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The authors studied the effect of prolonged physical exercise on the mechanical properties of rat aorta in relation to the amounts and qualities of arterial connective tissue fibrous proteins. Twelve male rats were divided into two groups: 6 sedentary rats (S) and 6 training rats (T), which were forced to swim from nine weeks to twenty-five weeks of age. The ultimate tensile stress and the ultimate tensile extension ratio of ring specimens at the descending thoracic aorta were larger in T than in S (192.3 +/- 47.9 g/mm2, mean +/- SD, vs 147.8 +/- 26.0, p less than 0.05; 3.52 +/- 0.13 vs 3.18 +/- 0.27, p less than 0.05; respectively). The elasticity parameter, calculated by fitting stress-strain curves to exponential function in the stress level of 0-20 g/mm2, was lower in T than in S (1.79 +/- 0.15 vs 2.13 +/- 0.24, p less than 0.01). The contents of elastin (alkali-insoluble elastin preparation) and collagen were higher in T than in S (0.44 +/- 0.11 g/g dry aorta vs 0.30 +/- 0.06, p less than 0.05; 0.15 +/- 0.04 g/g dry aorta vs 0.11 +/- 0.04, NS, respectively). Although the aortic calcium content did not significantly change in the training rats (T 1.17 +/- 0.23 mg/g dry aorta, S 0.95 +/- 0.34), the content of calcium in elastin was lower in T than in S (1.75 +/- 0.51 mg/g dry elastin vs 2.63 +/- 1.00, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of epinephrine in platelet activation and the effect of an alpha 2-adrenoceptor antagonist, midaglizole, during insulin-induced hypoglycaemia in Type 2 (non-insulin-dependent) diabetes mellitus were examined. The action of midaglizole as a platelet alpha 2-antagonist was confirmed by in vitro studies using platelet-rich plasma and washed platelet suspension. Hypoglycaemia was induced by a bolus injection of short-acting insulin in 24 diabetic patients. They were divided into two groups, a control group (n = 12) and an alpha 2-group (n = 12), and midaglizole was administered orally 60 min before insulin injection in the latter. Blood glucose and plasma C-peptide levels were significantly decreased (p less than 0.005) by insulin injection in both groups. Counter-regulatory hormones, including epinephrine, and arginine vasopressin were similarly increased at the hypoglycaemic nadir compared with the levels at 0 min in both groups. Plasma beta-thromboglobulin was increased at the hypoglycaemic nadir (165.5 +/- 12.6 ng/ml) compared with the level at 0 min (121.0 +/- 11.5, p less than 0.005) in the control group, whereas no significant increase was demonstrated in the alpha 2-group. These results suggest that plasma epinephrine plays an important role in platelet activation during hypoglycaemia in Type 2 diabetes mellitus, and that the platelet activation is prevented by alpha 2-adrenoceptor antagonist.

An excessive glucagon secretion to intravenous arginine infusion was found in obese hyperinsulinaemic patients with glucose intolerance. This study was designed to determine whether the glucagon hyperresponsiveness to arginine in these patients would improve by insulin infused at a high enough dose to overcome insulin resistance. By infusing high dose insulin during arginine infusion, the previously exaggerated glucagon response to arginine could be normalized. To normalize the abnormal glucagon response, insulin doses of 4.2 +/- 0.7 and 3.8 +/- 0.5 IU were required during arginine infusion in obese hyperinsulinaemic patients with impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetes mellitus, respectively. This achieved plasma peak insulin levels 3 to 4 times higher than those observed in non-obese healthy subjects. Furthermore, we clarified whether or not the effect of normalizing insulin action and/or glycaemic excursions contributed to normalizing the exaggerated glucagon response to arginine in these patients. Blood glucose was clamped while high dose insulin was infused at the same levels as observed during the arginine infusion test with no insulin infusion. As a result, normalization of the exaggerated plasma glucagon response was achieved, whether hyperglycaemia existed or not. These results clearly demonstrate that, similar to non-obese hypoinsulinaemic Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients, the exaggerated Alpha-cell response to arginine infusion in obese hyperinsulinaemic patients with glucose intolerance is secondary to the reduction of insulin action on the pancreatic Alpha cell, and that the expression of insulin action plays an important part in normalizing these abnormalities.

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