Effects of captopril on hemodynamics and blood gases in chronic obstructive lung disease with pulmonary hypertension.

The effects of Captopril, an angiotensin-converting enzyme inhibitor, on pulmonary hemodynamics and blood gases were studied in 9 patients with chronic obstructive lung disease (COLD) and pulmonary hypertension (PA-P greater than 20 mm Hg). Hemodynamic data were recorded prior to Captopril administration (50 mg per os) and for the next 60 min. Following Captopril administration, significant reductions in mean pulmonary artery pressure (PA-P) (p less than 0.05), in mean pulmonary wedge pressure (PW-P) (p less than 0.05), and in total pulmonary resistance (TPR) were noted; significant reductions in mean brachial artery pressure (BA-P) and systemic vascular resistance (SVR) were also recorded, while cardiac output, heart rate and blood gas tensions showed no significant changes. Furthermore, the higher the hypoxemia, the greater was the reduction in BA-P (p less than 0.05). We therefore feel that Captopril, when administered to COLD patients with pulmonary hypertension, may protect the pulmonary circulation from hypoxic pulmonary vasoconstriction.

Influence of ACE inhibition on pulmonary haemodynamics and function in patients in whom beta-blockers are contraindicated.

The effects of captopril have been studied in 19 patients suffering from chronic obstructive pulmonary disease (COPD). In 9 of these patients with pulmonary hypertension (mean pulmonary artery pressure greater than 20 mm Hg), we studied the effects of the drug on pulmonary haemodynamics, blood gases and systemic circulation. Haemodynamic data were recorded before oral captopril 50 mg and for the next 60 minutes. Following captopril administration, significant reductions in mean pulmonary artery pressure (PAP) (P less than 0.05), in mean pulmonary wedge pressure (PWP) (P less than 0.05) and in total pulmonary resistance (TPR) were noted; significant reductions in mean brachial artery pressure (BAP) and systemic vascular resistance (SVR) were also recorded, while cardiac output, heart rate and blood gas tensions showed no significant changes. Furthermore, the higher the hypoxaemia was, the greater the reduction in BAP (P less than 0.05). In the other 10 COPD patients with moderate essential hypertension, captopril was given as monotherapy (75-10 mg/day) for 60 days. We found no significant modification of the various respiratory function tests except for an increase in the vital capacity (P less than 0.05). Systolic blood pressure and diastolic blood pressure were reduced both in the supine and in the standing position and there were no side effects, in particular no bronchospasm even in the patients responsive to bronchodilator drugs. Our data suggest that captopril is an effective and safe drug when administered to COPD patients with essential hypertension. Moreover, in these patients, it may protect the pulmonary circulation from hypoxic pulmonary vasoconstriction.

Treatment of essential hypertension with captopril in patients with chronic obstructive pulmonary disease.

The effects of captopril have been studied in 10 patients suffering from chronic obstructive pulmonary disease (COPD) with moderate essential hypertension. Captopril was given as monotherapy (75-100 mg/day) over a period of 60 days. The following effects of captopril were seen in these patients: a significant reduction of systolic blood pressure (P less than 0.01) and of diastolic blood pressure (P less than 0.001), both in the supine and in the standing position; a significant increase of the vital capacity (P less than 0.05); no significant change in other various respiratory function tests or of heart rate, and no side effects, including bronchospasm in the patients sensitive to bronchodilator drugs. The present data suggest that in COPD patients with essential hypertension, captopril is an effective hypotensive agent and has no adverse effects in pulmonary function.

Sulphinpyrazone dose schedule in hyperuricemic patients with cardiovascular diseases: tolerability assessment.

Renal tolerability of four different dose schedule of sulphinpyrazone (S) was evaluated in a bi-centre, 2-week long open study performed in fifty-six cardiovascular patients of both sexes (47 males, 9 females; mean age 64 yrs) at different risk as regards serum uric acid levels. Each patient was allocated, according to his/her baseline values of serum uric acid or serum creatinine to four different sulphinpyrazone incremental dosage schedules. Renal function and other biochemical assessments (liver function; blood lipids; blood glucose) were assessed at the entry, after the 1st and the 2nd week. Reported signs and symptoms were collected at the 1st and the 2nd week, too. Renal function did not show any statistically and clinically significant impairment during the whole trial. General tolerability, both objective and subjective was particularly good. Only one patient was withdrawn because of reasons unrelated to the ongoing treatment. Sulphinpyrazone can be safely administered also in patients at risk as regards uric acid levels if the proposed therapeutic program is adopted.

Effects of afferent renal nerve stimulation on renal hemodynamic and excretory functions.

In anesthetized cats (n = 9) renal afferent fibers were electrically stimulated for 11 min, and the response of the contralateral innervated kidney was compared with that of the ipsilateral denervated one. Before stimulation, renal blood flow, glomerular filtration rate, and water and sodium excretions were significantly lower in the innervated kidney than in the denervated one. Afferent renal nerve stimulation augmented arterial pressure and also increased sodium and water excretions from both kidneys without concomitant changes in glomerular filtration rates and renal blood flows. Absolute and percent changes in sodium and water excretions from the innervated kidney were similar to those observed in the denervated one. The same results were obtained in cats (n = 4) which underwent bilateral adrenalectomy to avoid the effect of circulating catecholamines. In another group of cats (n = 5), the increase in renal perfusion pressure due to the stimulation was prevented by an aortic snare: this resulted in a slight but equal decrease of all variables in both kidneys. These experiments do not show a reflex control of renal function from renal afferents.

Cryoactivation fails to augment plasma renin activity in the cat.

1. Active and cryoactivated renin (plasma renin) activity after incubation at -5 degrees C for 4 days, were measured in cat plasma sampled before and during the following procedures: suprarenal aortic stenosis, electrical stimulation of the pons and mild hypotensive haemorrhage. 2. Under all experimental conditions the values of plasma renin activity for both the activated and non-activated samples were similar. 3. The absence of a cryoactivatable aliquot of renin suggests that in cat plasma the inactive form of the enzyme either is actually absent or has a liability to the action of cold different than in other animal species.