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

Blood pressure (BP) and hemodynamic responses (cardiac output [CO] and total peripheral resistance [TPR]) to a competitive reaction-time task, previously shown to increase beta-adrenergic activity, were compared in 20 Black and 20 White young men, once following infusion of saline placebo and later repeated after infusion of the nonselective beta-antagonist, propranolol. Both racial groups included subjects with marginal systolic BP (SBP) elevations (n = 6 Whites, n = 5 Blacks) and subjects with normal BP (n = 14 Whites, n = 15 Blacks). Blacks with marginal SBP elevations showed greater diastolic BP increases during the stressor than their White counterparts, both before and after beta-blockade. Both Blacks and Whites with marginal SBP elevations showed greater CO increases during the task than normotensives prior to blockade. Independent of BP status, Black subjects consistently showed higher TPR responses to the task than Whites (lesser decreases before blockade and greater increases after blockade). Blacks also showed greater diminution than Whites after blockade in ionotropic myocardial responses (stroke volume, pre-ejection period, and CO) to the stressor. The possible contributions of alpha-adrenergic and beta-adrenergic influences to these racial group differences are discussed.
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PMID:Race, borderline hypertension, and hemodynamic responses to behavioral stress before and after beta-adrenergic blockade. 256 Sep 75

Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.
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PMID:Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade. 285 27

A simple technique for cannulation of the thoracic epidural space in rats was described. 40-50 microliter of epidural bupivacaine 5 mg/ml induced a distribution of sensory analgesia from lower cervical to lower thoracic segments. With this model, effects of thoracic epidural anaesthesia (TEA) on mean arterial pressure (MAP), cardiac output (CO), systemic vascular resistance (SVR), stroke volume (SV), heart rate (HR), central venous pressure (CVP), left ventricular end-diastolic pressure (LVEDP) and maximal increase of pressure in the left ventricle (max dp/dt) were studied in six groups of animals: 1) In conscious animals (n = 10) MAP, CO, SV and HR decreased significantly by 12%, 25%, 10% and 16%, respectively, while SVR increased significantly by 20% during TEA; 2) In chloralose-anaesthetized animals (n = 7) the reduction in CO during TEA was less pronounced and there were no significant changes in SV or SVR; 3) In conscious animals (n = 6) LVEDP, CVP and max dp/dt decreased significantly during TEA; 4) Hexamethonium, when administered to pharmacologically vagotomized conscious animals during TEA (n = 8), induced a significant decrease in SVR (23%) but no change in HR; 5) Changes in haemodynamics after cardiac adrenoceptor blockade with metoprolol, in conscious animals (n = 12), did not differ significantly from those seen during TEA, except for an unchanged SV after metoprolol; 6) 50 microliters of bupivacaine (5 mg/ml) when given i.v. to conscious animals (n = 8) did not affect CO, SV, HR or TPR significantly, while MAP increased slightly but significantly. Thus, in this conscious animal model, TEA almost completely and rather selectively blocked probably mediated by a reflex activation of unblocked sympathetic efferents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thoracic epidural anesthesia in conscious and anaesthetized rats. Effects on central haemodynamics compared to cardiac beta adrenoceptor and ganglionic blockade. 289 22

Verapamil (1 mg/kg, i.v.) and nifedipine (0.3 mg/kg, i.v.) were tested at equi-antihypertensive doses for systemic hemodynamic responses in conscious spontaneously hypertensive rats (SHR) using the Fick method. Systemic hemodynamic effects of these agents were also evaluated in areflexic, spinal cord-transected and vagotomized SHR using the electromagnetic flowmetry technique. Both verapamil and nifedipine lowered mean arterial pressure (MAP:verapamil = -24%; nifedipine = -28%) in conscious SHR by decreasing total peripheral resistance (TPR:verapamil = -48%; nifedipine = -59%) with a concomitant rise in cardiac output (CO: verapamil = 48%; nifedipine = 86%) and stroke volume (SV:verapamil = 54%; nifedipine = 65%), but verapamil prevented tachycardia, whereas nifedipine increased heart rate (HR:13%). Verapamil and nifedipine also altered systemic hemodynamics in the areflexic SHR; verapamil reduced MAP (-31%) by reducing CO (-18%) with associated bradycardia (-25% HR), whereas nifedipine also lowered MAP (-21%) by decreasing TPR (-18%) without changes in CO and HR. It is concluded that, firstly, the antihypertensive action of verapamil and nifedipine in conscious SHR is due to systemic vasodilation that is associated with reflexly increased CO; secondly, that verapamil has a direct negative chronotropic effect, but nifedipine appears to be devoid of such an effect, and finally that the ability of verapamil to decrease TPR may depend upon resting sympathetic tone.
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PMID:Effects of verapamil and nifedipine on systemic hemodynamics in spontaneously hypertensive rats. 322 Oct 97

The compensatory cardiovascular response to hemorrhage includes a baroreceptor-induced activation of the sympathetic nervous system resulting in an attempt to reestablish MAP through peripheral vasoconstriction. If the hypotension is not reversed this compensatory vasoconstriction will progress to a loss of vascular tone known as vascular decompensation. The primary purpose of the present study was to compare the effectiveness of military antishock trousers (MAST) applied during the compensatory and decompensatory stages of hemorrhagic hypotension. MAST pressures of 30, 50, 70, and 90 mm Hg were applied during control, compensation, and decompensation. The results showed that MAST pressures up to 90 mm Hg were ineffective at raising mean arterial blood pressure (MAP) when applied to normotensive dogs; MAP increased 62% when MAST were applied during compensation as the result of a significant augmentation of cardiac output (stroke volume and heart rate) with no change in TPR; and a modest increase in MAP from 40 to 55 mm Hg occurred when MAST pressure was increased to 70 mm Hg during decompensation, which was accounted for entirely on the basis of an increased total peripheral resistance with no significant change in CO.
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PMID:Efficacy of military antishock trousers in compensatory and decompensatory hemorrhagic hypotension. 356 81

The purpose of this study was to investigate the effects of plasma volume expansion on the cardiac and peripheral components of the baroreceptor reflex. Nine male Rhesus monkeys were chronically instrumented to measure arterial pressure and aortic blood flow. The aortic arch was denervated at the time of surgery. Bilateral carotid artery occlusion (BCO) was used to elicit the carotid sinus reflex both before and after 25% plasma volume expansion with an iso-osmotic dextran solution. The BCO elicited significant increases in heart rate (HR, 29.8 +/- 5.3 bpm) mean arterial pressure (MAP, 55.0 +/- 8.2 mm Hg) and total peripheral resistance (TPR, 0.076 +/- 0.01 mm Hg/ml/min) coupled with a significant reduction in mean aortic flow (AF, -246.9 +/- 55.3 ml/min) and stroke volume (SV, -2.86 +/- 0.36 ml). Volume expansion significantly attenuated the HR (15.2 +/- 5.8 bpm), MAP (30.4 +/- 4.4 mm Hg) and TPR (0.036 +/- 0.006 mm Hg/ml/min) response to carotid sinus hypotension. The changes in mean AF and SV elicited by BCO, however, were not significantly different between the control and volume expansion conditions. These data suggest that plasma volume expansion significantly attenuates the baroreceptor reflex control of circulation with a similar reduction in both the peripheral resistance and heart rate components of the response.
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PMID:The effect of plasma volume expansion on the response to carotid occlusion in the non-human primate. 359 48

Hemodynamic effects of DBcAMP given at 0.05 to 0.3 mg/kg/min for 30 minutes to patients with low cardiac output less than 2.21/min/m2, to patients on IABP and on dopamine or dobutamine were investigated after open-heart surgery. Hemodynamic improvements were observed in cardiac index from 1.81 +/- 0.3 (mean +/- SD) to 2.56 +/- 0.401/min/m2 (p less than 0.001), stroke index from 20.5 +/- 5.2 to 26.4 +/- 5.2 ml/best/m2 (p less than 0.001). TRP decreased from 1963.8 +/- 682.8 to 1153.9 +/- 449.0 (p less than 0.001). These changes were similar to those of Groups II (3.0 greater than or equal to C1 greater than or equal to 2.21/min/m2) and of Group III (C1 greater than 3.01/min/m2). Increases were also observed in CI from 2.28 +/- 0.67 to 2.96 +/- 0.671/min/m2 (p less than 0.001) and in stroke index from 24.4 +/- 7.2 to 29.5 +/- 6.4 ml/best/m2 (p less than 0.001) and significant decreases were observed in TPR and PVR in patients receiving dopamine or dobutamine. These results strongly suggest the inotropic action of DBcAMP was independent on the beta receptor activity and could be a powerful adjunct in the treatment of low cardiac output patients on whom the dopamine or dobutamine was ineffective.
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PMID:[Hemodynamic effects of DBcAMP in patients with low cardiac output syndrome following open-heart surgery]. 608 11

Cardiac output (CO) and the distribution of blood flow were studied in chronically catheterized conscious rats during sustained (4 days) sepsis. Septicemia was induced by intraperitoneal administration of a pooled fecal inoculum, and tissue blood flow and CO were determined daily with 15-micron radioactive microspheres. Mean arterial blood pressure (MABP, 113 +/- 2 mmHg), CO (244.5 +/- 11.4 ml X min-1 X kg-1), and total peripheral resistance (TPR, 1.36 +/- 0.07 mmHg X ml-1 X min) were stable in control rats over the 4 days postinoculation. Septic animals showed a consistent tachycardia with MABP significantly reduced only on days 3 and 4 (86 +/- 4 mmHg). A hyperdynamic response to sepsis was indicated by an elevated CO (27%) and similarly reduced TPR on day 2. The calculated stroke volume averaged 0.22 +/- 0.01 ml/beat and did not vary over time or between the two groups. There was a 40-70% increase in blood flow to the heart, spleen, adrenal glands, and small intestine, and a greater than sixfold increase in hepatic arterial blood flow. The sustained elevation of coronary blood flow, observed in septic animals, was independent of myocardial work and is consistent with impaired myocardial function. Pancreas, stomach, and skeletal muscle blood flow was consistently compromised (24, 39, and 52%, respectively) during sepsis. Blood flow in other organs remained unchanged over time. Sepsis-induced changes in the fractional distribution of blood flow to various organs were similar to those described for absolute flow. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis. 670 86

Nine normal, healthy young males performed graded, maximal supine bicycle exercise with monitoring of hemodynamic and gated blood pool parameters. Right ventricular ejection fraction (RVEF) was greater than 0.45 in all acquisitions at rest (mean +/- SD = 0.53 +/- 0.05) and increased greater than 0.05 in all subjects with maximal exercise (mean +/- SD = 0.69 +/- 0.06 at stage 4). There was a very close correspondence between RV and LV stroke counts from the radionuclide angiograms at rest and all exercise levels in all patients. Cardiac output changes by radionuclide data from the RV correlated closely with those obtained by the Fick technique. Multivariate analysis of RVEF vs pulmonary artery pressure, total pulmonary resistance, and heart rate showed that RVEF was inversely related to total pulmonary resistance in these patients (n = 43 acquisitions, r = 0.61, RVEF = 0.75 -- 0.001 TPR in dynes-sec/cm5 Sy.x = 0.07) and positively related to heart rate (n = 43, 4 = 0.78, RVEF = 0.34 + 0.0025 x HR Sy.x = 0.05). RVEF was not significantly related to the other hemodynamic parameters. These results suggest that in normal subjects RV systolic function is afterload-dependent and that total pulmonary resistance may be a suitable afterload index. The results emphasize that heart rate must be considered when comparing RVEF changes.
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PMID:The normal right ventricular response to supine exercise. 714 Mar 95

Cardiovascular responses to adrenaline and acetylcholine (ACh) were investigated in anesthetized, artificially ventilated cats in control and after induction of acute normovolemic hemodilution. Progressive replacement of blood by high molecular weight dextran was performed in three steps of 20% each of the total estimated blood volume. Hemodynamic responses were recorded at four stages: the control stage and after the 1st, 2nd, and 3rd exchanges of blood for dextran. With the fall in hematocrit (Ht) there was a corresponding significant (p < 0.05) increase in heart rate (HR), cardiac output (CO), and stroke volume (SV), and a decrease in systemic vascular resistance (TPR). However, left ventricular systolic pressure (LVSP), left ventricular contractility (LV dP/dtmax), mean arterial pressure (MAP), and right atrial pressure (RAP) did not show any significant (p > 0.05) change due to hemodilution. The cardiovascular responses of intravenously administered adrenaline and ACh were significantly (p < 0.05) attenuated. Responses to sodium nitroprusside (SNP), a potent vasodilator and an exogenous source of nitric oxide, were also attenuated after hemodilution. The increase in SV and HR seem to be the contributing factors to the CO response. Our results indicate that the cardiovascular responsiveness to adrenaline, ACh and SNP is reduced during acute hemodilution which could be due to inadequate myocardial and vascular O2 supply. The possibility of a modulatory role of an endothelium-dependent mechanism and reflex regulatory responses by arterial baroreceptors during hemodilution also exists.
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PMID:Hemodilution-induced inhibition of cardiovascular responses to some vasoactive agents in anesthetized cats. 747 26


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