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The adrenoceptor-mediated responses in human skin (blanching and erythema) were studied by an iontophoretic technique. It is concluded that the receptors in superficial dermal blood vessels belong to the subclasses alpha 1 and beta 2.
The effect of hormonal interactions on human erythroid colony growth has been studied using the beta adrenergic agonist, isoproterenol. The growth of colonies derived from both erythroid burst-forming cells (BFU-E) and erythroid colony-forming cells (CFU-E) was enhanced in the presence of isoproterenol. While isoproterenol was effective at all concentrations of erythropoietin (Ep) in cultures of marrow cells, an increase in BFU-E-derived colonies in peripheral blood cultures could be detected only at suboptimal levels of Ep concentrations. The isoproterenol effect was blocked by an agent with beta 2 receptor specificity (butoxamine), and L-isomeric configuration (L-propranolol). The stimulatory effect appeared to be mediated by a receptor different from that for Ep or for phytohaemagglutinin-stimulated leucocyte conditioned medium. Circulating BFU-E from eight patients with polycythaemia vera were also studied. Those colonies which grew in the absence of added Ep increased with isoproterenol; in cultures from normal subjects and in patients with secondary erythrocytosis, agonist stimulation was seen only in the presence of Ep. These studies provide evidence that the growth of both normal and neoplastic erythroid progenitors may be modulated by hormonal interactions.
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Prenalterol was given to twenty five patients with acute myocardial infarction. Thirteen patients (group B) had signs of cardiac decompensation while twelve (group A) had not. Ejection fraction was determined with 99mTc-labelled red blood cells before and after prenalterol (50 micrograms kg-1 body weight), intravenously. In group B this procedure was repeated after digitalization 2 days later. The ejection fraction increased significantly in group A after prenalterol injection. In group B, prenalterol produced an increase, but this was not significant. After digitalis the ejection fraction increased significantly and prenalterol produced an additional significant rise. No significant changes in blood pressure occurred. Heart rate increased significantly in both groups after prenalterol injection and decreased significantly after digitalis.
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beta-Adrenoceptor stimulating agents possess anti-allergic effects in vitro and in vivo. To study the mechanism of action further we compared in 10 atopic subjects the effects on allergen-induced cutaneous reactions of intradermally (i.d.) injected prenalterol (1-10 microgram) terbutaline (2.5-250 ng) and KWD 2131 (100 ng-2.5 microgram), i.e. compounds with preferential actions on beta 1-, beta 2-adrenoceptors and on beta-adrenoceptors not fitting this classification. All injections were given according to a double-blind design. Terbutaline and KWD 2131 produced a dose-dependent inhibition of the skin reactions induced by injecting horse dander allergen 5 min later. Terbutaline was about 20 times as potent as KWD 2131 whereas prenalterol was inactive. Propranolol fully blocked the anti-allergic effect produced by terbutaline. The results suggest that the cutaneous anti-allergic effect of beta-adrenoceptor-stimulating drugs is mediated via activation of beta 2-adrenoceptors, possibly on the mast cell, resulting in inhibition of mediator release.
The hemodynamic effects of prenalterol, a new inotropic agent, were investigated in 10 patients with gram negative septic shock. In four of the patients, coronary sinus blood flow (CSF) and myocardial oxygen and lactate extraction were also determined. After baseline hemodynamic measurements, prenalterol was infused intravenously over a 10-min period to a total dose of 150 micrograms/kg. All patients responded within 15 min after completion of prenalterol infusion by increasing mean arterial pressure from 57 +/- 11 to 75 +/- 20 mmHg (7.58 +/- 46 to 9.97 +/- 2.66 kPa), (+32%), (P less than 0.01) and cardiac index from 2.65 +/- 0.40 to 3.80 +/- 0.47 1.min-1.m-2, (+44%) (P less than 0.001). There was no change in heart rate or systemic vascular resistance, nor were any arrhythmias recorded. The urinary output increased significantly. After prenalterol, CSF increased from 185 +/- 14 to 246 +/- 14 ml.min-1, (+33%), (P less than 0.001) and myocardial oxygen and lactate extraction rose from 19.8 +/- 2.1 to 26.6 +/- 2.1 ml O2.min-1, (+34%) (P less than 0.001) and from 33.2 +/- 2.3 to 44.7 +/- 2.1 mumol.min-1, (+35%), (P less than 0.001), respectively. The total body oxygen consumption increased from 287 +/- 13 to 348 +/- 23 ml O2.min-1, (+21%), (P less than 0.01) and the arterial lactate concentration decreased from 5.61+/- 0.55 to 3.94 +/- 0.16 mmol.l-1, (-30%), (P less than 0.01), suggesting improved tissue perfusion. The results demonstrate that prenalterol is a potent, highly selective inotropic agent inducing the same magnitude of increase in blood pressure and cardiac output as reported for dopamine in septic shock.
A patient undergoing prostatectomy under epidural analgesia developed clinical signs of a severe TURP syndrome. During resuscitation, it was revealed that serum sodium was only moderately decreased. Plasma oncotic pressure was, however, markedly decreased and the pressure gradient between plasma oncotic pressure and pulmonary capillary wedge pressure (approximately hydrostatic pressure) was 1 mmHg (0.13 kPa) only, allowing almost free filtration of fluid through the pulmonary capillary wall, resulting in a non-cardiogenic pulmonary edema. The patient was successfully resuscitated with albumin and inotropic stimulation with prenalterol.
Five patients with acute myocardial infarction and shock were treated with a new, highly selective beta-1-adrenoreceptor agonist, prenalterol. After 1 and 2 mg of the drug, all patients had markedly increased blood pressure and cardiac output, but no changes in heart rate or systemic vascular resistance. Left- and right-sided filling pressures decreased in three of the patients. In two of the patients, however, the increase in contractility and afterload was followed by a marked increase in left- and right-sided filling pressures, and myocardial lactate uptake changes to lactate production. After addition of sodium nitroprusside, blood pressure and filling pressures returned towards normal, and myocardial lactate uptake was restored. As anticipated from the hemodyanamic findings, myocardial oxygen consumption increased after prenalterol. It is suggested that the potent inotropic agent prenalterol may be used with great caution in cardiogenic shock.
The haemodynamic effects of prenalterol and dopamine were compared in 10 patients about 4 h after cardiac valve replacement during a phase of temporarily depressed myocardial function. The rate of infusion was adjusted to give similar increases in stroke volume with the two drugs (dopamine + 17% and prenalterol + 18%). Both drugs produced marked inotropic and chronotropic effects with significant increases in heart rate, cardiac output, arterial blood pressure, and left and right ventricular stroke work. The arterial blood pressure and the left ventricular stroke work increased significantly more with dopamine than with prenalterol, however. The systemic vascular resistance decreased significantly with prenalterol, whereas it was unchanged with dopamine. The effects of prenalterol could be traced after 90 min, whereas the effects of dopamine vanished within 15 min.
The effects of prenalterol infusion, 0.5 microgram/kg/min, on renal function were studied in 10 male volunteers. Systolic blood pressure increased by 22 mmHg (P less than 0.01) and diastolic pressure decreased by 11 mmHg (P less than 0.01). Heart rate increased by 11 beats/min (P less than 0.01). Plasma catecholamine levels and plasma renin activity were not altered. Renal haemodynamics were unchanged. Urine flow rate and fractional free water excretion decreased by 29% and 45%, respectively (P less than 0.01). Fractional sodium excretion increased by 19% (P less than 0.01) and fractional potassium excretion fell by 33% (P less than 0.05).
The effects of intravenous injection of prenalterol, a selective beta 1-adrenoceptor agonist, on central haemodynamics and the distribution of ventilation-perfusion (VA/Q) were assessed in eight patients after aortic and/or mitral valve replacement. VA/Q distributions were determined by the multiple inert gas elimination technique. Administration of prenalterol resulted in a significant increase in cardiac output and heart rate with no changes in mean pulmonary arterial pressure and wedge pressure. There was an insignificant fall in arterial oxygen tension from 14.3 to 12.4 kPa, accompanied by a significant increase in the inert gas shunt from 6.4 to 11.3% of cardiac output, while the configuration of the distribution of perfusion and ventilation on VA/Q remained unchanged. The increase in shunt was probably more an effect of the increase in cardiac output than a direct effect of the drug on the pulmonary vascular bed.
High lumbar epidural block was induced in seven dogs, causing a fall in mean arterial blood pressure (AP) from 24.5 +/- 2.9 to 12.0 +/- 3.1 kPa owing to reductions in cardiac output (QT) and systemic vascular resistance (SVR) to 67% and 68% of the pre-epidural values. Volume loading with dextran 10 ml X kg-1 b.w. increased QT nearly to the pre-epidural value. SVR decreased further to 61% of the pre-epidural value and AP was only slightly increased to 14.9 +/- 2.7 kPa. Subsequent administration of prenalterol 20 micrograms X kg-1 b.w. caused a further increase in QT to 17% above the pre-epidural value due to an increase in heart rate of 51 beats/min. AP did not change since SVR decreased further to 49% of the pre-epidural value. The hepatic arterial blood flow (QHA) was essentially unchanged during epidural block as well as during volume loading, while the portal venous blood flow (Qpv) was changed concurrently with (QT). In spite of the decrease in SVR, the preportal and hepatic arterial vascular resistances were not diminished following prenalterol. The increase in OT must therefore have favoured other vascular beds. Hepatic and pre-portal tissue oxygen uptakes were unchanged during the experimental procedure, while whole-body oxygen uptake decreased by 20% following the epidural block and increased nearly to the pre-epidural level following volume loading in combination with prenalterol.
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The haemodynamic effects of prenalterol, a new sympathomimetic agent, have been studied in anaesthetized open-chest pigs with acute myocardial ischaemia provoked by left anterior descending coronary artery ligation. A group of eight animals was infused with saline and served as control (C). In both groups the ligation of the left anterior descending coronary artery determined a significant (P less than 0.05) reduction of aortic flow, maximum left ventricular (LV) dp/dt with no changes in heart rate. The infusion of a first dose of 30 micrograms/kg of prenalterol restored the depressed haemodynamics but increased significantly the heart rate in the prenalterol group while the saline infused group did not show any significant changes. The haemodynamic effects of prenalterol were still evident 25 min after the infusion. The subsequent administration of a second dose of 60 micrograms/kg of prenalterol resulted in a further improvement of the aortic flow, LV dp/dt and heart rate which reached values higher than in the basal condition. The positive inotropic effect was not associated with changes in stroke volume, therefore the increase in aortic flow was essentially due to an increase of the heart rate. It is concluded that prenalterol is a powerful inotropic agent in acutely infarcted animals. Its action on aortic flow appears to be related to an increase in heart rate in contrast to some previous observations.