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Biomedical subjects

R Pedrinelli

Publications and source records attributed to R Pedrinelli.

133 records · Page 8Linked to original sources
PubMedDate not supplied

Naloxone does not modify the hemodynamic and neuroendocrine effects of clonidine in normal humans.

The relationship between central opioidergic and noradrenergic central control mechanisms of blood pressure was investigated in normal men by evaluating the interference exerted by naloxone, a specific opiate antagonist, on the cardiovascular (blood pressure and heart rate) and neuroendocrine [human growth hormone (HGH) stimulation] effects of clonidine, a centrally acting alpha-adrenergic agonist, according to two different protocols. In series 1, the effects of placebo (normal saline), clonidine (0.15 mg i.v.), and naloxone (0.4 mg i.v.) were compared with that of clonidine plus naloxone (0.15 and 0.4 mg i.v., respectively), in seven normal male subjects. Clonidine decreased blood pressure and heart rate, and increased HGH levels. Naloxone administered alone (0.4 mg i.v.) did not modify blood pressure, heart rate, and HGH levels, while naloxone (0.4 mg) pretreatment left unaltered the hemodynamic and neuroendocrine effects of clonidine. In series 2, in five additional normal males, the effect of increasing doses of naloxone (0.4, 2.0, and 8.0 mg i.v.) on the pharmacodynamic activity of clonidine (0.15 mg i.v.) was further evaluated. Clonidine alone decreased blood pressure and heart rate and increased HGH levels, while naloxone pretreatment, in the whole range of doses studied, did not significantly modify the action of clonidine. These data suggest that a central opioidergic tone does not modulate the effect of central alpha-noradrenergic stimulation in normal humans.

Adolescent↗
PubMedDate not supplied

Transcutaneous oxygen and carbon dioxide during treatment of critical limb ischemia with iloprost, a prostacyclin derivative.

The effect of intravenous iloprost treatment (median rate: 1.6; range 1-2 ng/kg/min; 6 h daily over 4 weeks) on transcutaneous pO2 and pCO2 was studied in 8 patients with bilateral peripheral obstructive arterial disease and monolateral critical limb ischemia. Tensiometric determinations were obtained at both metatarsi in the supine and dependent position. In critically ischemic limbs, supine transcutaneous p)2 changed erratically during iloprost treatment, increasing in only three out of eight lower limbs. At variance with its inconsistent behavior in the supine position, dependent pO2 increased during drug administration (p<0.02). Transcutaneous pCO2 was unchanged by iloprost. In the contralateral, non-symptomatic limb, both supine and dependent pO2 values were increased by the drug, suggesting that systemic hemodynamic changes may participate in its effect on transcutaneous gas tension, even at infusion rates clinically titrated to avoid evident changes in blood pressure and heart rate.

Aged↗
PubMedDate not supplied

Hemodynamic and humoral interactions between captopril and nifedipine.

Nine patients with uncomplicated essential hypertension received, according to a randomized sequence, captopril (25 mg three times daily), nifedipine (10 mg three times daily), and both drugs for 1 week, with each treatment period separated by a 1-week interval during which a placebo was given. Captopril significantly reduced blood pressure and plasma aldosterone, increased plasma renin activity (PRA), and did not change heart rate. Nifedipine exerted a similar effect on blood pressure and PRA, but it increased heart rate and did not change aldosterone. Captopril plus nifedipine further reduced blood pressure and increased PRA, did not change heart rate, and reduced aldosterone to values similar to those after captopril alone. The hypotensive effect of captopril was highly predictable by basal PRA values, and that of nifedipine by age, while PRA increments induced by captopril were unrelated to those induced by nifedipine. These data indicate that: 1) captopril and nifedipine exert an additive effect on blood pressure and renin; 2) captopril counteracts the heart rate increase induced by nifedipine; 3) nifedipine does not influence the aldosterone inhibition induced by captopril. It is suggested that the association of the two drugs can be usefully employed in the treatment of hypertension.

Adult↗
PubMedDate not supplied

[Pressor, renal and endocrine effects of systemic infusion of L-arginine in hypertensive patients].

In this study we compared the pressor, renal and endocrine effects of the physiological precursor of endothelial derived nitric oxide, L-arginine, with D-glucose, a substrate inactive on nitric oxide. Ten subjects with mild to moderate primary hypertension underwent infusion with either L-arginine (5 patients) or D-glucose (5 patients). The substances were infused over 25 min at equiosmolar rates, preceded and followed by a 25-min saline infusion. Blood pressure (BP) and heart rate were monitored at 3-min intervals; hormonal and humoral variables, inulin and para-aminohippurate clearance, and electrolyte excretion were measured at the end of each period at maximum diuresis. L-arginine and D-glucose brought about comparable increases in serum osmolality and similar hemodilution as compared with control saline. During L-arginine infusion, systolic and diastolic BP dropped by 16.6% and 11% respectively and recovered during the post-infusion period. Heart rate, plasma renin activity, and plasma norepinephrine did not change significantly. The percent BP decrease induced by L-arginine was significantly greater than that caused by D-glucose. Glomerular filtration rate remained stable, and renal plasma flow increased with both substances. However, only L-arginine stimulated markedly natriuresis, kaliuresis, and chloruresis. It also seemed to induce systemic acidosis, possibly as a consequence of hydrochloric acid generated during its metabolism. Circulating insulin, atrial natriuretic peptide, growth hormone, and glucagon levels increased, and plasma aldosterone remained unchanged during L-arginine infusion. During D-glucose infusion, insulin was stimulated and the other hormones were inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗