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

To determine left ventricular function during the stress of exercise and to evaluate the effects of propranolol on it in patients with hypertrophic cardiomyopathy (HCM), the ECG-multigated blood pool cardiac scintigraphy was performed in 12 without (HNCM) and 10 with (HOCM) left ventricular outflow obstruction at rest and during bicycle ergometer loading. The results were compared to those in 13 normal subjects. 1. Control measurements: Resting and exercise heart rates and blood pressures did not significantly differ between patients with hypertrophic cardiomyopathy and normal subjects. Ejection fraction (EF) was normal or higher in HCM than in normal subjects at rest, but during exercise it failed to increase normally. The increment in cardiac output was half of the normal value. Responses of count-derived end-diastolic volume (EDV) and stroke volume (SV) were different between HOCM and HNCM. They were unchanged during exercise in HNCM and declined in HOCM. End-systolic volume (ESV) was unchanged in HNCM and slightly decreased in HOCM. Responses of the peak ejection rate (PER) and time to the peak ejection rate (TPE) were not significantly different from normal subjects. Left ventricular (LV) ejection time (ET) and TPE/ET were not different from normal subjects. The peak filling rate (PFR) was significantly higher than normal in HOCM at rest and during exercise. The time to peak filling rate was prolonged at rest in HOCM, but not during exercise. 2. Effects of propranolol: Heart rates significantly decreased especially after intravenous propranolol administration. Cardiac output (CO) and SV were unchanged. EDV and ESV increased significantly. The PER was unchanged. The PFR decreased, but not significantly. TPE, time to the PFR (TPF) and ET were prolonged. The ratio of TPE/ET decreased initially, but abruptly increased later. In conclusion, in the control state of HCM patients, the responses of LVEF, EDV and ESV to exercise were abnormal and CO remained half of the normal. There was no difference between patients with and without obstruction. The effect of propranolol on left ventricular function was more obvious in patients with obstruction than without obstruction, especially in ESV, EDV, PFR and TPF. Propranolol did not improve LV systolic and diastolic functions, but the double product decreased depending on the decrease of heart rate maintaining CO by Frank-Starling mechanism due to increased EDV, which may play a part in improving subjective complaints.
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PMID:[Left ventricular function at rest and during exercise and the effects of propranolol in patients with hypertrophic cardiomyopathy]. 350 82

Effects of isosorbide 5-mononitrate (5-ISMN) on cardiovascular function were compared with those of verapamil hydrochloride and propranolol hydrochloride in anesthetized open-chest dogs. Intravenous injection of 5-ISMN (3 mg/kg) considerably lowered systolic blood pressure (SBP). Especially, stroke volume (SV), cardiac output (CO), cardiac work (CW) and systolic right ventricular pressure (SRVP) were significantly decreased. 5-ISMN also produced a continuous reduction in mean pulmonary artery pressure (MPAP), mean pulmonary capillary wedge pressure (MPCWP) and mean right atrium pressure (MRAP), while heart rate (HR) and total peripheral resistance (TPR) were not altered significantly. Intravenous injection of verapamil (0.3 mg/kg) considerably lowered diastolic blood pressure (DBP). Verapamil also caused a significant decrease in HR, CW and TPR and a slight decrease in SRVP and MPCWP. However, SV was significantly increased, and slight increases in MPAP and MRAP were also observed. Propranolol (0.5 mg/kg, i.v.) greatly decreased HR together with CO, CW, SRVP and MPAP and slightly decreased MPCWP, while it caused a considerable increase in 3V and a slight increase in TPR. The finding that administration of 5-ISMN resulted in reduction of pre-load and after-load suggests the possibility that this drug might decrease venous return and thereby reduce myocardial oxygen requirements.
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PMID:[Effects of isosorbide 5-mononitrate on cardiovascular function. (II). Effects on pre-load and after-load]. 408 31

The effects of dobutamine ([+/-]-4-[2-[[3-(p-hydroxyphenyl)-1-methyl propyl] amino] ethyl] pyrocatechol hydrochloride), a new synthetic cardioactive sympathomimetic amine, were examined on direct and continuous measurements of left ventricular (LV) diameter (D), pressures (P), velocity of shortening (V), dP/dt, dP/dt/P, arterial pressure, cardiac output, and regional blood flows in the left circumflex coronary, mesenteric, renal, and iliac beds in healthy, conscious dogs. At the highest dose of dobutamine examined, 40 mug/kg/min, the drug increased dP/dt/P from 65+/-3 to 128+/-4 s(-1) and isolength velocity from 72+/-4 to 120+/-7 mm/s without affecting LV end diastolic D significantly. Mean arterial P rose from 92+/-2 to 104+/-3 mm Hg and heart rate from 78+/-3 to 111+/-7 beats/min, while LV end systolic D fell from 24.1+/-1.4 to 19.9+/-1.8 mm, reflecting a rise in stroke volume from 30+/-4 to 42+/-3 ml. Cardiac output rose from 2.41+/-0.23 to 4.35+/-0.28 liter/min, while calculated total peripheral resistance declined from 0.042+/-0.005 to 0.028+/-0.003 mm Hg/ml/min. The greatest increases in flow and decreases in calculated resistance occurred in the iliac and coronary beds, and the least occurred in the renal bed. Propranolol blocked the inotropic and beta(2) dilator responses while vasoconstricting effects mediated by alpha adrenergic stimulation remained in each of the beds studied. When dobutamine was infused after a combination of practolol and phentolamine, dilatation occurred in each of the beds studied. These observations indicate that dobutamine is a potent positive inotropic agent with relatively slight effects on preload, afterload, or heart rate, and thus may be a potentially useful clinical agent. The one property of this drug which is not ideal is its tendency to cause a redistribution of cardiac output favoring the muscular beds at the expense of the kidney and visceral beds.
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PMID:Effects of dobutamine on left ventricular performance, coronary dynamics, and distribution of cardiac output in conscious dogs. 482 24

Propranolol (P) .13 mg./kg. was given to seven patients with mitral valve obstruction the changes in resting and exercise hemodynamics were followed by means of combined right and left heart catheterization. Changes were variable. At rest there was a decrease in heart rate of 10 beats/min. with no consistent change in stroke volume, cardiac output, left ventricular systolic (LVS) or left atrial (LA) pressure after P. Mean left ventricular end-diastolic (LVED) pressure was increased 3 mm., mean pulmonary artery (PA) pressure was increased 4 mm., and mean mitral valve gradient was reduced 3 mm. Hg by P. During exercise, mean LVS pressure was decreased 31 mm., mean LVED pressure increased 3 mm., mean LA pressure decreased 3 mm., and mean mitral valve gradient was reduced 5 mm. Hg after P. Mean exercise PA pressure was unchanged, cardiac output was reduced 0.9 1./min., and mean heart rate was reduced 37 beats/min., while stroke volume increased 3 ml./beat after P. Exercise pulmonary vascular resistance was increased from 6.1 to 8.2 units by P. Despite a slower heart rate, the diastolic filling period was not increased. P has no place in the treatment of the majority of patients with mitral stenosis because it further reduces cardiac performance below normal.
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PMID:Hemodynamic response to exercise after beta-adrenergic blockade with propranolol in patients with mitral valve obstruction. 595 14

Antihypertensive effects of three beta-adrenergic blocking drugs, acebutolol, propranolol, and practolol were studied for 11 weeks. Spontaneously (SHR); one-clip, two-kidney (CLIP); and deoxycorticosterone and salt (DOC) hypertensive rats were used. The drugs were given orally, 100 mg/kg per day, 5 days per week before development of hypertension. Propranolol inhibited blood pressure (BP) increase significantly in SHR. Acebutolol and practolol also lowered BP in SHR. Three drugs did not affect BP in CLIP, but an apparent inhibition was seen when the results were analyzed including the cases of which BP stayed below 150 mmHg. Either of three drugs did not show antihypertensive effects in DOC. Acebutolol rather increased BP more rapidly. Practolol also increased BP slightly more rapidly. Cerebral stroke was seen in DOC. The incidences of the stroke in the groups given the solvent, acebutolol, propranolol, and practolol were 3/6, 4/7, 2/6, and 3/6, respectively. Acebutolol seemed to cause stroke earlier with the more rapid BP elevation. Acebutolol, propranolol, and practolol decreased incidence of the vascular disease in CLIP. Propranolol also decreased it in DOC. Plasma renin activity was suppressed by these drugs in SHR and CLIP. The mechanisms of antihypertensive effects of beta-adrenergic blocking drugs are unknown. The present study denies those due to inhibition of cardiac function, or renin release from the kidney. A better experimental model is necessary to study this. The possibility that acebutolol and other beta-blockers might accelerate BP elevation and incidence of stroke must be reexamined.
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PMID:Effects of beta-adrenergic blocking drugs in hypertensive rats. 611 Jul 12

Neither stroke volume nor external cardiac work (the integral of pressure times flow during ejection) has been considered an important correlate of myocardial oxygen consumption. An initial set of experiments re-examined this question of independently varying heart rate, systolic blood pressure, and stroke volume in seven closed-chest, anesthetized dogs. This was achieved by cardiac pacing, a pressure control reservoir, phenylephrine infusion, and adjustment of arteriovenous shunts. Propranolol was used to minimize changes in contractility which might affect myocardial oxygen consumption. Stroke volume in the form of external work had a significant effect on oxygen consumption. From these results, a new pressure-work index of myocardial oxygen consumption was devised, and fitting parameters for the following indexes were determined: systolic pressure-rate product, estimated wall tension, external left ventricular work, triple product, mean pressure-rate product, Et (Bretschneider), and tension-time index. These indexes were prospectively applied to a second set of experiments in 11 closed-chest, anesthetized dogs given norepinephrine, isoproterenol, dobutamine, Nembutal, and propranolol to alter myocardial contractility. Inotropic oxygen wasting was observed with the tension-time, mean pressure-rate, triple product, and estimated wall tension indexes, but not with the pressure-work or systolic pressure-rate indexes. It is concluded that stroke work is an important correlate of myocardial oxygen consumption, and that the pressure-work of systolic pressure-rate indexes can account for catecholamine-induced, changes in myocardial oxygen consumption without postulating an oxygen-wasting effect.
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PMID:Work as a correlate of canine left ventricular oxygen consumption, and the problem of catecholamine oxygen wasting. 612 48

In propranolol-pretreated dogs (2 mg . kg -1) the immediate cardiovascular effects of sufentanil (0.01 mg . kg -1) or morphine (4 mg . kg -1) were compared. Besides a 40% decrease in cardiac index (CI), sufentanil and morphine initiated quite different hemodynamic changes. Sufentanil did not significantly change mean arterial pressure (MAP), central venous pressure (CVP) and mean pulmonary artery pressure (MPAP), while the pulmonary capillary wedge pressure (PCWP) increased by 50%. After morphine, MAP declined significantly by about 65%, and significant decreases in MPAP (14%) and PCWP (33%) were also observed. Propranolol reduced heart rate by 16%, and morphine caused no further reduction in HR. A significant decrease of about 30% was seen in HR after sufentanil. Sufentanil significantly raised systemic vascular resistance index (SVRI) by 15%, whereas morphine decreased it by 32%. Pulmonary vascular resistance index (PVRI) was unchanged after sufentanil, but significantly increased after morphine. Right ventricular stroke work index (RVSWI) was unaffected by both analgesics, and morphine decreased left ventricular work index (LVSWI) significantly by 80%. Oxygen transport index declined significantly after both analgesics. Sufentanil reduced oxygen consumption by 20%, while morphine left this parameter unaffected. We conclude that the administration of high-dose sufentanil leads to a stable circulation, even when a total beta-blockade exists.
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PMID:High-dose analgesic anesthesia with morphine or sufentanil in propranolol-treated dogs. 612 28

The effects of 90 min intravenous histamine (10 micrograms base . kg-1 . min-1) with and without beta (propranolol)-receptor blockade on lung water and hemodynamics were studied. In anesthetized dogs cold 3% saline was used as the indicator to determine cardiac index, central blood volume, and lung extravascular thermal volume. Propranolol alone decreased stroke volume and cardiac index but increased central blood volume, total peripheral resistance, and mean pulmonary arterial and pulmonary arterial wedge pressures. Pulmonary vascular resistance, mean arterial pressure, and lung extravascular thermal volume were not changed. Histamine with propranolol further reduced stroke volume and cardiac index, whereas mean pulmonary arterial and pulmonary arterial wedge pressures returned to control values. Mean arterial pressure, central blood volume, and total peripheral resistance decreased, pulmonary vascular resistance increased, and lung extravascular thermal volume remained unchanged. In all experiments postmortem extravascular lung water-to-dry weight ratio was unchanged. We conclude that histamine does not increase lung water content and that beta-receptor blockade does not modify this response.
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PMID:Effects of histamine on lung water and hemodynamics after beta-blockade. 613 42

In two identical experiments, A and B, we studied the effect of the simultaneous l.v. injection of propranolol (Inderal, 0.5 mg/kg) on the circulatory effects of triiodothyronine (T3 500 microgram/kg i.v. 3 hours before measuring). The two substances act at different rates and so the blocking effect of propranolol preceded the development of the circulatory effects of T3. Cardiac output was measured by the Evans blue dilution method, the heart rate was calculated from the ECG recording and blood pressure was measured with a mercury manometer; stroke volume and total peripheral vascular resistance were also calculated. The isolated injection of T3 was followed by a significant increase in cardiac output (experiment A: 129%, B: 118%) and stroke volume (A: 125%, B: 118%) and by a drop in total peripheral vascular resistance (A: 82%, B: 85%). There was no change, in this early phase, in the heart rate or blood pressure. No changes were found 3 hours after the isolated administration of Inderal (the maximum effect of propranolol is attained in 30-60 min). During the same period, the above initial effects of T3 were completely suppressed by the simultaneous injection of Inderal. These results were probably related to the experimental conditions (early and not very marked changes after T3), but they demonstrate that the initial effects of T3 on cardiac performance and on the peripheral blood vessels can be completely suppressed by a block of beta receptors. From this it can be concluded that beta-adrenergic regulation is an important part of the mechanism of the early haemodynamic action of T3.
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PMID:Inhibition of the early circulatory effects of triiodothyronine in rats by propranolol. 645 55

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.
Stroke
PMID:Treatment of acute focal cerebral ischemia with propranolol. 672 77


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