A randomized prospective study was conducted to determine whether the insulin regimen for NIDDM subjects poorly controlled on oral therapy should be designed primarily to control basal metabolism or to control mealtime hyperglycaemia. Grossly obese subjects were excluded. After a 2-month run-in phase involving intensive education, subjects were randomized to therapy with twice daily isophane or three times daily soluble insulin. Both Protaphane and Actrapid brought about similar improvement in HbA1 (9.5 +/- 0.5 and 9.7 +/- 0.4%) compared with baseline (11.7 +/- 0.5%; p < 0.001). Diurnal blood glucose profiles showed that despite the good post-prandial control achieved by pre-meal soluble insulin, loss of control occurred overnight, resulting in higher fasting blood glucose levels compared with Protaphane therapy (8.0 +/- 0.8 vs 10.6 +/- 0.8 mmol l-1; p < 0.05). The overall rate of hypoglycaemia was 0.44 patient-1 year-1. Thirty-two mild hypoglycaemic episodes occurred on Protaphane therapy and 79 on Actrapid therapy. Using formal psychometric tests it was shown that insulin therapy was associated with improved treatment satisfaction and that this was greater on Protaphane therapy (p < 0.05). Overall well-being increased similarly in the two groups. All subjects wished to continue with insulin therapy after the conclusion of the study. The insulin regimen for moderately or poorly controlled non-insulin-dependent diabetes should primarily be designed to correct the basal insulin deficiency rather than to mimic normal meal-induced insulin secretion.

R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t s

We administered sodium nitroprusside (SNP) or nifedipine intravenously to patients who became hypertensive after elective coronary revascularization and compared their effects on hemodynamics and the electrocardiogram in a parallel, randomized, open-label study. Four of 21 patients treated with nifedipine required the addition of SNP to maintain mean arterial pressure less than 90 mm Hg, compared with 4 of 28 patients in the SNP group who required the addition of nifedipine. The success rates of nifedipine (81%) and SNP (86%) were not significantly different. There was no difference in the incidence of adverse ST-segment changes during drug infusion (4% versus 5%) or perioperative myocardial infarction (9.5% versus 10.7%) in the nifedipine versus SNP groups, respectively. The plasma nifedipine concentration (mean value +/- SD) at steady state for 21 patients receiving nifedipine was 119 +/- 42.5 ng/mL. The pharmacokinetic variables for nifedipine were as follows (mean values +/- SD): systemic clearance, 0.525 +/- 0.228 L.h-1.kg-1; apparent volume of distribution, 0.738 +/- 0.446 L/kg; and elimination half-life, 1.02 +/- 0.51 h. These values are similar to those reported previously in healthy volunteers. We conclude that intravenous nifedipine can be used safely to control hypertension after coronary revascularization but were unable to demonstrate an advantage of nifedipine compared with SNP in preventing postoperative ischemia or infarction in this group of patients who had good left ventricular function.

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