee intake on ischemic heart disease one would need larger numbers. But in the light of our most important finding--that mortality from all causes is not increased in the high coffee consuming group--the finding of increased ischemic heart disease death rates with high coffee consumption would have to be compensated by a provocative, lower rate for other causes of death.
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PMID:Coffee consumption and mortality in a community study--Evans Co., Ga. 96 3

Cerebral blood flow was measured with the 133Xenon clearance method in anesthetized cats under controlled ventilation. An acute pressure increase in the carotid system increases the cerebrovascular permeability to Evans blue, indicating damage to the blood-brain barrier. In these conditions the reactivity or cerebral blood vessels toward changes in the acid-base balance is altered: the CO2 reactivity is less pronounced, while the effect of increasing the plasma (HCO-3) is more pronounced than in normal cats. Autoregulatory capacity toward moderate alterations in arterial blood pressure or in intracranial pressure is well maintained in these conditions.
Stroke
PMID:Cerebral blood flow in cats after an acute hypertensive insult with damage to the blood-brain barrier. 112 18

Dichloroacetate (DCA) activates the pyruvate dehydrogenase complex enhancing carbohydrate and lactate utilization in animals. As a result it is used clinically in the treatment of acute lactic acidosis and has therapeutic potential in the treatment of stroke. Adverse effects of chronic DCA treatment include polyneuropathy and testicular degeneration. Since DCA is a principal product of the aqueous chlorination of fulvic acids concern has arisen regarding the agent's impact on environmental health. We treated male Long-Evans rats with 0, 31.25, 62.5, or 125 mg DCA/kg/day by oral gavage for 10 weeks. Compared to controls, preputial gland and epididymis weights were reduced at 31.25 mg/kg, body and liver weights at 62.5 mg/kg, and accessory organ weights at 125 mg/kg. Epididymal sperm counts were reduced and sperm morphology was impacted at the 62.5 and 125 mg/kg doses levels. Histologic examination of the testis and epididymis revealed inhibited spermiation in testes at the 125 mg/kg dose level. Computer-assisted sperm motion analysis revealed reductions in percentage motile sperm, curvilinear and straight-line velocity, linearity, and amplitude of lateral head displacement at both the 62.5 and the 125 mg/kg dose levels. In the assessment of fertility after an overnight mating, the number of viable implants on Day 14 of gestation was decreased only in the highest dose group. These studies demonstrate adverse effects of NaDCA treatment on the rat male reproductive system, primarily on the accessory organs and sperm within them at lower doses (31.25 and 62.5 mg/kg), and on the testis at the highest dose (125 mg/kg).
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PMID:Adverse male reproductive effects following subchronic exposure of rats to sodium dichloroacetate. 139 2

The Evans blue dilution method and ultrasound dopplerography were used to study the effect of nicergolin on the systemic and cerebral hemodynamics in 31 patients with dyscirculatory encephalopathy against the background of atherosclerotic lesions of the major head arteries. It was established that nicergolin reduces the arterial pressure, diminishes the minute blood volume, cardiac and stroke indices, increases the specific peripheral vascular resistance, the linear blood flow velocity prevailingly in the stenosed major head arteries, results in a regression of the subjective and objective neurological symptomatology. Considering the cardiodepressive effect of nicergolin, this agent is indicated in patients with the hyperkinetic type of the systemic hemodynamics.
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PMID:[The effect of nicergoline on the systemic and cerebral hemodynamics of patients with circulatory encephalopathy and an atherosclerotic lesion of the major cerebral arteries]. 148 25

1. In the present study, the extent to which baroreflexes contribute to the cardiac effects of NG-nitro-L-arginine methyl ester (L-NAME) was assessed in conscious, Long Evans rats chronically instrumented with thoracic electromagnetic flow probes for the measurement of cardiac haemodynamics. 2. L-NAME (10 mg kg-1, i.v.) was administered in the absence (n = 6) and in the presence (n = 7) of atropine (1 mg kg-1) and atenolol (1 mg kg-1). 3. L-NAME caused a marked increase in mean arterial pressure and marked reductions in total peripheral conductance, cardiac output, heart rate, stroke volume, peak thoracic flow and the maximum rate of rise of aortic flow. 4. Administration of atropine, after the maximal bradycardic effect of L-NAME was established, restored the heart rate to resting levels. Concurrently, there was a reduction in stroke volume, such that cardiac output, although transiently elevated, did not show a sustained increase. No other variables were significantly affected by atropine. Additional administration of atenolol had no effect other than to cause a slight bradycardia, such that in the presence of atropine and atenolol, heart rate was not different from that in animals receiving atropine and atenolol before L-NAME. 5. In the presence of atropine and atenolol, L-NAME had similar pressor, vasoconstrictor and cardiac haemodynamic effects to those in untreated animals, although the bradycardia was significantly attenuated. However, there was still a significant reduction in heart rate following L-NAME in the presence of atropine and atenolol.6. These results indicate that the major component of the bradycardia following L-NAME is indirect and mediated through an increase in vagal efferent activity. However, the substantial reduction in cardiac function caused by L-NAME is not dependent on the autonomic control of the heart but rather, may depend on the increase in afterload and/or a direct effect of L-NAME on the heart and/or its vasculature.
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PMID:The influence of atropine and atenolol on the cardiac haemodynamic effects of NG-nitro-L-arginine methyl ester in conscious, Long Evans rats. 162 53

Focal cerebral ischemia was produced by occluding the left middle cerebral artery in 769 rats. Permeability of the blood-brain barrier to small or large molecules was evaluated qualitatively using Evans blue or sodium fluorescein and quantitatively using the transfer indexes of iodine-125-labeled bovine serum albumin or [14C]sucrose. Water content was determined using wet and dry weights and sodium and potassium contents using flame photometry. Cortical tissue in the middle cerebral artery territory was sampled less than or equal to 14 days after occlusion. A significant increase in the albumin transfer index was first found 12 hours after occlusion, and the index remained approximately the same until water content peaked 3 days after occlusion. In contrast, the sucrose transfer index increased gradually, significantly correlated with increases in the water and sodium contents. Tissue staining by sodium fluorescein was more extensive than that by Evans blue. As edema fluid decreased gradually 4-10 days after occlusion, the albumin and sucrose transfer indexes increased markedly. These findings indicate that disruption of the blood-brain barrier to small molecules is accompanied by accumulation of edema fluid during the later stages of ischemia. Opening of the barrier to serum protein is probably related to the resolution of edema.
Stroke 1990 Apr
PMID:Brain edema and cerebrovascular permeability during cerebral ischemia in rats. 169 34

1. Comparisons were made of the full haemodynamic profiles of the known cardiostimulant, (+/-)-dobutamine, and the putative inotropic peptide, human alpha-calcitonin gene-related peptide (human alpha-CGRP), in conscious, chronically-instrumented Long Evans rats. Both substances were administered continuously i.v. for 60 min at two doses ((+/-)-dobutamine, 2 and 10 mumol kg-1 h-1; human alpha-CGRP, 0.15 and 1.5 nmol kg-1 h-1). 2. In spite of their similar (small) effects on mean arterial blood pressure, the low doses of (+/-)-dobutamine and human alpha-CGRP influenced cardiac haemodynamics differently. Thus, (+/-)-dobutamine caused an increase in cardiac index (due to a tachycardia), accompanied by rises in peak aortic flow, maximum rate of rise of aortic flow (dF/dtmax) and total peripheral conductance. However, the latter waned during the infusion, and after the infusion there was a significant systemic vasoconstriction and reductions in peak aortic flow, dF/dtmax and stroke index. Such 'off' effects following dobutamine infusion have not been described previously. The infusion of the lower dose of human alpha-CGRP caused only a transient fall in central venous pressure. 3. The rise in total peripheral conductance during infusion of the lower dose of (+/-)-dobutamine was associated with increases in hindquarters and common and internal carotid vascular conductances. The fall in total peripheral conductance after infusion was associated with renal vasoconstriction. Although there was no significant change in total peripheral conductance during the infusion of the lower dose of human alpha-CGRP there were hindquarters and carotid vasodilatations together with mesenteric vasoconstriction. 4. Infusion of the higher dose of ( )-dobutamine had greater effects than the lower dose on all cardiac haemodynamic variables and additionally, increased stroke index. However, the negative cardiac haemodynamic effects following the offset of infusion were also enhanced in association with marked renal and mesenteric vasoconstrictions. While infusion of the higher dose of human alpha-CGRP increased cardiac index, peak aortic flow, dF/dtmax and total peripheral conductance, stroke index fell together with central venous pressure. 5. (+/-)-Dobutamine caused greater cardiostimulation and increases in hindquarters blood flow than did human alpha-CGRP. However, the latter at the higher dose caused substantially greater common and internal carotid hyperaemia than did (+/-)-dobutamine, possibly indicating a selective and additional effect of human alpha-CGRP on cranial blood flow. Furthermore, there were no adverse cardiovascular effects following infusion of human alpha-CGRP.
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PMID:Differential effects of (+/-)-dobutamine and human alpha-CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats. 188 4


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