Biomedical subjects

R Seitelberger

Publications and source records attributed to R Seitelberger.

At least 55 records · Page 3Linked to original sources

PubMed1988

Early diastolic filling dynamics during experimental mitral regurgitation in the conscious dog.

Diastolic flow into the left ventricle during mitral regurgitation must increase as total stroke volume increases in response to the volume overload. The mechanisms that allow augmented diastolic filling are not fully defined. Accordingly, the left ventricle of five dogs was instrumented with a micromanometer and sonomicrometers and studied during the conscious state before (control) and after the creation of significant mitral regurgitation. Serial measurements were made at control and up to 4 weeks after the creation of the volume overload. Heart rate, peak systolic wall stress, and peak positive dP/dt showed no significant changes between control and subsequent observations. End-diastolic volume and total stroke volume progressively and significantly increased during the 4-week course. When compared with the control state (51 +/- 4, mean +/- SD), the filling fraction during the first 40% of diastolic time was increased at 4 days (67 +/- 10%, p less than 0.001), 2 weeks (72 +/- 6%, p less than 0.001), and 4 weeks (76 +/- 10%, p less than 0.001). During the period of adaptation to the volume overload, filling fraction correlated with end-diastolic volume (r = 0.52, p less than 0.02) and total stroke volume (r = 0.80, p less than 0.001). Compared with the control state (0.81 +/- 0.04), eccentricity of the left ventricle at end systole decreased at 4 weeks (0.79 +/- 0.06, p less than 0.05); the absolute change in this ratio during the first 40% of diastolic time was significantly augmented at 2 weeks (0.09 +/- 0.02, p less than 0.05) and 4 weeks (0.11 +/- 0.04, p less than 0.005) compared with control (0.05 +/- 0.02). Ventricular elastance (pressure/volume) at end systole (minimum volume) was 1.70 +/- 0.50 mm Hg/ml at control, 1.09 +/- 0.46 at 4 days (p less than 0.05), 0.96 +/- 0.42 at 2 weeks (p less than 0.01), and 0.99 +/- 0.22 at 4 weeks (p less than 0.01). Moreover, the elastance change during the rapid-filling phase was significantly diminished after creation of mitral regurgitation. Thus, during the volume overload of mitral regurgitation, the left ventricle accommodates a higher percentage of its total stroke volume during early diastole; this adaptation can be correlated with augmented systolic shortening, and thereby with increased restorative forces or elastic recoil, and with reduced chamber elastance and eccentricity during the early part of diastole. Other potential mechanisms include altered systolic and relaxation loading, augmented elastic recoil of the left atrium, left atrium and left ventricular pressure gradient, accelerated myocardial inactivation, and increased adrenergic stimulation.

Animals↗

PubMed1988

Intracoronary alpha 2-adrenergic receptor blockade attenuates ischemia in conscious dogs during exercise.

Studies on the role of alpha-adrenergic constrictor tone in the coronary vascular bed during ischemia were performed in dogs running on a treadmill. The animals were instrumented with a left ventricular pressure transducer, and regional systolic wall thickening (%WTh) was assessed by sonomicrometry in the anterior and posterior walls of the left ventricle. An intracoronary catheter was implanted chronically in the circumflex coronary artery, and a hydraulic cuff was placed proximally around the artery. After beta-adrenergic blockade with propranolol (0.8 mg/kg i.v.), acute stenosis of the coronary artery was performed during running in five dogs to induce severe regional myocardial dysfunction in the posterior wall. Intracoronary infusion of the selective alpha 2-adrenergic blocking agent idazoxan (80 micrograms/kg) improved %WTh in the ischemic region from 5.1 +/- 1.6 to 10.8 +/- 2.8% (p less than 0.05), without any significant effect on the anterior wall. Blood flow to the subendocardium of the posterior wall (radioactive microspheres) increased from 0.17 +/- 0.05 to 0.45 +/- 0.30 (ml/min)/g (p less than 0.05). It is concluded that in exercising dogs subjected to beta-adrenergic blockade, significant postjunctional alpha 2-adrenergic receptor-mediated coronary vasoconstriction exists, even during severe ischemia. Regional alpha 2-adrenergic receptor blockade can reduce regional ischemia and improve contractile function by attenuating exercise-induced sympathetic vasoconstriction in this conscious animal model.

Adrenergic alpha-Antagonists↗

PubMed1988

Temporal Fourier transform of digital angiograms for left ventricular regional wall motion analysis.

To determine whether or not the first harmonic of a temporal Fourier transform, applied pixel-by-pixel on time-intensity curves, can detect the subtle wall motion abnormalities due to ischemia, 6 dogs were instrumented with a micromanometer in the left ventricles, a hydraulic cuff occluder around the circumflex coronary artery, and sonomicrometers on the inferior (ischemic) and anterior (non-ischemic) walls. Left ventricular images, obtained after contrast injection via the pulmonary artery, were compared with dimension signals in control and 3 progressive levels of coronary stenosis (Stenosis I, II and III). Normalized, digital functional images (512 x 512 matrix, 256 shades of gray/pixel) were divided into anterior, apical, and inferior areas to acquire regional mean phase (degrees) and amplitude (intensity units) values. After inducing stenosis, phase in ischemic region significantly increased at all 3 levels of stenosis, whereas amplitude significantly decreased at Stenosis II and III. However, amplitude images showed clearly the topographic site of ischemia. There was a progressive increase in phase and decrease in amplitude in ischemic areas as the percent wall thickening (%WTh) fell (phase vs. %WTh: r = -0.55, p less than 0.005; amplitude vs. %WTh: r = 0.71, p less than 0.001). Heart rate and peak systolic pressure showed no significant changes during stenosis. We conclude that quantitative functional images, generated from a temporal Fourier transform, are sensitive to the detection of left ventricular regional wall motion abnormalities during mild, moderate, and severe degrees of ischemia.

Animals↗

PubMed1987

Role of heart rate reduction in the treatment of exercise-induced myocardial ischaemia.

The role of bradycardia in reducing exercise-induced ischaemia and wall dysfunction was examined in dogs with single vessel chronic coronary artery stenosis created using an ameroid constrictor. Treadmill exercise produced significant regional myocardial ischaemia (blood flow measured using microspheres) and contractile dysfunction (systolic wall thickening measured with sonomicrometers). Dogs were initially studied during a control run before and during a second identical run after administration of the cardioselective beta-adrenergic blocker atenolol, which improved regional ischaemic function from 4.4 +/- 3.7% to 8.5 +/- 2.8% and subendocardial perfusion from 0.43 +/- 0.23 to 0.55 +/- 0.29 ml min-1 g-1. In another group of dogs during a run with atenolol, the heart rate was paced to match the rate observed in the control run. During the atenolol run with pacing, all beneficial effects of atenolol observed at the reduced exercise heart rate were lost. A third group of dogs received the bradycardic agent UL-FS 49 (1.0 mg kg-1, i.v.) prior to exercise. UL-FS 49 produced a heart rate reduction during exercise from 230 +/- 19 to 139 +/- 10 beats min-1; this was associated with an increase in systolic wall thickening from 9.3 +/- 5.0% (during the control run) to 21.5 +/- 8.4%, thereby eliminating the exercise-induced contractile dysfunction. Transmural myocardial blood flow per beat to the poststenotic myocardium was improved significantly from 4.8 X 10(-3) +/- 1.9 X 10(-3) ml beat-1 to 9.8 X 10(-3) +/- 1.7 X 10(-3). Atrial pacing to match heart rate to the control exercise rate during the UL-FS 49 run did not eliminate all of the improvement in systolic wall thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Contractile responses to sympathetic activation after coronary instrumentation.

The consequences of acute coronary dissection and chronic coronary instrumentation on contractile responses to sympathetic activation were examined in dogs. Stimulation of the left ventrolateral cervical cardiac nerve in seven anesthetized dogs after acute dissection of the left circumflex coronary artery (CX) did not change the increase in systolic shortening velocity. After acute dissection of the left anterior descending coronary artery (LAD), nerve stimulation increased shortening velocity of the posterior wall in all dogs but enhanced that of the anterior wall in only five dogs. In six conscious dogs with chronic instrumentation of the CX, reflex sympathetic activation induced by occlusion of the inferior vena cava comparably increased thickening velocities of both the anterior wall and posterior walls both at 1 and 3 wk after instrumentation. In six other dogs with chronic instrumentation of the LAD, responses to caval occlusion were nonuniform and correlated to the morphological degree of sympathetic denervation. Therefore, acute dissection and chronic instrumentation of the LAD may produce sympathetic denervation but do not cause functionally significant sympathetic denervation of the CX region.

Animals↗

PubMed1987

Attenuation of exercise-induced myocardial ischemia in dogs with recruitment of coronary vasodilator reserve by nifedipine.

There is now evidence that under resting conditions coronary vasodilator reserve exists even in the presence of myocardial ischemia. Therefore, we tested the hypothesis that a vasodilator reserve may exist during exercise so that during exercise-induced ischemia a reduction in coronary constrictor tone can be produced that attenuates the decreases in regional myocardial blood flow and function distal to a severe coronary stenosis without changing the determinants of myocardial oxygen demand. Nine dogs were instrumented with an ameroid constrictor on the left circumflex coronary artery and were studied 2 to 3 weeks later. During a control treadmill run, heart rate increased from 119 +/- 20 to 225 +/- 20 beats/min and peak left ventricular pressure increased from 144 +/- 17 to 163 +/- 28 mm Hg. Poststenotic subendocardial blood flow (measured by a microsphere technique) fell from 1.19 +/- 0.36 to 0.51 +/- 0.30 ml/min X g and systolic wall thickening (by sonomicrometry) decreased from 24.3 +/- 5.8% to 6.0 +/- 6.1%. During an identical run after nifedipine (10 micrograms/kg iv), systemic hemodynamics were not significantly altered. However, subendocardial blood flow was increased to 0.85 +/- 0.51 ml/min X g (p less than .05) and systolic wall thickening to 11.4 +/- 7.8% (p less than .01). We conclude that in this study the amelioration of exercise-induced myocardial ischemia was due to the recruitment by nifedipine of coronary vasodilator reserve.

Animals↗

PubMed1987

Elimination of exercise-induced regional myocardial dysfunction by a bradycardiac agent in dogs with chronic coronary stenosis.

We have previously demonstrated that the beneficial effect of cardioselective beta-blockade on exercise-induced ischemia is due entirely to negative chronotropism. Therefore we studied the effect of a new bradycardiac agent (UL-FS 49) in 10 dogs with chronic coronary artery stenosis produced by an ameroid constrictor. Regional myocardial function (sonomicrometers, wall thickness) and blood flow (microspheres) were measured during a control treadmill exercise bout and an identical run 3 hr later after the administration of UL-FS 49 (1.0 mg/kg iv). In the control run, heart rate increased from 114 +/- 20 to 230 +/- 19 beats/min and systolic wall thickening (%WT) in the poststenotic myocardium decreased from 23.3 +/- 5.2% at rest to 9.3 +/- 5.0%, a 60% reduction. Subendocardial blood flow in the ischemic area decreased from 1.04 +/- 0.30 to 0.55 +/- 0.40 ml/min/g, blood flow per beat decreased from 9.1 X 10(-3) to 2.5 X 10(-3) ml/g, and mean transmural flow failed to increase (1.06 +/- 0.30 vs 1.08 +/- 0.39 ml/min/g). During exercise with UL-FS 49, heart rate increased from 89 +/- 10 to only 139 +/- 10 beats/min. End-diastolic left ventricular pressure was increased compared with that during the control run (35.7 +/- 3.0 vs 28.9 +/- 5.5 mm Hg) but left ventricular peak systolic pressure and dP/dt were unchanged. %WT in the ischemic zone did not change significantly during exercise with UL-FS 49 (23.3 +/- 7.9% at rest, 21.5 +/- 8.4% during the run), and in the nonischemic zone it increased to the same extent as during the control run.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Mechanism of beneficial effect of beta-adrenergic blockade on exercise-induced myocardial ischemia in conscious dogs.

We examined the importance of decreased heart rate in the beneficial effect of beta-adrenergic blockade on exercise-induced regional myocardial ischemia and contractile dysfunction in conscious dogs with single vessel coronary stenosis (ameroid constrictor). Studies were performed during control treadmill exercise, which produced regional myocardial ischemia (blood flow measured with microspheres) and wall dysfunction (measured using sonomicrometers). A second run was performed after the administration of atenolol (0.3-1.0 mg/kg i.v.), and the reduced heart rate caused by atenolol during early steady-state running was then prevented by atrial pacing during the latter portion of the run. Atenolol reduced the exercise heart rate from 217 +/- 25 beats per minute (SD, n = 9) to 166 +/- 15, and ischemic zone wall thickening during systole improved from 27 +/- 22% of the resting value in the control run to 50 +/- 25% of the resting value in the atenolol run (p less than 0.01). Atrial pacing then increased heart rate to 217 +/- 23 beats per minute, and regional wall thickening deteriorated to 15 +/- 25% of the resting value. Regional subendocardial blood flow in the ischemic zone during atrial pacing with atenolol was slightly less than that observed in the control run, in both ischemic and control zones, indicating no remaining beneficial effect of atenolol when heart rate reduction was eliminated. We conclude that the only significant mechanism for the improvement in exercise-induced ischemia and wall motion produced by atenolol is a reduction in the exercise heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Scanning electron microscopy of circulating platelets reveals new aspects of platelet alteration during cardiopulmonary bypass operations.

Seventeen male patients undergoing cardiopulmonary bypass (CPBP) surgery for aorto-coronary bypass grafting were investigated by scanning electron microscopy (SEM) for alterations of the surface morphology of circulating platelets. An initial decline in the percentage of unactivated smooth discocytes (SD) to 87 +/- 12% was found after thoracotomy. Three minutes after the onset of CPBP, the percentage of SD had dropped drastically to 59 +/- 13%, and by the 8th minute of CPBP it had dropped to its lowest point (49 +/- 19%). On the other hand, the percentage of shape-changed platelets (SC) increased to 17 +/- 9% after 3 minutes, and the percentage of pseudopod discocytes (PD) to 25 +/- 13% after 8 minutes. Surprisingly, a remarkable recovery of platelet morphology could be observed after even 15 minutes of CPBP, and by the end of bypass 78 +/- 15% of the circulating platelets had regained the smooth discoid (SD) appearance of unactivated platelets. We conclude that this recovery of platelet morphology is due to an increasing insensitivity of the platelets to activating stimuli during the course of CPBP. Our study provides evidence that the only major platelet activation occurs during the first minutes of CPBP, and that CPBP-caused platelet activation is much less pronounced than generally believed.

Journal Article↗

PubMed1986

Experimental exercise-induced ischemia: drug therapy can eliminate regional dysfunction and oxygen supply-demand imbalance.

The purpose of this study was to test the hypothesis that moderately severe exercise-induced regional myocardial ischemia can be prevented by combined pharmacologic intervention. Eight chronically instrumented dogs were studied using an ameroid constrictor to produce critical stenosis of the left circumflex coronary artery. The dogs were studied during steady state treadmill exercise that induced regional myocardial dysfunction (reduced systolic wall thickening; sonomicrometers) and ischemia (reduced subendocardial blood flow; microspheres). During a control exercise run, wall thickening in the ischemic posterior wall decreased from 21.4 to 13.3% whereas subendocardial blood flow failed to increase normally (36% of that in the normal zone). In the control anterior wall, both wall thickening and subendocardial blood flow increased significantly during the control run. Wall thickness-left ventricular pressure loop areas were calculated as an index of regional work; this index increased abruptly with the onset of exercise in both regions but became significantly depressed in the ischemic region during the steady state exercise. Therapy with a combination of atenolol (0.3 mg/kg body weight orally), diltiazem (0.3 mg/kg intravenously) and isosorbide dinitrate (2.0 mg/kg orally) effectively prevented regional myocardial ischemia and regional dysfunction. After drug therapy, wall thickening in the posterior wall increased from 17.3% at rest to 18.8% during exercise, and the regional transmural blood flow pattern was markedly improved. The initial overshoot of the regional work index during exercise was blunted by the drug therapy, and at steady state no differences between the ischemic and control regions were detected. Thus, combined drug therapy can eliminate exercise-induced regional myocardial ischemic dysfunction and appears to normalize the oxygen supply-demand imbalance.

Adrenergic beta-Antagonists↗

PubMed1986

Exercise-induced regional dysfunction with subcritical coronary stenosis.

The hypothesis was tested that regional myocardial contractile dysfunction can detect subtle regional coronary blood flow maldistribution induced by exercise. In seven dogs, left ventricular pressure (micromanometer), regional systolic wall thickening (WTh, sonomicrometry), and myocardial blood flow (MBF, microspheres) were measured when mild degrees of coronary artery stenosis were produced during treadmill exercise. During exercise without coronary stenosis, WTh increased by 21 +/- 12% (SD), and transmural MBF increased uniformly. In each dog, two levels of coronary stenosis were produced during exercise by adjusting the coronary hydraulic cuff: (1) St-Ex I, where WTh during exercise failed to increase significantly (average change 0 +/- 7%), and (2) St-Ex II, where WTh during exercise decreased moderately from the resting control value (average -20 +/- 8%). In the potentially ischemic zone coronary hyperemia occurred with each run: resting subendocardial MBF was 1.09 +/- 0.30 mg/g/min, and it was 3.04 +/- 0.83 during control exercise, 2.48 +/- 0.75 during St-Ex I, and 1.55 +/- 0.59 ml/g/min during St-Ex II (p less than .01 compared with control exercise and control area). The subendocardial-subepicardial blood flow ratio fell from 1.32 +/- 0.27 during control exercise to 1.07 +/- 0.20 (p less than .05) during St-Ex I, and to 0.64 +/- 0.15 (p less than .01) with St-Ex II. Changes in the subendocardial electrogram and reactive hyperemia occurred more consistently during St-Ex II than St-Ex I. Thus, failure of regional function to increase during exercise detected slight maldistribution of regional MBF, whereas reduction of regional function during exercise of 10% or more below the resting value was a reliable marker of a regional flow defect and was always associated with other evidence of ischemia. Therefore, regional dysfunction during exercise can detect subcritical but functionally significant coronary stenosis, which may allow regional wall motion to be used for detecting coronary artery disease at a relatively early stage.

Animals↗

PubMed1984

Evidence against the adenosine-catecholamine antagonism under in vivo conditions.

Experiments were carried out in anaesthetized, thoracotomized dogs. The dose dependent positive inotropic and chronotropic effects of intracoronary (i.cor.) infusions or bolus injections of isoproterenol (ISO) were neither antagonized by adenosine (0.46, 1.0, and 2.91 x 10(-5) mol/l) nor by the adenosine analogue N6-phenylisopropyl-adenosine (PIA, 3.23 x 10(-7) mol/l). The results indicate, that adenosine and PIA do not have any antagonistic effects on isoproterenol induced positive inotropy and chronotropy in the intact dog heart. Consequently it can be assumed that an adenosine-catecholamine antagonism is of no physiological relevance.

Adenosine↗

PubMed1984

Effects of indomethacin on changes in renal blood flow induced by adenosine and its analogues in conscious dogs.

The effects of indomethacin on changes in renal blood flow induced by adenosine, NECA (adenosine-5'-N-ethyl-carboxamide) and 2',3'-dinitro-NECA were investigated in 6 chronically instrumented conscious dogs. Adenosine (187.5, 375 and 750 nmol/kg, i.v.) induced a dose-dependent initial decrease, followed by a reactive increase in renal blood flow. NECA (1.5 nmol/kg, i.v.) also induced an initial decrease, which was, however, followed by a prolonged reactive increase in renal blood flow. 2',3'-dinitro-NECA (50 nmol/kg, orally) induced only an increase in renal blood flow. Indomethacin (27.9 mumol/kg, i.v.) caused no relevant change of the initial decrease and a significant attenuation of the reactive increase in renal blood flow induced by adenosine. NECA-induced changes in blood flow were affected by indomethacin in the same direction but to a greater extent than were adenosine-induced changes in blood flow. Indomethacin reversed the increase to a decrease in renal blood flow induced by 2',3'-dinitro-NECA. Thus, prostaglandins seem to be involved in mediating the response of renal blood flow to adenosine, NECA and 2',3'-dinitro-NECA.

Adenosine↗

PubMed1984

A canine model of transient myocardial dysfunction regional shortening in the presence of critical stenosis and cardiac stimulation.

An experimental model of exercise-induced angina pectoris was developed in anesthetized dogs. Two i.v. bolus injections of isoproterenol (ISO, 0.25 microgram/kg; time interval: 10 min) were administered, followed by constriction of the circumflex coronary artery (LCX; critical stenosis). Further i.v. bolus injections of ISO were administered before and after i.v. infusion of 0.9% NaCl (control infusion). Stenosis of the LCX did not modify regional function at rest as assessed with ultrasonic crystals implanted subendocardially both in the distribution areas of the circumflex coronary artery and of the left anterior descending coronary artery (LAD). In the presence of critical stenosis, ISO induced a reproducible, transient decrease in systolic shortening and percent systolic shortening in the area supplied by the LCX and a marked increase in systolic shortening and percent systolic shortening in the area supplied by the LAD. During a 60-min observation period following control infusion, no further substantial changes in regional dimensions were observed. The ISO-induced hemodynamic changes were reproducible during this period. The experimental model of exercise-induced angina pectoris presented in this study can be assumed to provide a reliable basis for evaluating the efficacy of various therapeutical interventions.

Anesthesia↗

PubMed1984

Blood pressure response and renin release following 4 days of treatment with dihydralazine and urapidil in conscious dogs.

The magnitude and the persistence of blood pressure reduction by dihydralazine and urapidil were investigated following treatment over a period of 4 days. The experiments were performed on six normotensive dogs, trained to submit to puncture of the femoral artery and to stand quietly in a special frame. The first-dose effects of orally administered dihydralazine (1.42, 7.1 mg X kg-1) and urapidil (2.0, 10.0 mg X kg-1) on heart rate, arterial blood pressure and plasma renin activity (PRA) were compared with the effects of the substances after 4 days of treatment. Both compounds caused a dose-dependent decrease in blood pressure but in contrast to urapidil the effect of dihydralazine was accompanied by large increases in heart rate and PRA. Dose-dependent tolerance to dihydralazine but not to urapidil was observed after treatment over only 4 days. However, basal blood pressure was significantly lowered after 4 days of treatment with urapidil at the high dosage and no further reduction was achieved on the fifth day. The importance of persistent counterregulation in the development of tolerance to the antihypertensive effect of dihydralazine is discussed.

Animals↗

PubMedDate not supplied

Dihydroergotoxine, an ergot alkaloid without marked hypotensive effect, improves blood flow and metabolism in the underperfused canine myocardium.

Regional myocardial blood flow was assessed in 6 anaesthetized dogs using radiolabelled microspheres. Lactate, H+, and O2 content were measured in arterial and local venous blood, obtained from the area supplied by the circumflex branch of the left coronary artery (LCX). Constriction of LCX by 67% led to considerable hemodynamic changes indicative of depressed global myocardial function. A significant release of lactate from the underperfused part of the left ventricle was recorded. Infusion of 0.7 micrograms/kg dihydroergotoxine over a period of 5 min induced a decrease in heart rate, left ventricular dp/dt max, and cardiac output, a sustained increase in total peripheral and femoral resistance and a transient increase in mean arterial blood pressure. Dihydroergotoxine markedly reduced lactate release and even, in some cases, induced lactate uptake and led to a significant increase in the endocardial blood flow both in the underperfused and normally perfused left ventricle. It is concluded that dihydroergotoxine, due to its ability to reduce myocardial oxygen demand and owing to its alpha-sympatholytic activity, which is not accompanied by any marked decrease in arterial blood pressure, causes improvement in blood flow in the underperfused myocardium and a marked amelioration of the impaired metabolic processes.

Animals↗

PubMedDate not supplied

Effects of dihydroergotamine (DHE) on blood flow and metabolism in the underperfused myocardium in anaesthetized dogs.

The study was carried out in 13 mongrel dogs. Regional myocardial blood flow was measured using radiolabelled microspheres. Lactate, H+-ions, and O2 content were measured in arterial and local venous blood. Partial occlusion of the ramus circumflexus (LCX) led to a decrease in left ventricular dp/dt max, systemic arterial pressure, and a marked release of lactate from the underperfused myocardium. With DHE (2 micrograms/kg infused within 5 min, 8 dogs), a slight decrease in heart rate, left ventricular dp/dt max, LCX-resistance and a small increase in femoral and total peripheral resistance as well as in arterial and left and right atrial pressure was observed. In the normally perfused and in the underperfused part of the left ventricle microsphere assessed blood flow was unchanged or slightly elevated with DHE. Lactate release from the underperfused myocardium was markedly reduced. None of the DHE-induced effects on hemodynamic and metabolic parameters were observed in control experiments with infusion of 0.9% NaCl (5 ml). The results indicate that DHE leads to an amelioration of impaired metabolism in the underperfused myocardium and exerts no vasoconstriction in this area.

Animals↗

PubMedDate not supplied

The influence of repeated administration of prazosin on its hypotensive effect and on renin release in conscious dogs. A comparison with urapidil.

The effects of prazosin (0.1, 0.5 and 2.5 mg/kg, orally) on blood pressure, heart rate and PRA were investigated after acute and chronic administration in conscious, normotensive dogs. The acute administration of prazosin caused a reduction in both systolic and diastolic blood pressure and an increase in heart rate and PRA. After chronic administration, twice daily for four days, tolerance developed, which was not due to persistent counterregulation. On comparison with urapidil, another alpha-adrenoceptor antagonist, the hypotensive and counterregulatory response to acute administration were similar with both substances; the development of tolerance to prazosin after chronic administration contrasted with the results with urapidil.

Antihypertensive Agents↗