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

1 The use of radioactive microspheres is described for the measurement of cardiac output in anaesthetized rabbits and its redistribution after the administration of drugs which lower blood pressure. 2 Hydralazine increased peripheral vascular conductance by 123%. The vascular beds in which it had most effect were those of the carcass (mainly muscle) and the kidneys. 3 SK&F 24260, (1,4 dihydro-2, 6-dimethyl-4(2-trifluoremethylpheny)-3,5,-pyridinedicarboxylic acid diethyl ester), had similar vasocilator actions. Its effect in the carcass contributed relatively more to the increase of total peripheral conductance. It also caused a remarkable degree of cerebral vasodilatation. 4 Guanethidine had a relatively small effect on total peripheral conductance and lowered blood pressure mainly by reducing stroke volume and cardiac output.
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PMID:The use of radioactive microspheres to compare the effects of hydralazine, guanethidine and SK & F 24260 on the redistribution of cardiac output in anaesthetized rabbits. 0 Nov 34

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.
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PMID:Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure. 49 13

The severity of mitral regurgitation is, in part, determined by aortic impedance to left ventricular outflow. Sodium nitroprusside acutely decreases regurgitant flow, but the importance of its dual vasodilating effects, the lowering of peripheral vascular resistance and increasing of venous capacitance, is unclear. We studied the hemodynamic response to intravenous hydralazine, which selectively acts on the arteriolar resistance bed, in 10 patients with severe mitral regurgitation. Hydralazine produced a 50% increase in forward stroke volume (22 +/- 2 to 33 +/- 3 ml/m2, P less than 0.001) and a 33% reduction in regurgitant stroke volume (40 +/- 6 to 27 +/- 6 ml/m2, P less than 0.001), with a resultant fall in pulmonary capillary wedge v wave and mean pressures. Unlike nitroprusside, it did not alter left ventricular end-diastolic volume or pressure. Oral hydralazine maintained this hemodynamic improvement for at least 48 hours and, in three patients, provided more sustained clinical improvement. We conclude that hydralazine, by virtue of its selective lowering of aortic impedance, reduces the amount of mitral regurgitation and thus may be a useful mode of interim or chronic therapy in selected patients.
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PMID:Beneficial effects of hydralazine in severe mitral regurgitation. 66 75

Hydralazine is shown to have a very complex cerebral hemodynamic effect. It raises the intracranial pressure which, together with its effect upon systemic blood pressure, reduces the cerebral perfusion pressure. In spite of this and a concomitantly induced hyperventilation by hydralazine, CBF increases with some delay. The conclusion is that hydralazine is a cerebral vasodilator acting immediately upon cerebral capacitance vessels but later upon the resistance vessels as well.
Stroke
PMID:A paradoxical cerebral hemodynamic effect of hydralazine. 115 77

Felodipine, a potent dihydropyridine calcium antagonist with a pronounced vascular selectivity, was given intravenously (0.006-0.025 mumol kg-1) to anaesthetized, open-chest dogs with denervated hearts. The result was a dose-dependent decrease in mean arterial pressure (MAP) and total peripheral resistance (TPR), while heart rate (HR), stroke volume (SV) and left ventricular end-diastolic pressure remained relatively unchanged. Cardiac tension work (TTI) and oxygen consumption (MVO2) were reduced, probably due to the decrease in afterload. The relative reduction of the coronary vascular resistance (CVR) was greater than that of TPR. The hypotensive effect of verapamil (0.05-0.20 mumol kg-1) was small and MAP decreased mainly via a decrease in HR and SV. Higher doses of verapamil which induced vasodilatation could not be given without the development of complete atrio-ventricular dissociation. Hydralazine (11-45 mumol kg-1) decreased TPR and CVR in parallel but the decrease in MAP was partly counteracted by a powerful increase in HR, SV and cardiac inotropy which was associated with elevated catecholamine levels in plasma. When MAP and HR were maintained constant by means of aortic balloon inflation and atrial pacing, felodipine markedly increased coronary blood flow and coronary sinus oxygen saturation while SV, TTI, inotropy and MVO2 remained relatively unchanged. It is concluded that felodipine markedly dilates peripheral resistance vessels, and in particular those in the coronary vascular bed, without any cardiodepressant effects.
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PMID:Acute haemodynamic effects of felodipine, verapamil and hydralazine in the anaesthetized dog. 186 91

The effects of hydralazine and prostaglandin E1 on regional myocardial function were studied in dogs. Sixteen dogs were randomly assigned to one of two drug treatment groups of eight dogs each. The first group (G1) was treated with 0.4 mg/kg hydralazine administered as a bolus. The second group (G2) received prostaglandin E1 given as an infusion for a total dose of 0.8 micrograms/kg. Regional myocardial function was assessed through the measurement of myocardial segment shortening during systole. We call this index percent systolic shortening (%SS). An ischemic heart preparation was created by partial occlusion of coronary blood flow. The degree of induced ischemia was determined by following the reduction in %SS. Hydralazine reduced %SS of the ischemic myocardium while increasing the cardiac index, stroke volume index, and coronary blood flow. Prostaglandin E1 increased %SS, cardiac index, and stroke volume index in the ischemic heart preparation. Hydralazine, therefore, induced dissociation between global ventricular function and regional myocardial function whereas prostaglandin E1 did not. The present findings emphasize that evaluation of vasoactive drugs should consider their effects on regional myocardial function as well as on global hemodynamics.
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PMID:Effects of hydralazine and prostaglandin E1 on regional myocardial function in the ischemic canine heart. 198 67

In order to assess the relative value of digoxin, nifedipine and hydralazine on left ventricular performance at rest and during exercise, we studied 10 men with moderately severe chronic aortic regurgitation using two-dimensional echocardiography. Digoxin after one month at therapeutic serum levels increased resting ejection fraction as compared to control [0.54 +/- 0.08 (SD) vs 0.47 +/- 0.08, respectively, P less than 0.03]. Ejection fraction decreased during exercise but the difference between digoxin and control was maintained. Stroke volume also was higher on digoxin than control at rest (93 +/- 15 vs 83 +/- 17 ml, P less than 0.02) and the larger stroke volume on digoxin was maintained during exercise. By contrast, stroke volume was reduced by one month of therapy with maximally tolerated nifedipine doses compared to control (74 +/- 8 vs 83 +/- 17 ml, P = 0.03) and this difference was maintained during exercise. Hydralazine in doses up to 225 mg/day for one month produced no significant changes in left ventricular performance compared to control at rest or during exercise. However, compared to digoxin ejection fraction at peak exercise was significantly less on hydralazine (0.39 +/- 0.9 vs 0.52 +/- 10, P less than 0.02). These data suggest that digoxin improved left ventricular performance and may be of benefit in the treatment of patients with chronic aortic regurgitation.
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PMID:Effect of digoxin and vasodilators on left ventricular function in aortic regurgitation. 273 81

Isolated tail arteries from stroke-prone spontaneously hypertensive rats (SHRSP), but not normotensive Wistar-Kyoto (WKY) rats, exhibit oscillatory contractions in response to norepinephrine. To establish whether this vascular abnormality is secondary to elevated arterial pressure, SHRSP and WKY were treated with hydralazine and hydrochlorothiazide from weaning to 4 months of age. Hydralazine and hydrochlorothiazide treatment significantly attenuated hypertension development in SHRSP (systolic blood pressure: control SHRSP = 219 +/- 9 mmHg; treated SHRSP = 143 +/- 5 mmHg at 15 weeks of age). Helically-cut tail artery strips from all rats were mounted in tissue baths for isometric force recording and exposed to norepinephrine (6 x 10(-10)-6 x 10(-6) M) for 20 min at each concentration. Oscillatory activity was defined as the sum of the magnitudes of all phasic contractions occurring during the final 10 min of NE incubation. There was no significant difference in the magnitude of oscillatory activity between hydralazine/hydrochlorothiazide-treated SHRSP and control SHRSP. From these results we conclude that norepinephrine-induced oscillatory activity in SHRSP is a primary vascular abnormality that is not secondary to high blood pressure.
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PMID:Effect of antihypertensive therapy on a vascular change in genetically hypertensive rats. 343 74

We evaluated the acute hemodynamic responses to hydralazine during cardiac catheterization in 13 infants with idiopathic dilated cardiomyopathy. Ages ranged from 2 to 13 months (6.7 +/- 4.0 months, mean +/- SD). Each infant had congestive heart failure and angiographic evidence of markedly depressed left ventricular ejection fraction (0.24 +/- 0.11; normal = 0.58-0.78) with left ventricular dilation (left ventricular end-diastolic volume = 349 +/- 125% of normal). Hydralazine (0.5 to 1.0 mg/kg administered intravenously) acutely decreased systemic arteriolar resistance from 21.1 +/- 3.3 to 12.0 +/- 2.7 U/m2 (p less than 0.001). This 41 +/- 14% decrease in systemic resistance was accompanied by a 45 +/- 16% increase in cardiac index (3.24 +/- 0.53 to 4.71 +/- 0.99 L/min/m2; p less than 0.001). Mean arterial blood pressure declined from 70 +/- 8 to 60 +/- 11 mm Hg (p less than 0.001). Hydralazine also increased heart rate (122 +/- 19 to 138 +/- 18 bpm; p less than 0.001), but this increase did not account entirely for the change in cardiac index as evidenced by a rise in stroke volume index (26.9 +/- 4.9 to 34.5 +/- 7.5 ml/beat/m2; p less than 0.001). Pulmonary arteriolar resistance and pulmonary capillary wedge pressure fell slightly in response to hydralazine. Subsequently, oral hydralazine was included in the treatment regimen of 10 infants followed for 3 to 38 months (mean = 15 months). Of these, eight demonstrated sustained clinical improvement. We conclude that hydralazine may be a beneficial adjunct to the management of congestive heart failure in young infants with a dilated cardiomyopathy.
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PMID:Hemodynamic effects of hydralazine in infants with idiopathic dilated cardiomyopathy and congestive heart failure. 379 28

The mechanism by which hydralazine improves cardiac function in patients with heart failure is not well characterized. Hydralazine may improve left ventricular (LV) function by decreasing afterloading wall stress or by increasing myocardial contractility. The effect of intravenous hydralazine was assessed in 8 patients with severe idiopathic dilated cardiomyopathy. Hydralazine increased stroke volume index (from 24 +/- 8 to 40 +/- 9 ml/m2, p less than 0.01) and decreased systemic vascular resistance from 1,603 +/- 619 to 810 +/- 317 dynes s cm-5, p less than 0.01) and peak LV wall stress (from 476 +/- 118 to 410 +/- 68 kdynes/cm2, p = 0.02). Two groups were defined by normal or high LV wall stress. Patients with high LV stress had higher LV end-diastolic pressure (38 +/- 12 vs 17 +/- 8 mm Hg, p less than 0.01), LV end-diastolic volume index (184 +/- 24 vs 149 +/- 7 ml/m2, p less than 0.01) and systemic vascular resistance (1,423 +/- 686 vs 846 +/- 293 dynes s cm-5, p = 0.01). Hydralazine decreased stress more in these patients (-101 +/- 57 vs -6 +/- 9 kdynes/cm2, p = 0.02), LV end-diastolic pressure (-12 +/- 7 vs 2 +/- 2 mm Hg, p = 0.02), systolic pressure (-15 +/- 13 vs 3 +/- 4 mm Hg, p = 0.03) and systemic vascular resistance (-1,053 +/- 247 vs -363 +/- 83 dynes s cm-5, p less than 0.01) than in patients with normal LV stress. Decreased LV stress was caused by decreased systolic and diastolic pressures and/or volumes. Late systolic pressure-volume relations in patients with normal LV stress suggested increased myocardial contractility, but this was not confirmed by LV dP/dt. Hydralazine improves LV function in patients with dilated cardiomyopathy by reducing elevated LV wall stress, with little inotropic effect.
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PMID:Effects of hydralazine on pressure-volume and stress-volume relations in congestive heart failure secondary to idiopathic dilated cardiomyopathy. 405 Jul 8


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