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

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.
J Thorac Cardiovasc Surg 1979 Feb
PMID:Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration. 3 98

18 patients without valvular pathology, coronary artery disease, or idiopathic hypertrophic subaortic stenosis were haemodynamically and angiographically investigated in order to analyse the effects of a ventricular extrasystolic beat upon the post-extrasystolic left ventricular peak pressure. In eight normal patients (group I), the post-extrasystolic peak pressure (P.ES.P.P.) was lower than that of the pre-extrasystolic beat; in 10 patients with symptoms of left ventricular failure (group II) the P.ES.P.P. significantly increased. The reasons are: 1) cardiac origin: stroke volume increased more in group II; 2) arterial origin. a) aortic compliance was lower in group II (this is probably related to the older age of patients in group II), and by decrease in end-diastolic aortic pressure was smaller in group II. Part of this arterial effect (2b) may probably be explained from the fact that post-extrasystolic compensatory pauses are equal in both groups, but the decay time of arterial pressure during diastole (assuming an exponential decay) is larger in group II. At the same age and with the identical aortic compliance only the two factors 1 and 2b play a part in the changes in P.ES.P.P.
Cardiovasc Res 1979 Jun
PMID:Post-extrasystolic left ventricular peak pressure with and without left ventricular failure. 8 10

The norepinephrine (NE) concentration of cardiac ventricles was determined by radioenzymatic assay in normotensive Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone rats (SPR) at 3-6, 14-19, and over 31 weeks of age. There was no difference between strains prior to hypertension, but a progressive decrease in cardiac NE concentration occurred in SHR and particularly in SPR relative to WKY after hypertension was established. This decrease was not due to cardiac hypertrophy. The cardiac neuronal NE storage capacity in rats over 31 weeks of age was analyzed by determining the maximum concentration of NE obtained in a cardiac microsomal fraction, after saturation in vivo with exogenous NE. The results indicated that, after a long period of hypertension, there was a reduction in cardiac NE storage capacity resulting from a loss either of sympathetic nerve endings or of storage vesicles. Moreover, in addition to this reduction in the total size of the cardiac NE store, there was an independent reduction in the degree of filling of this store in both SHR and SPR. This could reflect an increased turnover of cardiac NE in chronically hypertensive SHR and SPR.
J Cardiovasc Pharmacol
PMID:Changes in cardiac norepinephrine in spontaneously hypertensive and stroke-prone rats. 9 73

The long-term hemodynamic effects of atenolol were studied in 10 patients with previously untreated essential hypertension in WHO stage I. Oxygen consumption, heart rate, cardiac output, and intra-arterial brachial pressure were recorded at rest in supine and sitting positions and during steady-state work at 50, 100, and 150 W. The patients were treated with 100 mg atenolol daily (200 mg in 1 patient) as the sole antihypertensive drug and were restudied after 1 and 5 years. After 1 year the blood pressure was reduced approximately 18% both at rest and during exercise, and the heart rate about 25%. The cardiac output was reduced 16% at rest supine, 27% at rest sitting, and about 20% during exercise. The calculated total peripheral resistance was not decreased compared to pretreatment values. After 5 years on treatment, the hemodynamic parameters were almost identical to those seen after 1 year. There was no increase in stroke volume or cardiac output and no decrease in the total peripheral resistance. Thus prolonged beta-blocker treatment over several years does not seem to normalize hemodynamics in patients with mild to moderate essential hypertension.
J Cardiovasc Pharmacol
PMID:Hemodynamic consequences of long-term beta-blocker therapy: a 5-year follow-up study of atenolol. 9 5

ASI-222 [3-beta-O-(4-amino-4,6-dideoxy-beta-D-galactopyranosyl) digitoxigenin HCl] is a semisynthetic aminosugar cardiac glycoside that has been shown to have a greater therapeutic index than ouabain or digoxin in dogs. We have compared the effects of ASI, digitoxigenin, digitoxigenin-beta-D-galactose, and digoxin in the dog heart-lung preparation. Minute work and stroke work were calculated. Controls were obtained before and after the hearts were failed with sodium pentobarbital. ASI-222 is about three times more potent than digitoxigenin and about twice as potent as digitoxigenin-beta-D-galactose in producing similar increases in the left ventricular stroke work. ASI-222 is about three times more potent than digoxin in creasing left ventricular stroke work. Our results indicate that the addition of an aminosugar group to the genin further increased potency over that observed with the addition of a single neutral sugar and prolonged the duration of activity in failing myocardial tissue.
J Cardiovasc Pharmacol
PMID:Structure-activity relationships of an aminosugar cardiac glycoside, ASI-222 HCl, in the heart-lung preparation of the dog. 9 11

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.
J Cardiovasc Pharmacol
PMID:Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain). 9 26

A Doppler velocity meter for measuring blood flow velocity in the human aorta is described. Using pulsed ultrasound, this instrument allows the velocity to be measured at selected depths. The instrument has been tested in laboratory experiments, and appears to give accurate estimates of mean flow velocity for both steady and pulsatile flows. Flow velocities and estimates of stroke volume have been obtained from the ascending aorta in 18 patients. It is suggested that at present only relative values for flow and flow velocity can be measured. A method for obtaining absolute values for these parameters, based on scanning in the aortic arch, is proposed.
Cardiovasc Res 1976 May
PMID:Transcutaneous measurement of blood flow velocity in the human aorta. 13 58

In an experimental model of chronic cardiac volume overloading, ie chronic A-V block, evaluations of cardiac function were performed during the phase of the development of hypertrophy (one and two weeks of A-V block) and at stable hypertrophy (ten weeks of A-V block). During a time period of ten weeks of volume overload left ventricular muscle mass increased to 1.41 of normal hearts. Cardiac performance measured from cardiac index, stroke volume, and left ventricular ejection fraction was not depressed at any evaluated state of hypertrophy. Normal cardiac performance was also demonstrated when the heart was stressed by high ventricular pacing rates. The contractile state of the intact heart was expressed as the velocity of the isometric left ventricular pressure rise (dP/dt) at comparable loading conditions. Increased dP/dtmax at a stage before stable hypertrophy was reached, even when preload is normalised by ventricular pacing (70/min) implies that the volume overloaded heart during the development of hypertrophy mobilises part of its contractile reserve. It is assumed that increased contractility is a functional cause of an increase in oxygen demand; and that an adequate energy availability is covered by the enlargement of the mitochondrial mass. At stable hypertrophy when the contractile material has also increased, a new steady state is reached and an again normal contractility indicates an also stable dynamic situation.
Cardiovasc Res 1977 Mar
PMID:Role of cardiac contractility in hypertrophy from chronic volume loading. 14 5

Actomyosin was extracted from myocardial homogenates from male rats of different ages of a long-inbred Fischer rat colony maintained under controlled conditions of temperature, humidity, and light. ATPase specific activity rose to a maximum at 2 months of age; this was followed by a progressive decline by about 25% at 16 months of age. However, the extractable actomyosin remained constant during this period. This loss in actomyosin ATPase specific activity is in good agreement with previously reported decrements in both stroke index and myocardial calcium content and an increase in myocardial contraction duration in aged rats.
Cardiovasc Res 1977 May
PMID:Reduced myocardial actomyosin adenosine triphosphatase activity in the ageing male Fischer rat. 14 29

Myocardial function, flow and O2 consumption were compared in cardiac hypertrophy induced by pressure-loading (P) and by volume overloading (V). Increases in LV-to-body weight ratios in P and V hypertrophied hearts were comparable. Indices of LV function such as cardiac output, stroke volume, stroke work, minute work, peak LV dP/dt, ratio of peak LV dP/dt-to-isovolumic pressure and -to-LVEDP, and Vmax were significantly reduced from normal only in hypertrophy induced by V. Left ventricular coronary flow was reduced from 167.1 +/- 27.2 in normal dogs to 146.2 +/- 17.1 cm3/min-100 g-1 in P hypertrophy, and was reduced further to 82.5 +/- 8.2 cm3/min-100 g-1 in V hypertrophy. Flows decreased similarly in epicardium and endocardium in both hypertrophied hearts. Cardiac O2 extraction in P and V hearts was greater than in control hearts. Myocardial O2 consumption was maintained at control values in P hypertrophy, and decreased by 54 +/- 3% in V hypertrophy. These findings indicate that LV function is impaired at rest in hypertrophy induced by V and is normal in hypertrophy induced by P.
Cardiovasc Res 1977 Jul
PMID:Cardiac function, coronary flow and MVO2 in hypertrophy induced by pressure and volume overloading. 14 80


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