Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydralazine reduces pulmonary vascular resistance in patients with primary and secondary pulmonary hypertension, but the effects on right ventricular function of a change in resistance without a reduction in pulmonary arterial pressure are not known. We evaluated the hemodynamic effects of hydralazine, 50 mg, administered orally every 6 hours for 48 hours in 14 patients with right ventricular failure and pulmonary hypertension resulting from various causes. Hydralazine reduced mean right ventricular end-diastolic pressure from 17.4 +/- 5.6 to 11.6 +/- 5.3 mm Hg (p less than 0.001) and increased cardiac output and stroke volume by more than 40%. In nine patients who had no change in mean pulmonary arterial pressure after hydralazine, total pulmonary resistance decreased from 15.9 +/- 6.0 to 10.6 +/- 4.3 (p less than 0.001) and cardiac index increased from 2.07 +/- 0.51 to 2.97 +/- 0.91 (p less than 0.005). There was a close correlation between the reductions in total pulmonary resistance and right ventricular end-diastolic pressure (r = 0.73)). These data suggest that hydralazine can increase cardiac output and reduce right ventricular end-diastolic pressure even when pulmonary arterial pressure remains unchanged.
 ...
PMID:The effects of oral hydralazine on right ventricular end-diastolic pressure in patients with right ventricular failure. 707 95

Arterial oxygen transport (cardiac output x arterial oxygen content) may be decreased in heart failure. We studied the determinants of arterial oxygen transport in 15 patients with chronic, severe myocardial failure at rest and during cycle ergometry. During control therapy at rest, arterial oxygen tension was normal (81 +/- 8 mm Hg, mean +/- SD) and increased slightly during exercise (90 +/- 14 mm Hg). During hydralazine therapy at rest, arterial oxygen tension was slightly higher (87 +/- 9 mm Hg) and also increased during exercise (92 +/- 15 mm Hg). Hydralazine did not increase arterial oxygen tension (0.10 greater than p greater than 0.05), but exercise did (p less than 0.02). Arterial oxygen saturation and content were normal and did not change under any condition or treatment. During control therapy at rest, arterial oxygen transport was low (313 +/- 74 ml/min . m2) and remained abnormally low during exercise (434 +/- 124 ml/min . m2). During hydralazine therapy, arterial oxygen transport was higher at rest (457 +/- 100 ml/min . m2) and during exercise (577 +/- 131 ml/min . m2). Hydralazine increased arterial oxygen transport (p less than 0.01) because it increased stroke volume at rest and during exercise, but it did not change arterial oxygenation. Arterial oxygenation is normal in chronic heart failure patients at rest and during exercise. Hydralazine increases cardiac output and arterial oxygen transport without changing arterial oxygenation.
 ...
PMID:Arterial oxygenation and arterial oxygen transport in chronic myocardial failure at rest, during exercise and after hydralazine treatment. 708

We studied the effects of afterload reduction in chronic severe aortic insufficiency by measuring the hemodynamic response to oral hydralazine in 10 consecutive patients. Hemodynamics were also measured during maximal exercise in eight of these patients. At rest, hydralazine reduced pulmonary artery wedge pressure from 14 to 9 mm Hg (p less than 0.01), and increased cardiac index by 70% and stroke volume index by 35% (both p less than 0.001). Before hydralazine, pulmonary artery wedge pressure exceeded 20 mm Hg in five patients during maximal exercise; with hydralazine, at identical levels of exercise, pulmonary artery wedge pressure remained below 20 mm Hg in all patients. For the group, hydralazine reduced pulmonary artery wedge pressure from 21 to 12 mm Hg (p less than 0.05) and increased cardiac index by 31% (p less than 0.05) during exercise; changes in stroke volume index were more variable and there was no significant increase for the group, although several patients increased stroke volume substantially and the overall increase was 34%. These data show that afterload reduction has beneficial effects on cardiac performance in chronic severe aortic insufficiency both at rest and during exercise. Hydralazine may be of use in such patients either in preparation for valve replacement or as interim therapy.
 ...
PMID:Beneficial effects of hydralazine on rest and exercise hemodynamics in patients with chronic severe aortic insufficiency. 737 85

To determine how arteriolar dilation improves cardiac performance in aortic insufficiency, we evaluated the acute effects of hydralazine in 10 patients with chronic severe aortic insufficiency. Control measurements of intracardiac and intravascular pressures, cardiac output and left ventricular volumes were obtained at cardiac catheterization. Hydralazine, 0.3 mg/kg i.v. (maximal dose 20 mg), was administered and all measurements were repeated 30 minutes later. A reduction in systemic vascular resistance from 1264 to 710 dyn-sec-cm-5 was associated with significant increases in forward cardiac index (2.9 to 5.1 l/min/m2) and stroke volume index (37 to 55 ml/m2). Left ventricular end-diastolic pressure was reduced from 19 to 12 mm Hg. There was a significant reduction in mean arterial pressure (88 to 83 mm Hg) and a significant increase in heart rate (81 to 94 beats/min). Regurgitant stroke volume was reduced by more than 10 ml/m2 in seven patients and for the group was significantly reduced, from 65 to 53 ml/m2. Regurgitant fraction was reduced in all patients; the overall reduction from 0.64 to 0.48 was highly significant. Ejection fraction increased more than 0.10 in four patients, by 0.08 in an additional patient and for the group increased significantly from 0.50 to 0.57. Left ventricular end-diastolic volume decreased by more than 25 ml/m2 in four patients, by 19 ml/m2 in an additional patient and was decreased significantly, from 208 to 190 ml/m2, for the group. Arteriolar dilators improve cardiac performance in aortic insufficiency by reducing the amount of aortic regurgitation and, in some patients, by substantially improving systolic pump fraction. These data suggest a role for arteriolar dilators in the management of selected patients with aortic insufficiency.
 ...
PMID:Mechanism for improved cardiac performance with arteriolar dilators in aortic insufficiency. 744 51

This study was performed to examine the effects of blockade of the renin-angiotensin system on the development of hypertension and renal damage in stroke-prone spontaneously hypertensive rats (SHR-sp), using a non-peptide angiotensin II receptor antagonist, CV-11974. We examined changes in blood pressure, urinary protein excretion, creatinine clearance and renal morphology in CV-11974-treated SHR-sp rats and compared these variables with those in non-treated SHR-sp and Wistar Kyoto (WKY) rats, as well as in hydralazine-treated SHR-sp rats. CV-11974 lowered systolic blood pressure in a manner similarly to hydralazine (CV-11974 204 +/- 3, hydralazine 200 +/- 3, non-treated SHR-sp 284 +/- 9, WKY 155 +/- 5 mmHg), but reduced urinary protein excretion more than hydralazine (p < 0.01). There were no significant differences in creatinine clearance among experimental groups. The glomerulosclerosis index was greater in non-treated and hydralazine-treated SHR-sp rats than in CV-11974 treated SHR-sp and WKY rats (p < 0.01). Hydralazine-treated SHR-sp rats had a lower glomerulosclerosis index than the non-treated SHR-sp rats (p < 0.01). No significant differences were found in glomerulosclerosis index between CV-11974-treated SHR-sp and WKY rats. Tubular atrophy, tubular casts and interstitial fibrosis were observed in non-treated SHR-sp rats and, occasionally, in hydralazine-treated SHR-sp rats, but not in CV-11974-treated SHR-sp rats or WKY rats. These results indicate that the angiotensin II receptor antagonist was superior to hydralazine as far as renal protection was concerned. This suggests that renal damage in SHR-sp rats is associated not only with hypertension but also with activation of the renin-angiotensin system.
 ...
PMID:Renal protective effects of angiotensin II receptor I antagonist CV-11974 in spontaneously hypertensive stroke-prone rats (SHR-sp). 788 3

1. The effect of the selective histamine H3 receptor agonist, R-alpha-methylhistamine given intravenously (10-100 micrograms kg-1) was examined on baseline total peripheral resistance (TPR), and cardiovascular haemodynamics in bilaterally vagotomized, anaesthetized guinea-pigs. 2. R-alpha-methylhistamine produced a dose-dependent hypotension and fall in TPR at 30 and 100 micrograms kg-1. A decrease in heart rate (HR) was observed at a dose of 100 micrograms kg-1. R-alpha-methylhistamine (10-100 micrograms kg-1) also produced a dose-dependent fall in rate pressure product (RPP). There was no effect on cardiac output (CO) or stroke volume (SV) at these doses. 3. Histamine H1 and H2 blockade in animals pretreated with a combination of chlorpheniramine (0.3 mg kg-1) and cimetidine (3.0 mg kg-1) did not alter the haemodynamic actions of R-alpha-methyl-histamine (100 micrograms kg-1, i.v.). Pretreatment with the selective H3 antagonist, thioperamide (1 mg kg-1), completely blocked the action of R-alpha-methylhistamine on haemodynamic parameters. 4. To study the mechanism of action of R-alpha-methylhistamine, the vasodilator hydralazine (1 mg kg-1, i.v.) was used. Hydralazine lowered BP, TRP and RPP in guinea-pigs pretreated with ipratropium (50 micrograms kg-1, i.v.). Hydralazine had no effect on HR, SV or CO. 5. R-alpha-methylhistamine (100 micrograms kg-1) did not affect the vasopressor action and increases in TPR produced by adrenaline (1 and 3 micrograms kg-1). On the other hand, the vasodilator hydralazine (1 mg kg-1, i.v.) inhibited the effects of adrenaline (3 micrograms kg-1) on TPR and RPP. The effect of both doses of adrenaline on BP were attenuated by hydralazine. Therefore, the inhibitory effects of R-alpha-methylhistamine are not mediated through a direct action on vascular smooth muscle.6. In adrenalectomized guinea-pigs, R-alpha-methylhistamine (100 microg kg-1) produced a drop in BP and HR.There was no difference between the effects of R-alpha-methylhistamine on blood pressure and heart rate in adrenalectomized and non-adrenalectomized guinea-pigs.7. These results show that activation of peripheral H3 receptors lowers basal BP, HR and TPR, most likely by a peripheral prejunctional mechanism. The fall in BP and TPR is probably due to a decrease in noradrenaline release from sympathetic effector nerves innervating the resistance blood vessels.
 ...
PMID:Production by R-alpha-methylhistamine of a histamine H3 receptor-mediated decrease in basal vascular resistance in guinea-pigs. 790 73

Hydralazine was administered at cardiac catheterization to eight children with a ventricular septal defect (age: 2.2-8.8 years), and the extent of afterload reduction was determined using aortic input impedance and wall stress. The pulmonary to systemic blood flow ratio decreased from 2.2 +/- 0.8 to 1.8 +/- 0.4 (p < 0.05) and the pulmonary systemic resistance ratio increased from 0.11 +/- 0.08 to 0.13 +/- 0.10 (p < 0.05) after hydralazine administration. Hydralazine reduced mean aortic pressure and the amplitude of the late systolic peak of the aortic pressure wave. Peak flow velocity in the descending aorta increased from 62 +/- 14 to 81 +/- 24 cm/sec (p < 0.05). Peripheral resistance decreased significantly from 13.3 +/- 5.9 to 6.6 +/- 3.7 10(3) dyn sec/cm3 (p < 0.05). The modulus of the first harmonic, indicating pulse wave reflection, decreased from 1196 +/- 575 to 815 +/- 382 dyn sec/cm3 (p < 0.05). The characteristic impedance, indicating aortic stiffness, did not change. End-systolic wall stress decreased significantly from 54.4 +/- 16.7 to 34.8 +/- 10.2 g/cm2 (p < 0.01). Hydralazine acutely achieved afterload reduction by reducing both peripheral resistance and pulse wave reflection, and increased stroke volume.
 ...
PMID:Afterload reduction by hydralazine in children with a ventricular septal defect as determined by aortic input impedance. 808 27

Our previous studies have shown that ethanol selectively counteracts centrally mediated hypotensive responses. This study investigated the role of cardiac output and peripheral resistance in the antagonistic interaction between ethanol and antihypertensive drugs. Changes in blood pressure, heart rate, cardiac index, stroke volume, and peripheral resistance elicited by clonidine and subsequent ethanol or saline administration were evaluated in conscious rats. The aortic barodenervated rat was employed because it exhibits greater hypotensive responses to clonidine compared with the intact rat. Aortic barodenervation elicited acute rises in blood pressure, heart rate, and peripheral resistance, whereas cardiac index and stroke volume were not altered. The blood pressure of conscious aortic barodenervated rats returned to sham-operated levels by 48 hours due to concomitant reductions in cardiac index and stroke volume; the peripheral resistance, however, remained significantly elevated. Clonidine (30 microg/kg, I.V.) elicited greater decreases in blood pressure in aortic barodenervated compared with sham-operated rats. The hypotension was caused by decreases in cardiac index and stroke volume because peripheral resistance did not change. Ethanol (1 g/kg, I.V.) counteracted the hypotensive effect of clonidine and raised blood pressure to levels higher than preclonidine values. Significant (P<.05) increases in cardiac index and stroke volume and decreases in peripheral resistance accompanied the pressor effect of ethanol. Additional control groups were included in the study to determine the selectivity of the interaction. A dose of hydralazine (0.5 mg/kg, I.V.) was used that produced similar hypotension to that evoked by clonidine in aortic barodenervated rats. Hydralazine-evoked hypotension was similar in denervated and control rats and resulted from significant reductions in peripheral resistance. Reflex increases in heart rate and stroke volume and hence cardiac output were observed. Ethanol given after hydralazine produced a short-lived pressor effect (<5 minutes versus 40 minutes in the case of clonidine) and counteracted the sympathetically mediated increases in cardiac output, stroke volume, and heart rate. These findings support our hypothesis that ethanol selectively counteracts hypotensive responses of central origin by reversing the reduction in cardiac output elicited by clonidine.
 ...
PMID:Role of cardiac output in ethanol-evoked attenuation of centrally mediated hypotension in conscious rats. 926 Sep 94

Our previous studies showed that ethanol selectively counteracts centrally mediated hypotensive responses. In this study, we investigated the role of sympathetic nerve activity, cardiac output (CO), and total peripheral resistance (TPR) in this antagonistic hemodynamic interaction between ethanol and clonidine. Changes in blood pressure (BP), heart rate (HR), CO, stroke volume (SV), and TPR elicited by intracisternal (i.c.) clonidine and subsequent ethanol or saline were evaluated in conscious freely moving spontaneously hypertensive rats (SHRs). Clonidine (0.5 microg, i.c.) evoked hypotension was due to a significant reduction in TPR (from 3.6+/-0.21 to 2.8+/-0.17 mm Hg/ml/min/100 g), which was associated with a significant (p < 0.05) reduction in plasma norepinephrine (NE, from 660+/-115 to 310+/-50 pg/ml), measured as index of sympathetic activity. Ethanol (1 g/kg, i.v.) counteracted the hypotensive effect of clonidine and produced significant (p < 0.05) increases in plasma NE and TPR. Further support for the hypothesis that ethanol selectively counteracts centrally mediated hypotension was sought by investigating the effect of ethanol on peripherally mediated hemodynamic responses to hydralazine. Hydralazine (0.4 mg/kg, i.v.) produced a hypotension similar in magnitude to that produced by clonidine, which was also due to a significant reduction in TPR. However, unlike the case with clonidine, reflex increases in HR, SV, and hence CO were evident. Ethanol given after hydralazine produced a short-lived pressor effect (<10 min vs. 60 min in case of clonidine) in spite of a sustained increase in TPR. The latter was offset by the simultaneous decreases in CO, SV, and HR. A 30% increase in plasma NE caused by hydralazine returned to baseline level after ethanol or saline. Blood ethanol concentrations were similar in all treatment groups. These findings suggest that ethanol selectively counteracts centrally evoked hypotensive responses by counteracting the sympathoinhibition-mediated decreases in TPR elicited by centrally administered clonidine in conscious SHRs.
 ...
PMID:Role of the sympathetic control of vascular resistance in ethanol-clonidine hemodynamic interaction in SHRs. 1051 Nov 36

Hypertensive crises are situations when arterial hypertension shows its immediate damaging potential, and in such circumstance, antihypertensive therapy provides its life-saving effectiveness. Among these situations are hypertensive emergencies, hypertensive urgencies, hypertensive encephalopathy, and also accelerated-malignant hypertension characterised by the presence of grade 3 or grade 4 Keith-Wagener retinopathy and numerous complications (acute renal failure, heart failure, haemorrhagic brain stroke or acute coronary events). Despite of antihypertensive therapy, the mortality rate of accelerated-malignant hypertension is about 25% after the 5th year. We present the case of a thirty-three years old male, with a five-year history of non-treated hypertension, who develops accelerated- hypertension with heart failure, microangiopathic haemolytic anaemia and renal failure that requires renal replacement therapy. After a strict control of blood pressure; initially using parenteral agents such as Solinitrin and Urapidil, followed by angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-adrenergic receptor blockers, calcium channel blockers and Hydralazine, the patient partially recovers his renal function, resulting in the withdrawal of haemodialysis.
 ...
PMID:[Accelerated arterial hypertension in a young male]. 1521 76


<< Previous 1 2 3 4 Next >>