Our data suggest that group follow-up as the sole means of follow-up after structured education for individuals with type 1 diabetes is as effective as a return to one-to-one clinic visits.

Objective-To study underlying vascular responses in chronic heart failure in patients without ACE inhibitor treatment, and to compare them with age matched controls. Design-Forearm blood flow was studied using venous occlusion plethysmography in patients with chronic heart failure (n = 12) and matched controls (n = 13), after infusion of L-NMMA (a nitric oxide synthase inhibitor), glyceryl trinitrate (an endothelium independent vasodilator), and serotonin (an endothelium dependent vasodilator). Results-L-NMMA produced significant vasoconstriction in normal subjects (forearm blood flow reduced by 24%), but not in patients (6%; diVerence between groups p < 0.03). The vasodilator responses to glyceryl trinitrate were impaired in patients (p < 0.02). In normal controls, serotonin produced initial dilatation, followed by vasoconstriction at high doses. In patients, no vasodilator responses were observed, only late vasoconstriction (p < 0.03). Conclusions-The vascular responses of patients are confirmed as being abnormal. The lack of response to L-NMMA suggests that nitric oxide does not contribute to basal vascular tone in patients with chronic heart failure. The responses to glyceryl trinitrate and to serotonin suggest that there is both smooth muscle and endothelial dysfunction in patients with chronic heart failure.

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Microvascular disease is an important cause of morbidity in diabetes. There is evidence that impaired autoregulation of blood flow is involved in the pathogenesis of diabetic microangiopathy. The vascular endothelium plays a central role in the regulation of vascular tone. Endothelin (ET)-l is a potent endothelium-derived vasoconstrictor substance that contributes to basal vascular tone. Impaired vasoconstriction in response to endogenous ET could result in hyperperfusion and subsequent microvascular damage. The purpose of our study was to determine whether vascular responses to locally administered ET-1 are impaired in NIDDM. Nine patients with NIDDM and 12 control subjects underwent cannulation of the nondominant brachial artery. Forearm blood flow (FBF) was measured at baseline and during the drug infusion using strain-gauge venous occlusion plethysmography. ET-1 (5 pmol/min) was infused for 60 min at a rate of 1 ml/min. FBF was measured during the first 5 min of the infusion and at 5-min intervals thereafter. Results were expressed as change in FBF from baseline (ml • 100 ml" 1 • min" 1 ) and were analyzed using repeated measures analysis of variance and Dunnett's test of multiple comparisons. Control subjects showed a gradual onset of vasoconstriction in response to ET-1, which reached maximum at 35 min (1.1 ml • 100 ml" 1 • min" 1 ; P < 0.01). There was no reduction in FBF in response to ET-1 in the diabetic group. The differences between the diabetic and control groups were significant (P < 0.03). In conclusion, ET-1 infused locally at 5 pmol/min does not cause vasoconstriction in patients with NIDDM. Diabetes 45:105-107, 1996 M icrovascular disease is an important cause of morbidity and mortality in both IDDM and NIDDM. It can result in retinopathy and nephropathy, and it contributes to foot pathology, diabetic cardiopathy, and neuropathy. Despite this, the pathogenesis of diabetic microangiopathy is uncertain. The hemodynamic hypothesis argues that an early increase in precapillary blood flow and capillary hypertension precede the adaptive changes that lead to microvascular sclerosis (1-3). Although the majority of evidence for the hemodynamic hypothesis relates to IDDM, increased renal plasma flow and impaired maximum vasodilatation to thermal injury have been described in patients with NIDDM (4,5). These findings indicate that autoregulation of blood flow is disturbed in this group also. The vascular endothelium plays a central role in the regulation of vascular tone through the production of several vasoactive substances, including endothelin (ET)-l, nitric oxide, and cyclooxygenase products. Previous studies in this department have demonstrated impaired endothelium-dependent vasodilatation in patients with NIDDM, probably due to impaired release of nitric oxide or increased production of a cyclooxygenase-derived constrictor substance (6). ET-1 was first discovered in 1988 in the supernatant of aortic endothelial cells (7). It is a 21-amino acid peptide formed by proteolytic cleavage of its precursor...

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