Peak Mean Arterial Pressure Research Articles

Neurocirculatory Regulation in Cortisol-Induced Hypertension

Effects of chronic glucocorticoid treatment on arterial baroreflex function and on cardiac beta- and vascular alpha-adrenoceptor-mediated responses were assessed in conscious, unrestrained Wistar-Kyoto rats. Cortisol (25 mg/kg/day) was administered for seven days using a subcutaneous reservoir pump. Arterial baroreflex-cardiac sensitivity was assessed by examining the relationship of the cardiac interbeat interval to the mean arterial blood pressure during phenylephrine or nitroprusside challenge; baroreflex-sympathoneural sensitivity was assessed from the ratio of the increase in the arterial norepinephrine concentration to the decrease in mean arterial pressure at 15 min during intravenous infusion of nitroprusside; cardiac beta-adrenoceptor-mediated responsiveness was estimated from heart rate responses to bolus-injected isoproterenol; and vascular alpha-adrenoceptor-mediated responsiveness was estimated from peak mean arterial pressure responses to bolus-injected phenylephrine. Cortisol treatment increased mean arterial pressure, decreased heart rate, and increased heart rate responses to isoproterenol, whereas baroreflex-vagal sensitivity, baroreflex-sympathoneural sensitivity, and pressor responses to phenylephrine were unaffected. The results indicate that hypertension due to chronic cortisol administration is not associated with decreased sensitivity of the baroreceptor-cardiac reflex. Baroreflex-sympathoneural sensitivity and alpha 1-adrenoceptor responsiveness also remain normal, whereas beta-adrenoceptor responsiveness is increased. The findings suggest that the pattern of neurocirculatory adjustment in glucocorticoid hypertension differs from that seen in other forms of hypertension.

Validation of Doppler-derived pulmonary arterial pressure in patients with ductus arteriosus under different hemodynamic states.

Twenty-nine patients with a patent ductus arteriosus (PDA) in isolation (n = 17) or in combination with other lesions (n = 12) underwent simultaneous hemodynamic assessment and evaluation of PDA flow velocity by the Doppler method. The accuracy with which Doppler velocity across the PDA predicted pulmonary arterial pressure and the influence of PDA size and shape on the Doppler velocity-pressure relationship were examined. Seventy percent had a cone-shaped PDA (narrowest at the pulmonary artery end), and the remainder were tubular. Narrowest PDA diameter ranged from 1.5 to 9 mm (mean 3.5 mm). Peak systolic and mean pulmonary arterial pressure ranged from 10 to 116 and 8 to 72 mm Hg, respectively. Twenty-one patients (group 1) had left-to-right shunting only. The following variables showed significant correlation in this group: peak instantaneous systolic aortic-to-main pulmonary arterial (MPA) pressure gradient and maximum Doppler velocity across the PDA (slope = 1.03, SEE = 13 mm Hg, r = .94, p less than .001), mean aortic-to-MPA pressure gradient and mean Doppler velocity (slope = 1.06, SEE = 10 mm Hg, r = .95, p less than .001), and end diastolic aortic-to-MPA pressure gradient and minimum Doppler velocity (slope = 1.12, SEE = 8 mm Hg, r = .96, p less than .001). Eight patients (group 2) had bidirectional shunting. In this group peak instantaneous aortic-to-MPA pressure gradient significantly correlated with maximum Doppler velocity measured from the left-to-right shunt (slope = .70, SEE = 2 mm Hg, r = .92, p less than .002) and mean pressure gradient correlated with mean Doppler velocity (slope = .83, SEE = 3 mm Hg, r = .78, p less than .003). Right-to-left Doppler velocities showed no correlation with pressures. In six patients with pulmonary hypertension Doppler velocity changes accurately predicted the effect of pulmonary vasodilation on pulmonary arterial pressure. Doppler velocity of PDA flow reliably predicts pulmonary arterial pressure over a wide range of pressures and PDA shapes and sizes.

Systemic hemodynamic effects of leukotrienes C4 and D4 in the rat.

Although local administration of the sulfidopeptide leukotrienes into cutaneous and coronary vascular beds indicates that these naturally occurring metabolites of arachidonic acid are vasoconstrictors, their systemic administration has produced both pressor and depressor responses. The systemic hemodynamic effects of intravenous leukotriene C4 (LTC4) and leukotriene D4 (LTD4) were assessed in ether-anesthetized rats and compared with the effects produced by equimolar doses (2 X 10(-10) to 4 X 10(-8) mol/kg) of norepinephrine and angiotensin. Mean arterial pressure, right atrial pressure, and cardiac output (electromagnetic flowmetry) were recorded during bolus administrations of these vasoactive compounds. LTC4 and LTD4 had similar hemodynamic effects that were characterized by moderate pressure elevations produced by dose-dependent increases in total peripheral resistance, since cardiac output declined. Although the peak mean arterial pressure levels produced by LTC4 and LTD4 (135 +/- 7 and 129 +/- 5 mmHg, respectively) were less than those by norepinephrine (157 +/- 3 mmHg) and angiotensin (174 +/- 5 mmHg), the peak total peripheral resistance values of LTC4 and LTD4 (2.23 +/- 0.32 and 1.86 +/- 0.17 mmHg X ml-1 X min-1, respectively) were between those of the well-known vasopressors, norepinephrine (1.50 +/- 0.09) and angiotensin (2.72 +/- 0.41). The pressor response to LTC4 and LTD4 was less marked than that to norepinephrine and to angiotensin because of the concomitant reduction in cardiac output. These results indicate that LTC4 and LTD4 are systemic vasoconstrictors with potencies similar to those of norepinephrine and angiotensin.

Hemodynamic differences between supine and upright exercise in patients with congestive heart failure.

Although the differences in hemodynamic responses to supine and upright exercise have been studied in normal subjects and in patients with angina pectoris, no such comparison has been made in patients with congestive heart failure. Many investigators measure exercise hemodynamics in heart failure patients to assess the effect of vasodilator and inotropic drugs. Both modes of exercise have been used and have often yielded differing results. We compared the hemodynamic response to supine and upright exercise in 14 patients with stable, New York Heart Association class III chronic heart failure. During upright exercise, peak heart rate was higher (124 +/- 15 vs 115 +/- 18 beats/min, p less than 0.025) and peak mean arterial pressure was lower (102 +/- 15 vs 95 +/- 17 mm Hg, p less than 0.25), yielding similar double products. Although the peak left ventricular filling pressure was slightly lower during upright exercise (40 +/- 7 vs 35 +/- 10 mm Hg, p less than 0.05), the maximum cardiac and stroke indexes were not significantly different (3.6 +/- 0.8 vs 3.4 +/- 0.8 l/min/m2 and 30 +/- 8 vs 30 +/- 6 ml/m2, upright vs supine exercise). In contrast to these relatively similar hemodynamic responses, exercise capacity was significantly greater during upright exercise (peak work load 336 +/- 84 vs 293 +/- 73 kpm/min, p less than 0.1; maximum oxygen consumption 12.1 +/- 2.4 vs 9.8 +/- 1.9 ml/min/kg, p less than 0.001). We conclude that either exercise method may be used to assess the hemodynamic effects of drugs, but that exercise capacity should be measured in the upright position.

Cerebral and extracerebral blood volume in generalized seizures in the baboon Papio papio

Relative variations of the cerebral and extracerebral blood volume (CBV) were measured continuously by a novel atraumatic method in baboons to explore the relationship between changes in the systemic circulation and in the cerebral (and extracerebral) vascular responses, before, during and after generalized seizures induced by photic stimulation. Major bursts of generalized spikes and waves are accompanied by an increase of the mean arterial pressure and of the cerebral blood volume and a decrease of the nasal blood volume. During the seizure discharge a substantial increase in CBV occurs, associated with a dramatic increase in arterial pressure. However, the greatest increase in CBV occurs after the peak mean arterial pressure. The results show that the CBV does not passively follow the blood pressure and demonstrate the dramatic responsiveness of the nasal region to seizure discharge.