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

The effects of intravenous captopril and intravenous digoxin given separately and in combination on rest and exercise hemodynamics were studied in 16 patients with severe heart failure and sinus rhythm. When given separately, both captopril and digoxin decreased the pulmonary capillary wedge pressure by, respectively, 24% (p = 0.003) and 34% (p = 0.004) and systemic vascular resistance by 23% (p = 0.09) and 20% (p = 0.03). Only digoxin increased cardiac index by 23% (p = 0.03) and stroke work index by 52% (p = 0.01). During maximal exercise, captopril alone decreased systemic vascular resistance by 28% (p = 0.0002) and increased cardiac index by 33% (p = 0.02). Digoxin alone decreased pulmonary capillary wedge pressure by 11% (p = 0.04) and increased stroke work index by 44% (p = 0.01). The combination of captopril and digoxin resulted in a decrease in pulmonary capillary wedge pressure and systemic vascular resistance and an increase in cardiac index and stroke work index both at rest and during exercise that was greater than values observed with either drug given alone. Cardiac index response to the combination of captopril and digoxin correlated with baseline serum aldosterone concentration (r = 0.81, p less than 0.001) and plasma renin activity (r = 0.74, p less than 0.0002). A significant decrease in norepinephrine concentration was noted after digoxin was administered alone or added to captopril. These findings demonstrate that in patients with severe heart failure, the acute administration of captopril and digoxin has an independent salutary hemodynamic effect. The combination of these agents, however, has an adjunctive effect on cardiac function at rest and during exercise.
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PMID:Comparative hemodynamic and neurohormonal effects of intravenous captopril and digoxin and their combinations in patients with severe heart failure. 256 44

The specific competitive alpha 1-postsynaptic blocking action and haemodynamic effects of prazosin (Minipress) have been summarized. Prazosin causes dilatation of arterioles and veins, reduces total peripheral resistance as well as preload and afterload. Cardiac output does not change at rest, stroke volume and subsequent cardiac output increase during exercise. The changes in heart rate have non-significant. It does not cause sympathetic counter-regulation, plasma renin activity does not increase, aldosterone level decreases, salt- and fluid retention may rarely be observed. It does not provoke angina. The authors report on the results of their examinations with the first dose of prazosin in 61 patients (in 33 cases by the double-blind cross-over method by placebo control), and summarize the observations made with the drug in long-term treatment in Hungary. The authors and other teams used prazosin as a long-term treatment (of approximately 3 months) in combination with other drugs in a total of 344 patients, and as monotherapy in 159 patients. In the course of combination treatment side-effects were observed in 15% of the patients (dizziness, headache, weakness, occasionally palpitation). During monotherapy, side-effects occurred in 12% of the patients (tachycardia, headache, weakness, dizziness). Hungarian results confirm the usefulness of prazosin in all stages of hypertension. It is effective in 30-35% of the cases as a monotherapy (this rate is congruent with the efficacy of beta-blockers, calcium antagonists and antihypertensive drugs of central action). Earlier prazosin had been used as a third agent in combination treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the action of Minipress. Examinations in hypertension. 257 64

The sequential effects of an increased daily NaCl intake on hemodynamics, fluid electrolyte balances, and hormonal responses were evaluated in dogs (n = 7) with fixed circulating levels of angiotensin II (ANG II). During the control period, ANG II was infused at 3 ng.kg-1.min-1 while dogs were maintained on an 8 meq NaCl/day diet. Water intake was fixed at 700 ml/day. Continuously recorded (24 h/day) changes of total body weight (TBW) were used as an index of total body water. Cardiac stroke volume and arterial pressure were recorded, and each beat was digitized to provide hourly and 24-h average cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR). After three stable control days, daily salt intake was increased to 120 meq for 7 days. TBW increased gradually to 448 +/- 111 g (2.9%, P less than 0.05) above control by day 3. An 11% expansion of blood volume (P less than 0.05) was found (51CR-labeled red blood cells) on day 2 of high NaCl. CO rose 12% and MAP 20% (P less than 0.05) in parallel with TBW by day 4. By day 7, CO remained only 5% elevated, whereas MAP had stabilized at 20% above control levels. TPR remained significantly elevated from days 3 through 7. A positive Na balance averaging 91 +/- 8 meq (P less than 0.05) occurred on day 1. Plasma Na concentration was increased 2-3 meq/l above control throughout the period of high-salt intake. Plasma renin activity and aldosterone levels decreased to nearly undetectable levels, vasopressin rose slightly, and atrial natriuretic peptide levels increased significantly. Dogs maintained at 8 meq/day NaCl during the same infusion of ANG II showed no changes in MAP, CO, TPR, or TBW. In summary, the salt-induced hypertension was consistently related to small but significant fluid retention, blood volume expansion, elevations of cardiac output, and a gradual increase in TPR.
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PMID:Hemodynamics and blood volume in angiotensin II salt-dependent hypertension in dogs. 258 96

We were able to show that spontaneously hypertensive stroke-prone rats (SHR-SP) have a lower number of glucocorticoid receptors (P-value is of borderline significance, 0.01 greater than P less than 0.05) with a highly significant lower Kd (P less than 0.0005), i.e higher affinity in their mononuclear leukocytes, compared to normotensive Wistar-Kyoto rats (WKY). The plasma levels of corticosterone, aldosterone and 18-hydroxycorticosterone of the two strains do not differ.
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PMID:Glucocorticoid receptors and dissociation constant (Kd) are decreased in mononuclear leukocytes of spontaneously hypertensive rats (SHR-SP) as compared to normotensive Wistar-Kyoto rats (WKY). 262 28

This study aims to clarify the neurohumoral regulation of cardiovascular circulatory adjustments and to analyze changes in renal function and their relationship to cardiovascular hemodynamics in the early stage of heart failure. Cardiac and peripheral (calf segment) hemodynamics, neurohumoral factors and renal function were investigated in totally 139 patients with acute myocardial infarction (AMI). Capacitance vessel constriction was observed in patients with uncomplicated AMI (Killip-I, Forrester HS-I) and constriction of capacitance and resistance vessels in patients complicated by heart failure (Killip II, Forrester HS-II) or cardiogenic shock (Killip III-IV, Forrester HS-IV). Augmented sympathoadrenal discharge significantly related to the degree of pump dysfunction (elevation of heart rate, central venous pressure, pulmonary capillary wedge pressure (PCWP) and decrease of stroke volume index (SVI] and activation of the renin-angiotensin-aldosterone system significantly related to fall in tissue perfusion pressure (mean blood pressure and calf vascular resistance) would be a possible mechanism for these compensatory mechanisms. However these would contribute to excessive vasoconstriction in limbs resulting in exercise intolerance or renal glomerular function impairment. The derangement of creatinine clearance, serum creatinine (Scr), blood urea nitrogen and beta 2-microglobulin were related to Killip classification, and it was clarified that PCWP tended to elevate more in patients with preexisting renal function disturbance, and when cardiac output (CO) depressed much lower, reduction of CO per se caused more severe prerenal renal insufficiency. That is, there were significant correlations between renal function parameters and cardiovascular hemodynamics. The Cardio-Renal Subset (CRS) was originally developed according to the initial SVI and Scr, and it was demonstrated that the CRS would be of definite predictive value in early identification of high risk patients.
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PMID:Cardiovascular circulatory adjustments and renal function in acute heart failure. 265 39

Twelve essential hypertensive patients with normal renal function were treated once daily with a new angiotensin converting enzyme inhibitor, enalapril maleate, for about two months. In all patients, the drug-induced changes in blood pressure (BP), systemic and renal hemodynamics, plasma renin activity (PRA), and urine aldosterone (UA) were evaluated. Mean arterial pressure was significantly lowered. No significant changes in cardiac index, heart rate, and stroke index were observed, while peripheral vascular resistance index was significantly decreased. Plasma and blood volumes were not significantly altered. The effects on renal hemodynamics consisted of a significant increase in renal plasma flow (RPF), a decrease in renal vascular resistance, and no change in glomerular filtration rate (GFR). UA excretion was significantly reduced during enalapril therapy. The drug was well tolerated, and no side effects were observed. In summary, enalapril is able to reduce blood pressure through a vasodilatatory effect without change in cardiac output. It increases renal blood flow with no change in glomerular filtration rate.
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PMID:Systemic and renal hemodynamic changes after two-month treatment with enalapril in patients with essential hypertension. 283 Jan 96

Enalapril 40 mg or tolerated dose was given once daily to 21 patients with congestive heart failure (CHF), NYHA class III, in addition to treatment with digoxin and/or diuretics. After an 8-week open period, 19 patients were randomized to continue enalapril or to receive a placebo in a double-blind manner. After the first enalapril dose of 10 mg, maximal reduction of blood pressure (BP) occurred after 4 hours (mean 34/17 mmHg; p less than 0.001). No further reduction was found after higher doses. After the open period significant improvement was shown as judged by NYHA class (p less than 0.01), stroke volume (p less than 0.05), maximal working capacity (p less than 0.05), heart volume (p less than 0.01) and maximum rate pressure product (RPPmax) (p less than 0.001). Urinary aldosterone markedly decreased (p less than 0.01), whereas serum potassium and serum creatinine slightly increased (p less than 0.05). At the end of the blind period enalapril was superior to placebo concerning NYHA class (p less than 0.01), heart volume (p less than 0.05) and RPPmax (p less than 0.05). Other parameters, including aldosterone in urine, did not differ between the groups. Carry-over effects may have diminished the differences between enalapril and placebo. Diarrhoea (n = 5) and hypotension (n = 5) were the most common side-effects. Overall, enalapril was well tolerated and seems to be useful in single daily doses in the treatment of CHF.
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PMID:Once daily dosing of enalapril in congestive heart failure. 283 90

1. To test the hypothesis that NaCl increases blood pressure, while NaHCO3 does not, we measured the effect of an NaHCO3-containing mineral water on blood pressure in stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto (WKY) rats. We compared mineral water with equimolar amounts of NaCl and demineralized drinking water in six groups of 20 rats each over 24 weeks. 2. NaCl consistently increased blood pressure in both SHR-SP and WKY compared with demineralized water, while mineral water did not. 3. We studied the possible role of sodium-regulating hormones. Sodium, potassium-dependent adenosine triphosphatase activity was decreased by NaCl and by age, but not by mineral water. The concentration of atrial natriuretic peptide was greater in SHR-SP, but was not influenced by the two regimens. Components of the renin-angiotensin-aldosterone system and 18-hydroxydeoxycorticosterone tended to decrease with NaCl, but not with mineral water. 4. Plasma pH values in the six groups of rats were not different; however, SHR-SP had consistently lower PCO2 and HCO3- values and higher anion gap values than WKY rats. These values were not influence by the two regimens. 5. NaCl elevates blood pressure in SHR-SP while NaHCO3 does not. The changes in hormones regulating sodium homoeostasis suggest that NaCl induces volume expansion while NaHCO3 does not. The effect may be related to influences on renal sodium reabsorption by chloride and bicarbonate. The possible role of increased proton excretory activity in SHR-SP remains to be determined.
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PMID:Effect of sodium chloride and sodium bicarbonate on blood pressure in stroke-prone spontaneously hypertensive rats. 284 Feb 35

This study was undertaken to clarify the relationship between mild transient hypertension and dilated cardiomyopathy. Fifty-five patients were studied: group 1--controls (12 patients), group 2--hypertensives without clinical evidence of heart failure (14 patients), group 3--patients with hypertensive heart failure and diastolic blood pressure above 100 mmHg (10 patients), group 4--patients with possible dilated cardiomyopathy with mild hypertension, i.e. diastolic blood pressure of 90-100 mmHg (8 patients), group 5--patients with dilated cardiomyopathy and normal blood pressure (11 patients). The haemodynamic status and cardiac contractility indices were measured in each patient on admission, using M-mode echocardiography. Serum sodium and potassium as well as the urinary sodium, potassium and vanillyl mandelic acid excretions were also measured. The stroke volume, cardiac output and cardiac index fell with heart failure, but much more remarkably in group 4. The peripheral vascular resistance was higher in groups 2, 3 and 4 than in groups 1 and 5; so also were the aortic diameter, left posterior wall thickness and left ventricular mass. The plasma volume, aldosterone and cortisol levels were higher and the urinary sodium and potassium excretion lower in patients with heart failure (groups 3, 4 and 5). It is concluded that the raised blood pressure found in some patients suspected to have dilated cardiomyopathy is not due to the haemodynamic and biochemical changes that occur in heart failure. Such patients are 'chronic' hypertensives with hypertensive heart failure. Their presenting blood pressure is low because of their markedly reduced cardiac output.
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PMID:Mild hypertension in patients with suspected dilated cardiomyopathy: cause or consequence? 284 18

The atrial natriuretic peptides (ANP) are a family of newly discovered peptides which are released from atrial tissue and have potent diuretic/natriuretic, vasodilating and aldosterone inhibitory properties. Plasma concentration of ANP was measured and related to haemodynamic changes after acute blood volume expansion (10 and 20%) in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Acute blood volume expansion resulted in an increase in central (CBV) and peripheral blood volume (PBV), central venous pressure (CVP), stroke volume (SV) and cardiac output (CO), while total peripheral resistance (TPR) and heart rate (HR) were decreased. Mean arterial pressure (MAP) was unchanged. There were larger increases in CBV, CVP and CO in SHR than in WKY rats. In contrast, the increase in PBV and the decrease in HR were more marked in the WKY rats. Basal plasma ANP concentrations were similar in both groups. Blood volume expansion caused a linear increase in plasma ANP in the WKY rats, while the increase in plasma ANP concentration was attenuated in the SHR. It is concluded that acute blood volume expansion is more centralized in the SHR than in the WKY rats. Interestingly, the ANP release in response to blood volume expansion seems to be attenuated in SHR compared with WKY rats, as maximal plasma ANP concentrations were found at 10% volume load.
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PMID:Plasma atrial natriuretic peptide and haemodynamics in conscious normotensive and spontaneously hypertensive rats after acute blood volume expansion. 285 25


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