Hg Decrease In Systolic Pressure Research Articles

Is the hypotension of cirrhosis a GABA-mediated process?

Systolic and diastolic blood pressures were recorded in 176 ambulant patients with chronic liver disease, including 36 patients with compensated cirrhosis (Group I), 119 patients with noncirrhotic chronic liver disease (Group II) and 21 patients with benign structural or functional liver disease (Group III). Group I patients had significantly lower systolic (113.0 +/- 2.2 mm Hg, mean +/- S.E.) and diastolic (65.3 +/- 1.7 mm Hg) pressures than Group II patients (125.8 +/- 3.5 and 76.6 +/- 1.5 mm Hg, respectively (p less than 0.0001) or Group III patients (125.1 +/- 3.4 and 77.5 +/- 2.4 mm Hg, respectively) (p less than 0.0001). Serum levels of GABA, a potent amino acid neurotransmitter with known vasodilatory effects in vitro, were higher in Group I patients (1.12 +/- 0.26 microM, mean +/- S.E.) than in Group II patients (0.41 +/- 0.05 microM) (p less than 0.005) or Group III patients (0.34 +/- 0.03 mM) (p less than 0.05). A constant infusion of GABA into the systemic circulation of six adult dogs, at rates required to achieve serum GABA levels within one order of magnitude of those observed in humans with cirrhosis, resulted in a 17.0 +/- 4.3 mm Hg decrease in systolic pressure (p less than 0.05) and a 10.8 +/- 3.7 mm Hg decrease in diastolic pressure (p less than 0.05). Control amino acids were not vasoactive. The results of this study suggest that, in addition to other vasoactive compounds, a GABA-mediated process might contribute to the hypotension observed in patients with compensated cirrhosis.

Effects of nicardipine on left ventricular function and energetics in man

The effects of nicardipine, a new dihydropyridine calcium antagonist, on left ventricular function and energetics were studied in 13 patients. Nicardipine was administered as a 2 mg bolus (i.v.) followed by an infusion titrated to maintain a 10–20 mm Hg decrease in systolic pressure. Nicardipine increased heart rate 19% ( P < 0.001) while left ventricular end-diastolic pressure was not significantly changed and stroke volume (ml) increased 13% ( P < 0.01). Peak values for the first and second time derivatives of left ventricular pressure were increased by 26% ( P < 0.01) and 50% ( P < 0.02) respectively. Peak aortic blood flow, peak aortic blood acceleration, and the peak rate of change of ejection power were increased 86% ( P < 0.001), 123% ( P < 0.01), and 113% ( P < 0.001), respectively. Stroke work was not changed during nicardipine infusion. External power increased by 40% ( P < 0.01); however, the ratio of oscillatory to total power was not significantly different. Although the product of heart rate and systolic aortic pressure was not significantly altered with nicardipine, myocardial oxygen consumption increased 18% ( P < 0.02) with a disproportionate increase in coronary blood flow of 41% ( P < 0.001) and decrease in coronary resistance of 39% ( P < 0.001). The time constant for left ventricular isovolumic relation decreased 22% ( P < 0.001) during nicardipine infusion while the minimum value of dP dt was unchanged. Thus, when administered intravenously in man, nicardipine is a potent coronary and systemic vasodilator producing reflex tachycardia, increased indices of myocardial contractile state, and improved isovolumic relaxation with an associated increase in myocardial oxygen consumption.

Effects on blood pressure of calcium supplementation of women

The relationship between dietary and supplemental (1.5 g/d) calcium intake and blood pressure was examined in 81 normotensive and 34 medicated hypertensive women between the ages of 35 and 65 years who completed a 4-yr clinical trial to assess age-associated bone loss in women. Calcium intakes were monitored during the entire study. Resting blood pressures and systolic blood pressure response (SBPR) to a stress test were recorded three times during the study. At the end of the study there was no relationship between systolic or diastolic blood pressure or SBPR and total calcium intake in normotensive women (n = 81). In the medicated hypertensive group (n = 34) there was a 13 mm Hg decrease in systolic pressure of supplemented women (n = 18) and a 7 mm Hg increase in unsupplemented women (n = 16) over the 4 yr (p less than .02).

Coronary and systemic hemodynamic effects of nicardipine

Systemic and coronary hemodynamic effects of a new dihydropyridine calcium antagonist, nicardipine, were studied in 15 patients. Nicardipine was administered as a 2-mg bolus intravenously followed by an infusion titrated to maintain a 10 to 20-mm Hg decrease in systolic pressure. Nicardipine increased both heart rate from 69 ± 3 to 81 ± 3 beats/min and cardiac output from 7.3 ± 0.5 to 9.9 ± 0.5 liters/min (both p < 0.001) as systemic vascular resistance decreased from 1,183 ± 70 to 733 ± 33 dynes s cm −5 (p < 0.001). Left ventricular end-diastolic pressure remained constant, at 14 ± 1 vs 14 ± 1 mm Hg as stroke volume increased from 108 ± 6 to 123 ± 6 ml/m 2 (p < 0.001). Coronary blood flow increased from 102 ± 9 to 147 ± 13 ml/min, while coronary resistance decreased from 1.17 ± 0.1 to 0.7 ± 0.1 mm Hg/ml/min (both p < 0.001). Heart rate-systolic blood pressure product did not change (104 ± 5 vs 106 ± 5 beats/min mm Hg × 10 −2, difference not significant) with drug administration. At the same heart rate before and during nicardipine administration (using atrial pacing in 6 patients), significant augmentation of coronary flow was still observed. Thirteen of 14 patients showed a greater percent decrease in coronary resistance than systemic vascular resistance. Nicardipine differs from other calcium antagonists with respect to consistent augmentation of coronary blood flow. This effect appears to be the result, in part, of increased potency in the coronary bed compared with the systemic vascular bed.