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PubMed1983

Can right ventricular performance be assessed by equilibrium radionuclide ventriculography?

Although right ventricular function may be examined by following the passage (first pass) of a bolus of radionuclide through the right heart before it reaches the left heart, the counts detected with conventional gamma cameras in such a short time interval are low; moreover, repeated determinations would result in an unacceptable radiation burden to the patient. We have modified the gated equilibrium blood pool method to allow repeated assessment of the right ventricular ejection fraction (RVEF) and have compared the results with the first-pass method in 43 patients. Good agreement was obtained between the two methods (r = 0.91, p less than 0.001). The mean difference between the two methods was 0.04 with an intra-observer variation for the equilibrium studies of 0.03 and an inter-observer difference of 0.04. The mean difference in RVEF for seven patients studied on two separate occasions 30 minutes apart was only 0.02. In four patients the mean RVEF measured at rest was 0.44 +/- 0.05 (SEM) and after exercise it was 0.48 +/- 0.06. After infusion of isoprenaline at 1 microgram/min the mean rose to 0.64 +/- 0.04 (p less than 0.02) and after infusion of a new beta 1-sympathomimetic agent, prenalterol, at doses of 1 and 2 mg it was 0.56 +/- 0.02 (p less than 0.02) and 0.59 +/- 0.03 (p less than 0.01) respectively, where the significance levels are relative to the resting values. In nine patients with good ventricular function the vasodilator nifedipine caused right and left ventricular ejection fractions to increase by the same amount; while in six patients with severe impairment of left ventricular function due to ischaemic heart disease the RVEF increased from 0.58 +/- 0.03 to 0.73 +/- 0.03 (p less than 0.01) after 2 mg of prenalterol, but the left ventricular ejection fraction increased only from 0.22 +/- 0.04 to 0.26 +/- 0.04. We conclude that repeated estimation of right ventricular performance is possible by equilibrium radionuclide ventriculography.

Adrenergic beta-Agonists↗
PubMed1982

Effects of inotropic agents on arterial resistance and venous compliance in anesthetized dogs.

Systemic vascular effects of dopamine, dobutamine, and prenalterol were studied in 45 anesthetized open-chest dogs. Blood flow (Q) and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant Q showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. Dopamine (2.5-10 micrograms X kg-1 X min-1) was the most active drug with dose-related increases in heart rate 6-19%, arterial pressure (Pa) 3-36%, and venous compliance 2-25%. Small doses of dopamine (2.5 and 5 micrograms X kg-1 X min-1) reduced arterial resistance of the slow time-constant compartment increasing Q distribution to that compartment 21-42%, whereas larger doses increased both arterial resistance and venous compliance in that compartment. Arterial resistance in the fast time-constant compartment increased with all doses of dopamine. Dobutamine (2.5-10 micrograms X kg-1 X min-1) modestly increased heart rate 2-11% and Pa 9-12% without altering Q distribution demonstrating a relatively flat dose response. Dobutamine 2.5-5 micrograms X kg-1 X min-1 increased venous compliance 5-10% while 10 micrograms X kg-1 X min-1 had no effect or decreased compliance of both compartments. Prenalterol 3 micrograms X kg-1 X min-1 increased Pa 9% primarily by increasing arterial resistance in the fast time-constant compartment without altering heart rate or blood flow distribution. Doses of prenalterol 10-100 times greater caused dose-dependent reductions in Pa and vascular compliance. In this animal model of the circulation with a fixed cardiac output, dopamine had the greatest effect on the peripheral vasculature and chronotropy.

Animals↗
PubMed1982

beta 1- and beta 2-adrenoceptor agonists have different effects on rat parotid acinar cells.

To determine whether beta 1- and beta 2-adrenoceptors have similar functions in salivary glands, Sprague-Dawley rats were chronically treated with either the beta 1-selective (prenalterol), beta 2-selective (terbutaline), or the nonselective beta-agonist isoproterenol. All three agonists increased parotid and submandibular gland weight and acinar cell size. Isoproterenol and prenalterol caused marked quantitative and qualitative alterations in the granule population, whereas terbutaline had no effect. A single injection of isoproterenol caused a significant amylase release and accumulation of cAMP. Prenalterol was as potent as isoproterenol with regard to amylase release but was without effect on the cAMP content. In contrast, terbutaline had a minimal effect on amylase release but had the same effect as isoproterenol on cAMP accumulation. The in vitro perifusion experiments confirmed these in vivo results with respect to the effects of the selective beta-agonists. Thus, the present investigation using both morphological and biochemical methods suggests that beta 1- and beta 2-adrenoceptors may have different functions in rat parotid acinar cells. In addition, the stimulus-growth coupling seems to be unrelated to stimulus-secretion coupling.

Adrenergic beta-Agonists↗
PubMed1977

Cardiac function and metabolism during cholinergic stimulation in the newborn lamb.

This study was designed to assess the influences of cholinergic stimulation on coronary flow (CF), oxygen metabolism (MVO2) and contractility (MC) of the left ventricle in the newborn. Nineteen lambs, 1-7 days of age, were anesthetized with pentobarbital (20 mg/kg) and prepared for continuous measurement of CF, heart rate (HR), aortic (AP) and left ventricular end-diastolic (LVEDP) pressures, dP/dt max, and cardiac output (CO). HR, AP, and CO could be controlled as desired. Simultaneous arterial and sinus blood samples were analyzed for O2 content, hematocrit, pH, PO2, and PCO2. LV MVO2 and %O2 extraction (Ext) were calculated. Acetylcholine (ACh) infusion (30-50 microgram/min-kg) caused an increase of LVEDP (4 cmH2O), but no significant change in dP/dt max or HR with constant AP and CO. CF increased by 44%, but MVO2 per beat was unchanged. Similar changes were observed with constant HR (pace). Suramaximal efferent stimulation of right or left vagus nerves produced bradycardia (77-68 beats/min) but no significant changes in contractility, CF, Ext, or MVO2. These findings were unaltered by beta blockade. The changes elicited by ACh infusion or vagal stimulation were abolished by giving atropine. It is concluded that although cholinergic sensitivity can be demonstrated, vagal stimulation does not importantly influence MC, CF, or MVO2 in the lamb. This may relate to incomplete development of the adrenergic system.

Acetylcholine↗
PubMed1980

Blood pressure, plasma catecholamines, and sympathetic outflow in pithed SHR and WKY rats.

After destruction, by pithing, of the central nervous system, the blood pressure (BP) of the spontaneously hypertensive (SHR) rat falls, but remains higher than in the pithed normotensive (WKY) rat. At all ages examined, stimulation of the sympathetic outflow evoked greater increases in BP of pithed SHR rats, but the increases in plasma catecholamines were similar in the two strains. The BP increase evoked by administered norepinephrine was greater in old SHR than in old WKY rats, but this increased response was not found in young animals. Both young and old SHR rats, however, were more sensitive than WKY rats to the pressor effects of epinephrine. Results of selective pharmacologic blockade of cardiac or vascular beta-adrenoceptors suggest that a smaller vasodilator response in young SHR rats to the beta-adrenergic effects of epinephrine is responsible for the greater pressor response than in WKY rats. This factor diminishes in older SHR rats in which, as suggested by Folkow, structural changes in the resistance blood vessel diameter may account for the enhanced pressor responsivity of SHR rats.

Animals↗
PubMed1985

Chronic infarction decreases maximum cardiac work and sensitivity of heart to extracellular calcium.

Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery to cause an initial 40% loss of viable tissue by weight. Due to compensatory hypertrophy of the surviving myocardium and progression of the infarct to scar tissue, the infarct represented approximately 25% by weight of the whole heart after 1 wk. After 1 or 3 wk, these infarcted hearts were removed and perfused in vitro by the working hearts technique. Ventricular pressure development and positive dP/dt were lower in infarcted hearts compared with sham-operated ones. O2 consumption and glucose utilization by viable tissue per unit pressure development was the same in normal and infarcted hearts. Levels of creatine phosphate and free creatine were decreased, but ATP and total adenine nucleotides were well maintained. The inotropic response to decreases in extracellular [Ca2+] was much greater in infarcted hearts than in sham controls. Prenalterol increased ventricular function proportionally more in infarcted than in the sham-operated hearts, suggesting that down regulation of beta receptors was not a problem. The infarcted hearts were much more sensitive to verapamil than control hearts. It is concluded that the depressed function of the noninfarcted tissue of chronically infarcted hearts is due in part to loss of functioning tissue mass and in part to decreased sensitivity to extracellular Ca2+.

Adenosine Triphosphate↗
PubMed1975

Nonsustained pulmonary vasoconstriction during acute hypoxia in anesthetized dogs.

The objectives of this study were to describe in greater detail the initial rise and spontaneous decline in acute hypoxic pulmonary vasoconstriction and to investigate a number of mechanisms that could have caused this secondary vasodilation. With the onset of isocapnic hypoxia (Pao2 of 28, 44, or 56 mmHg), pulmonary vascular resistances increased to maximum values at 3 min and then spontaneously declined toward control values. Pulmonary perfusion pressures rose to maxima at approximately 4 min and then also declined. During severe hypoxic exposures (Pao2 of 30-37 mmHg) this secondary vasodilation was found not to be due to beta-adrenergic-induced vasodilation, withdrawal of alpha-adrenergic-induced vasoconstriction, vasodilation caused by a sustained increase in pulmonary blood flow, fatigue of the vascular smooth muscle contractile mechanism, or release of vasodilatory prostaglandins. It is suggested that the decline in hypoxic pulmonary vasoconstriction may be due to an exhaustion of a chemical mediator, release of a pulmonary vasodilator agent, or myogenic stress relaxation.

Animals↗
PubMed1975

Analysis of coronary vascular beta receptors in situ.

Observations were conducted in the isolated potassium-arrested dog heart to determine the direct vasodilator effects of adrenergic agonists and antagonists on the coronaryvascular beta receptors, independent of cardiac inotropic and chronotropic influences. Practocol (a selective beta-1-receptor antagonist) blocked coronary vasodilation activated by isoproternol (a combined beta-1-and beta-2-receptor agonist) only at the very high dose of 10-minus 3 M, whereas propranolol (a combined beta-1- and beta-2-receptor antagonist) blocked coronary vasodilation at 10-minus 7 to 10-minus 5 M. Salbutamol (a selective beta-2-receptor agonist) was one-eighth as potent as isoproterenol in producing coronary vasodilation. The potency ratio (1/8) is similiar to valuesreported for other beta receptors classified as type 2. It is concluded that the coronary vasodilator beta receptors are type 2, similiar to those found in peripheral bloodvessels.

Albuterol↗
PubMed1976

Erythropoietin production after renal denervation or beta-adrenergic blockade.

The ability of either beta-adrenergic blockade or bilateral renal denervation to alter erythropoietin (ESF) production in rabbits exposed to hypobaric hypoxia was studied. ESF elaboration during 5 h of exposure to hypoxia was not affected by beta-blockade, but was markedly reduced by prior surgical denervation of both kidneys. After 18 h of hypoxia plasma ESF levels in renal denervated rabbits did not differ significantly from those of sham-operated controls. Previous studies have shown that ESF production during this more prolonged exposure to hypoxia was significantly inhibited by some beta-adrenergic blocking agents. Combined renal denervation and beta-blockade were more effective than renal denervation alone in attenuating ESF production during 5 h of exposure to hypoxia. However, ESF elaboration during 18 h of hypoxia was significantly greater in animals with combined denervation and beta-blockade than in control rabbits. These results suggest the existence of two distinct mechanisms for ESF production in rabbits exposed to hypobaric hypoxia.

Adrenergic beta-Antagonists↗
PubMed1992

Preoptic norepinephrine-induced hypothermia is mediated by alpha 2-adrenoceptors.

We have shown previously that norepinephrine (NE) microdialyzed into the preoptic area of conscious guinea pigs evokes a fall in core temperature (Tco) that is mediated by a reduction in metabolic rate. To identify the adrenoceptor subtype(s) involved in this effect, we microdialyzed intrapreoptically various adrenergic agonists or antagonists singly or in combinations. Tco and ear skin temperatures of the animals were monitored throughout the experiments. alpha 1-, beta-, beta 1-, and beta 2-agonists and antagonists did not induce significant Tco changes. Although the alpha 2-antagonists yohimbine (Yoh) and rauwolscine (Rau) did not have thermal effects per se, the alpha 2-agonist clonidine evoked dose-dependent Tco falls that were abolished by codialyzed Yoh and Rau. The microdialysis of NE evoked, as before, a 0.7 +/- 0.2 degrees C Tco fall; it was abolished by the codialyzed alpha-antagonist phentolamine, Yoh, and Rau but not by the beta-antagonist propranolol. No adrenoceptor agonist induced changes in ear skin temperature. These results indicate that the hypothermizing effect of intrapreoptically microdialyzed NE is achieved by a reduction in metabolic heat production, mediated by alpha 2-adrenoceptors.

Animals↗
PubMed1984

Regional myocardial contractile response to the beta-adrenergic stimulant prenalterol in the conscious dog following myocardial infarction. Mechanism of hemodynamic effect.

In order to assess regional myocardial contractile responses to the beta-adrenergic stimulant prenalterol after recent myocardial infarction, 9 male mongrel dogs underwent left circumflex coronary artery (LCX) occlusion after implantation of miniature subendocardial sonomicrometer crystals in normal, marginally ischemic (border) and central ischemic zones. 90-min LCX occlusion with reperfusion resulted in substantial infarction (mean +/- SEM 24 +/- 3% of total left ventricular area) and characteristic regional functional alterations. In conscious, unsedated animals 72 h after infarction, intravenous prenalterol (30 micrograms/kg) significantly decreased end-diastolic and end-systolic segment length and increased percent systolic shortening in normal and border zones, but did not alter ischemic zone function. Heart rate increased significantly with prenalterol. Regional myocardial function before drug administration correlated closely with response to the inotropic agent. These results indicate that the mechanism by which prenalterol improves cardiac function 72 h after myocardial infarction is stimulation of normal and marginally ischemic myocardium.

Animals↗
PubMed1977

Exercise testing and indirect assessment of myocardial oxygen consumption in evaluation of angina pectoris.

Exercise testing is an important means of evaluating the patient with angina pectoris, providing objective data not available from conventional clinical assessment. In utilizing exercise to determine functional impairment in angina, it is essential to distinguish between external stress, or the load on the skeletal muscles, and internal or cardiac stress. Evaluation of external exercise capacity alone is limited as a measure of cardiac peformance since the relationship between external function and cardiac performance is not necessarily direct. A readily applicable approach to determination of cardiac capacity in angina is afforded by indirect assessment of myocardial oxygen consumption (MVO2). This is achieved through derived indexes utilizing heart rate and blood pressure, two major determinants of MVO2, in the form of the product of heart rate and systolic blood pressure. Although this approach does not encompass all the major determinants of MVO2, changes in the heart rate-blood pressure product bear a close correlation to alterations in directly measured MVO2. Within limits and employed with caution, indirect assessment of MVO2 is useful in elucidating mechanisms of action of extracardiac and intrinsic myocardial factors in the provocation and therapy of angina pectoris.

Angina Pectoris↗
PubMed1977

Peripheral blood lymphocytes in systemic lupus erythematosus. Relation to activity.

Peripheral blood lymphocytes from 20 patients with systemic lupus erythematosus (SLE), 3 patients with drug-induced lupus and 20 normal controls were studied. The absolute number of E-rosette-forming cells (ERFC) and surface immunoglobulin-bearing cells were determined during active and inactive stages of the disease. An attempt was made to establish the relationship between the number of ERFC and the clinical stages of the disease on one hand and treatment on the other. A decrease in ERFC was observed in all SLE patients, but it was most prominent in patients with active disease. No correlation was found between treatment and the decreased numbers of ERFC.

Humans↗