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Objectives: Self-administered intracavernous injections, notably with alprostadil are currently the most widely used non-psychotherapeutical treatment of erectile dysfunction. We assessed the effectiveness of this treatment after 6 months of self-injections., Methods: Efficacy, acceptability and tolerance to alprostadil self-administered via intracavernous injections for 6 months was evaluated in 144 men, age 24 to 72 years, and followed monthly after an initial training period and search for the optimal dose., Results: The mean number of self-injections was 5.5 at a mean dose of 18.6 micrograms per injection. From the first to sixth month, the frequency of complete erections after self-injection rose from 62% to 77% and failures declined from 8% to 3%. After six months, 40% of the patients had abandoned the treatment including 9% who abandoned during the first month, usually due to poor acceptance and because of cure in two patients (4.5%). Patients reported sexual intercourse after self-injections as satisfactory in 81% of the cases; 66% of their partners reported satisfactory intercourse. Tolerance assessment revealed pain in 14% of the patients and decreasing effect with time in two patients who discontinued self-injections for this reason. Other undesirable side effects were infrequent, usually related to technical injection errors and decreasing effect with time. One case of priapism and two indurations of the cavernous bodies were also observed., Conclusion: Self-administration of intracavernous alprostadil can lead to rigid erection in patients with erectile dysfunction. Patients are generally well satisfied and tolerance is good.

Objectives: To endoscopically evaluate the tolerance of gastroduodenal mucosa to methylprednisolone given orally and intravenously., Methods: Thirty two healthy volunteers (age range 18-39 years) were divided randomly into two groups of 16 each (8 males and 8 females). All were Caucasians, gave their informed consent and were considered normal after a complete clinical and laboratory work-up including gastroduodenal fibroscopy. Methylprednisolone (500 mg) was administered for three consecutive days at 9 a.m., orally in one group and intravenously in the second group. No other drugs were being taken and alcohol and smoking were prohibited from day 0 to day 11. Tolerance was evaluated on days 4 and 11 based on clinical examination, blood pressure, heart rate, oral temperature, body weight, blood and urine chemistry and by video-recorded gastroduodenal endoscopy. Two independent endoscopists, uninformed of the patient's regimen, scored lesions from 0 (normal) to 5 (more than 25 lesions including at least 2 erosions). In case of abnormal findings, follow-up was continued to normalization., Results: Endoscopically detectable lesions (stage I) attributed to corticosteroid therapy were observed in 4 subjects in the oral group and in 5 in the intravenous group. All regressed spontaneously. Duodenal lesions were observed only after oral administration while lesions of gastric mucosa were mostly found after intravenous administration. Systemic effects included abdominal pain after oral intake, 1 case of insomnia and bitter taste in the mouth after intravenous administration., Conclusions: These findings suggest that the effect of corticosteroid therapy, on the gastric mucosa, is basically systemic, and on the duodenal mucosa, basically local. No severe manifestations were observed after high-dose methylprednisolone given orally or by intravenous injection.

A tablet form of nifedipine was given to eight hypertensive hospitalized men (Stage I or II WHO, 45 +/- 10 years old). After an initial placebo test, 20, 40, and 60 mg of nifedipine were given at 8.00 a.m. in random order at 72-hour intervals in a single administration double-blind crossover study. Blood pressure and heart rate were measured twice by the same observer every 20 minutes from 7.00 a.m. to 8.00 a.m. and then hourly until 8.00 p.m., first with the patients recumbent and again after 1 minute of standing. Plasma nifedipine levels were assayed in samples drawn hourly from 8.00 a.m. to noon, every 2 hours from noon to 8.00 p.m., and at 24 and 48 hours after drug ingestion. The three doses all lowered blood pressure significantly. The reduction during recumbency was significantly larger (-18%) and lasted longer (12 hours) after 60 mg than after 20 mg (-11% at 7 hours). The three doses caused similar increases in heart rate (+29% to +38%), the maximum occurring at the second hour and lasting for 5 hours. The peak plasma concentrations and areas under the plasma concentration time curve were dose-dependent; kinetics were linear between 20 and 60 mg, and the half-life of nifedipine tablets was close to 10 hours. The decrease in mean arterial blood pressure correlated strongly with plasma nifedipine levels (r = 0.61; n = 190; p less than 0.001). Four patients experienced mild side effects (headaches, flushes, drowsiness, or weakness). The tablet form of nifedipine had a potent antihypertensive action that lasted longer than that of the capsule formulation.

A tablet formulation of nifedipine was given to 8 hospitalized hypertensive men, W.H.O. stage I or II, mean age 45 years. After an initial placebo test, nifedipine 20, 40 or 60 mg was given in random order at 72-h intervals, in a single administration crossover study. The placebo and the active drug were given at 8 a.m. Blood pressure and heart rate were measured twice by the same observer, every 20 min from 7 to 8 a.m., and then hourly until 8 p.m., first in recumbency and again after 1 min of standing upright. Plasma nifedipine was assayed in samples taken hourly from 8 a.m. to noon, every 2 h from noon to 8 p.m., and 24 and 48 h after drug administration. All 3 doses significantly lowered blood pressure; the fall during recumbency was significantly larger (-18%) and lasted longer (12 h) after 60 mg than after 20 mg (-11% and 7 h). All 3 doses caused a similar increase in heart rate (+29 to +38%), which reached its maximum after 2 h and lasted for 5 h. The maximum plasma concentration and the area under the plasma concentration--time curve were dose-dependent despite large inter-subject variation. Absorption, bioavailability and elimination were linear between the 20 and 60 mg doses. Plasma nifedipine levels were strongly correlated with the concomitant decrease in mean arterial blood pressure (r = 0.61, p less than 0.001). Four patients experienced mild side effects (headaches, flushes, drowsiness or weakness). This tablet form of nifedipine has a potent antihypertensive action which lasts longer than that of the capsule presentation.

In a double-blind versus placebo preliminary study conducted in seven mildly hypertensive patients, the 10-mg capsule form of nifedipine was able to reduce significantly systolic and diastolic blood pressure (-14%) for 3 h. In a single-dose, cross-over study, captopril (1 mg/kg) and nifedipine (20 mg) significantly reduced blood pressure in 12 patients with moderate essential hypertension, but the mean maximum arterial pressure reduction was faster and greater with nifedipine than with captopril (-23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively). Nifedipine did not significantly alter the renin angiotensin aldosterone system in supine and upright positions, and the blood pressure drop it induced was not related to the initial level of activation of that system. Associated with the stimulation of the sympathetic nervous system, an increased release of vasopressin was noted during nifedipine administration. Finally, nifedipine, a calcium antagonist, was a potent antihypertensive drug through its vasodilating properties. It provoked specific hormonal alterations, i.e., stimulation of catecholamines and vasopressin release, whereas the renin angiotensin aldosterone system was not significantly altered.