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

Cardiovascular responses have been studied in baboons, after total exchange transfusion with hemoglobin solutions having various P50 values. At the end of the exchange transfusion, the hematocrit was 1.5%, the mean hemoglobin concentration was 4.4 g/dl, and the P50 varied between 12 and 26 mm Hg. Cardiac output did not change during the study, although heart rate increased, and stroke volume and MAP decreased. Hemoglobin concentration, per se, does not appear to be the critical stimulus for an increase in cardiac output with hemoglobin solution. In addition, the position of the hemoglobin-oxygen dissociation curve does not appear to influence these hemodynamic responses. The physiological response to anemia in the presence of hemoglobin solution appears different from that observed in the absence of plasma O2 carriers.
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PMID:Cardiac output response to extreme hemodilution with hemoglobin solutions of various P50 values. 11 94

Comprehensive ascertainment of all possible new cases of stroke appearing between January 1, 1970 and June 30, 1971, and admitted to three major hospitals in Winnipeg, Manitoba, has been achieved by reviewing the Manitoba Health Services Commission claim reports. The medical records of these cases were reviewed, pertinent data were abstracted, and rigid criteria for diagnosis were followed. Also, data were obtained from death certificates, autopsy reports and long-term hospital records. A total of 606 ascertained cases (410 infarction, 137 hemorrhage, and 59 undetermined type) were matched for age, sex, residence and year of admission with 606 controls from admissions for other than cardiovascular and cerebrovascular disorders. The data were analyzed for elucidating the possible risk factors for infarction (INF) and hemorrhage (HGE). The findings suggested that hypertension was the main risk factor in hemorrhage, whereas in infarction, along with hypertension, other factors such as diabetes, heart enlargement in chest x-ray, ECG abnormalities, and smoking were suggested as risk factors. There was an association also between infarction, on one hand, and the history of receiving anticoagulants, diuretics, and medications for the heart, and the occurrence of myocardial infarction, on the other hand. These features indicate that infarction and ischemic heart disease have similar risk factors. Hemoglobin and hematocrit were higher in infarction cases than in their controls only when measured at stroke admission. No difference was revealed when they were measured prior to stroke. Their association with infraction therefore may be secondary to other factors and of no significance for its risk.
Stroke
PMID:Relative role of factors associated with cerebral infarction and cerebral hemorrhage. A matched pair case-control study. 13 18

Case control analysis of 204 patients with acute ischemic stroke revealed the matched pair odds ratio (and 95% confidence limits) for hypertension, ECG abnormality, heart disease of any type, diabetes, smoking and alcohol intake to be 3.95 (2.5, 6.2), 2.1 (1.4, 3.1), 2.1 (1.4, 3.2), 1.7 (1.1, 2.6), 1.8 (1.1, 2.8) and 1.5 (0.86, 2.6), respectively. Except alcohol intake, the other factors were statistically significant. Hemoglobin, packed cell volume (hematocrit), serum cholesterol, triglycerides and low-density lipoprotein cholesterol levels were not found to be significant. High-density lipoprotein (HDL) cholesterol and uric acid were significantly lower and the ratio of total cholesterol to HDL cholesterol (TC/HDL) was higher among stroke patients. The risk was considerably higher when there was any combination of hypertension, heart disease and HDL cholesterol level lower than 45 mg/dl. Logistic regression revealed hypertension, heart disease of any type, lower HDL cholesterol and uric acid and higher ratio of TC/HDL to be significant factors.
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PMID:Risk factors for ischemic stroke: a case control analysis. 160 91

Six male Quechua Indians (34.0 +/- 1.1 yr, 159.5 +/- 2.1 cm, 60.5 +/- 1.6 kg), life-long residents of La Raya, Peru (4,350-m altitude with an average barometric pressure of 460 Torr), were studied using noninvasive methods to determine the structural and functional changes in the cardiovascular system in response to a 6-wk deacclimation period at sea level. Cardiac output, stroke volume, and left ventricular ejection fractions were determined using radionuclide angiographic techniques at rest and during exercise on a cycle ergometer at 40, 60, and 90% of a previously determined maximal O2 consumption. Subjects at rest were subjected to two-dimensional and M-mode echocardiograms and a standard 12-lead electrocardiogram. Hemoglobin and hematocrit were measured on arrival at sea level by use of a Coulter Stacker S+ analyzer. After a 6-wk deacclimation period, all variables were remeasured using the identical methodology. Hemoglobin values decreased significantly over the deacclimation period (15.7 +/- 1.1 to 13.5 +/- 1.2 g/dl; P less than 0.01). The results indicate that the removal of these high-altitude-adapted natives from 4,300 m to sea level for 6 wk results in only minor changes to the cardiac structure and function as measured by these noninvasive techniques.
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PMID:Cardiovascular adaptations in Andean natives after 6 wk of exposure to sea level. 188 61

Endothelial cells modulate vascular tone by releasing endothelium-derived relaxing (EDRF) and contracting factors. An imbalance of these factors in hypertension could contribute to increased peripheral vascular resistance. Mesenteric resistance arteries of Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were suspended in a myograph filled with physiological salt solution (37 degrees C; 95% O2-5% CO2). In WKY rings contracted with norepinephrine, acetylcholine (10(-9)-10(-4) M) evoked endothelium-dependent relaxations (88 +/- 2%, IC50 7.3 +/- 0.1; n = 31). Hemoglobin (10(-5) M) but not meclofenamate (10(-5) M) reversed the relaxations delineating EDRF as the mediator. Nitric oxide (3 X 10(-9)-10(-5) M) induced comparable relaxations as acetylcholine. In SHRSP, relaxations to acetylcholine but not those to nitric oxide were impaired (61 +/- 5%, IC50 greater than 6.6 +/- 0.4; n = 24; P less than 0.005). In SHRSP, meclofenamate but not the thromboxane synthetase inhibitor CGS 13080 normalized endothelium-dependent relaxations. Relaxations to sodium nitroprusside were enhanced in SHRSP both in rings with and without endothelium. Thus our results are compatible with the concept that endothelium-dependent relaxations in resistance arteries are mediated by nitric oxide. In SHRSP, endothelium-dependent relaxations are impaired because of a cyclooxygenase-dependent substance interfering with the release and/or action of EDRF.
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PMID:Impaired endothelium-dependent relaxations in hypertensive resistance arteries involve cyclooxygenase pathway. 210 97

The frequency of pulmonary hemorrhagic lesions in stroke-prone spontaneously hypertensive rats (SHRSP) was higher in older than in younger rats. Hemoglobin and protein contents in pulmonary lavage fluid which may indicate alveolar hemorrhage showed an increase with the progress of age, but the difference of hemorrhagic levels was much more in older rats than that of younger ones. A strong relationship between hemoglobin and protein contents of pulmonary lavage fluid was observed. Morphologically, the most striking feature was fibrinoid degeneration of the vascular walls in the center of hemorrhagic lesions of the lung, not only in the capillaries but also in small arteries. In the early stage of hemorrhage, endothelial discontinuity exhibited intraluminal fibrin deposits in this area of the vessels. Erythrocytes and polygonal deposits of fibrin could also be seen within the same vascular walls. In the advanced stage, subendothelial spaces and medial layers of vascular walls contained an electron-dense amorphous material which was consisted to be a degradation product of fibrinogen. The occurrence of this substance was thought to be induced by the hemodynamic effects of hypertension, the results of increased permeability and the accumulation of blood components. From these results, we suggest that fibrinoid degeneration due to abnormal cellular permeability associated with hypertension in SHRSP may be in some way linked to the development of pulmonary hemorrhage.
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PMID:Vascular changes involved in pulmonary hemorrhage of stroke-prone spontaneously hypertensive rats. 262 47

To determine whether extraluminal or intraluminal hemoglobin inhibits endothelium-dependent relaxation, we measured the vascular responsiveness of rabbit basilar artery in an in vitro perfusion system and we performed immunohistochemical staining for hemoglobin. In the in vitro study, we applied agents from either the intraluminal or the extraluminal side of excised basilar arteries. KCl-induced contraction was the same with either application. Acetylcholine-induced maximal relaxations were 57.6 +/- 8.5% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 3.3 +/- 0.3% for intraluminal, and 34.9 +/- 8.6% for extraluminal applications. Adenosine triphosphate-induced maximal relaxations were 64.2 +/- 4.1% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 26.9 +/- 3.8% for intraluminal, and 42.2 +/- 6.0% for extraluminal applications. Hemoglobin's inhibition of acetylcholine- and adenosine triphosphate-induced relaxation was significantly greater with intraluminal than with extraluminal application (p less than 0.05). The immunohistochemical study revealed hemoglobin in the outer layer of the smooth muscle and in the adventitia when 10(-5) M hemoglobin was applied extraluminally for 5 minutes, whereas hemoglobin was observed on the surface of the endothelial cells after intraluminal application. Our findings suggest that hemoglobin inhibits acetylcholine- or adenosine triphosphate-induced relaxation by binding to endothelium-derived relaxing factor (EDRF) and by inhibiting production of EDRF. Hemoglobin's inhibitory effect on endothelium-dependent relaxation may be important in the pathogenesis of vasospasm after subarachnoid hemorrhage.
Stroke 1988 Dec
PMID:Comparison of intraluminal and extraluminal inhibitory effects of hemoglobin on endothelium-dependent relaxation of rabbit basilar artery. 326 26

The effect of simulated altitude erythrocythemia on hemoglobin flow rate and maximal O2 uptake (VO2max) was determined for nine women sea-level residents. Test conditions included normoxia and normobaric hypoxia (16% O2-84% N2). Cycle tests were performed under normoxia (T1-N) and hypoxia (T1-H) at prereinfusion control and under hypoxia 48 h after a placebo infusion (T2-H) and 48 h after autologous infusion of 334 ml of erythrocytes (T3-H). Hematocrit (38.1-44.9%) and hemoglobin concentration (12.7-14.7 g.dl-1) increased from control to postreinfusion. At peak exercise, VO2max decreased from T1-N (2.40 l.min-1) to T1-H (2.15 l.min-1) then increased at T3-H (2.37 l.min-1). Maximal arterial-mixed venous O2 difference decreased from T1-N to T1-H and increased at T3-H. Cardiac output (Q), stroke volume, heart rate, and total peripheral resistance during maximal exercise were unchanged from T1-N through T3-H. Hemoglobin flow rate (Hb flow) at maximum did not change from T1-N to T1-H but increased at T3-H. When compared with submaximal values for T1-N, VO2 was unchanged at T1-H and T3-H; Q increased at T1-H and decreased at T3-H; arterial-mixed venous O2 difference decreased at T1-H and increased at T3-H; Hb flow did not change at T1-N but increased at T3-H. For young women, simulated altitude erythrocythemia increased peak Hb flow and decreased physiological altitude (227.8 m) but did not affect maximum cardiac output (Qmax).
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PMID:Effect of simulated altitude erythrocythemia in women on hemoglobin flow rate during exercise. 337 98

A total of 1,377 patients with symptomatic obstructive cerebrovascular disease (most commonly, internal carotid artery occlusion) entered a trial in which they were randomized to either medical or surgical (extracranial-intracranial bypass) therapy. All but 8 had hemoglobin estimations performed at entry. The patients were followed for an average of 55.8 months. In the medical group, the 325 patients with high normal hemoglobin concentration (15 g/l or more) suffered no more ischemic strokes than the 382 patients with lower values (less than 15 g/l). Those strokes that did occur were no more severe in the high than the low hemoglobin group. Hemoglobin concentration did not emerge as a prognostic factor in those patients treated surgically (n = 662). This prospective study counters the hypothesis that high normal hemoglobin concentration is associated with poor outcome in patients with symptomatic obstructive disease of the carotid and cerebral arteries.
Stroke
PMID:Hemoglobin concentration and prognosis in symptomatic obstructive cerebrovascular disease. 381 Jul 72

A 47-year-old patient with severe decompensated alcoholic liver disease developed a progressive deterioration of her renal function (serum creatinine 4.0 mg/dL) with a renal failure index (RFI: UNa/U/PCr) consistently less than 1.0. In the absence of other causes of renal failure, these values supported the diagnosis of hepatorenal syndrome (HRS). A five-hour head-out water immersion (HWI) in a sitting position was carried out to increase the patient's "effective" blood volume (EBV) in an attempt to reverse the HRS. Hemodynamic monitoring (Swan-Ganz) was performed during the entire HWI procedure. Cardiac index increased by 64% during HWI (2.57 to 4.22 L/min/m2). Stroke volume index doubled (32.9 to 65.0 mL/m2) and systemic vascular resistance decreased by 48% (1426 to 754 dyne sec/cm). Increases in right atrium (RA) pressure (7.5 to 17.5 mm Hg) and pulmonary wedge (PW) capillary pressure (7.5 to 16.3 mm Hg) also occurred. Hemoglobin, hematocrit, and plasma protein concentrations decreased by 18% during HWI. Only a modest improvement in creatinine, urea, inulin, and para-aminohippurate (PAH) clearances was observed during HWI, and the RFI remained below 1.0. Plasma levels of antidiuretic hormone (ADH), aldosterone, and renin activity decreased during HWI. The patient's renal function progressively deteriorated over the next 15 days, but tubular function, as assessed by an RFI less than 1.0, was still intact seven days after our study. Our results indicate that a considerable increase in effective blood volume does not restore renal function in HRS.
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PMID:Effect of head-out water immersion on hepatorenal syndrome. 669 41


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