Treatment of uncomplicated gonorrhoea in women with a combination of rifampicin and erythromycin.

One hundred women with uncomplicated gonorrhoea (in five cases due to penicillinase producing strains of Neisseria gonorrhoeae (PPNG)) were treated with a single oral dose of rifampicin 900 mg and erythromycin stearate 1 g. N gonorrhoeae was reisolated from the oropharynx of one patient, who was infected with a PPNG strain, but was eradicated from the genital tract in 100% of cases. The combination eradicated Chlamydia trachomatis from only 10 (28%) of the 36 patients infected. Side effects were predominantly mild and consisted of transient nausea. The treatment merits evaluation in areas with a high incidence of PPNG strains.

Long-term treatment of hypertension with labetalol.

1 Thirty-two hypertensive patients have been treated with labetalol for periods of up to 7 years. 2 Ten patients observed for 6 years from time of stabilization of dosage, did not show any tolerance to labetalol. 3 Postural and exercise hypotension were not seen in these patients over this prolonged follow-up, although they were seen in other patients given over 2 g labetalol daily.

Long-term treatment of hypertension with labetalol.

1 Thirty-two hypertensive patients have been treated with labetalol for periods of up to 7 years. 2 Ten patients observed for 6 years from time of stabilization of dosage, did not show any tolerance to labetalol. 3 Postural and exercise hypotension were not seen in these patients over this prolonged follow-up, although they were seen in other patients given over 2 g labetalol daily.

Pharmacological basis for antihypertensive effects of intravenous labetalol.

Labetalol 1-5 mg/kg administered intravenously to normal subjects in the supine position produced an immediate mean fall in systolic (16%) and diastolic (25%) blood pressure with a concomitant increase in heart rate (12%). After graded exercise, intravenous labetalol inhibited increases in heart rate and blood pressure. Isoprenaline log dose response curves of increase in heart rate and reduction in diastolic pressure after intravenous labetalol shifted to the right in a parallel manner compared with pre-labetalol response curves suggestive of competitive antagonism at beta-adrenoceptor sites. Similarly, phenylephrine dose response curves of increase in systolic pressure before and after intravenous labetalol were suggestive of competitive antagonism at alpha-adrenoceptor sites. The ratio of relative potency alpha: beta adrenoceptor antagonism after intravenous labetalol was approximately 1:7, whereas in the same subjects after oral labetalol the ratio was approximately 1:3 as previously reported. Using the inhibition of isoprenaline tachycardia to estimate the potency of the beta-adrenoceptor antagonism of labetalol relative to that of propranolol the potency ratio was 1:6. However, using inhibition of Valsalva tachycardia as the index, the estimated ratio was approximately 1:3. Estimates of relative potency using inhibition of tilt tachycardia were complicated by the additional effects upon blood pressure after labetalol not seen after propranolol. Labetalol produced adrenoceptor blockade at both alpha and beta sites in man sufficient to explain its therapeutic antihypertensive effect.

A within-patient comparison of bethanidine, methyldopa and propranolol in the treatment of hypertension.

1. A within-patient comparison showed that bethanidine, methyldopa and propranolol produced similar control of the blood pressure. 2. Unlike bethanidine, propranolol did not produce postural and exercise hypotension; methyldopa was intermediate in effect. 3. Overall side effects were of a similar incidence though there were differences in incidence of particular side effects.

Labetalol in long-term treatment of hypertension.

1 Labetalol, a beta- and alpha-adrenoreceptor-blocking drug, has been used in the treatment of hypertension in a total of 32 patients for over 4.5 yr, 14 patients for 3 yr or more. 2 Labetalol seems to have a similarly potency of methyldopa and the adrenergic neurone-blocking drugs. 3 Postural hypotension was only observed at doses over 2 g/d. It was the reason for stopping treatment in two patients. 4 Dosage varied; average 889 mg/d, range 75-3,200 mg. Tolerance did not develop. 5 Side-effects led to drug withdrawal in four patients

Some haemodynamic effects of compound AH 5158 compared with propranolol, propranolol plus hydrallazine, and diazoxide: the use of AH 5158 in the treatment of hypertension.

1. Intravenous administration of compound AH 5158, which possesses alpha- and beta-adrenergic receptor-blocking properties, produces haemodynamic effects similar to those seen from the combined effects of propranolol and hydrallazine. 2. Chronic oral administration has demonstrated that compound AH 5158 is an effective hypotensive agent capable of controlling the blood pressure in patients previously requiring large doses of drugs such as methyldopa. Some postural and exercise hypotension may be seen with larger doses.

Interactions between sympathomimetic amines and antidepressant agents in man.

Intravenous infusions of phenylephrine, noradrenaline, adrenaline, and isoprenaline were given to healthy human volunteers after five to seven days on phenelzine, tranylcypromine, or imipramine, and cardiovascular responses were compared with those observed under control conditions. With monoamine oxidase inhibitors there was a 2-2(1/2) fold potentiation of the pressor effect of phenylephrine, but no clinically significant potentiation of cardiovascular effects of noradrenaline, adrenaline, or isoprenaline. With imipramine there was potentiation of the pressor effects of phenylephrine (2-3 fold), noradrenaline (4-8 fold), and adrenaline (2-4 fold); there were dysrhythmias during adrenaline infusions, but no noticeable or consistent changes in response to isoprenaline.Noradrenaline and adrenaline in amounts contained in local anaesthetics used in dentistry are not likely to be significantly potentiated in otherwise healthy patients receiving monoamine oxidase inhibitors. Hazardous potentiation of their cardiovascular effects might occur in patients receiving tricyclic antidepressants.Our observations do not indicate that the hazards associated with isoprenaline inhalation by bronchial asthmatics would be increased by coincident therapy with a monoamine oxidase inhibitor or tricyclic antidepressant.