Coronary collateral vessels reduce damage to ischemic myocardium after coronary obstruction. Factors that stimulate collateral formation are expected to have ameliorating effects on myocardial infarction. In a canine experimental myocardial infarct model, intracoronary injection of basic fibroblast growth factor (bFGF) improved cardiac systolic function and reduced infarct size. Treatment with bFGF increased the number of arterioles and capillaries in the infarct. Thus, the angiogenic action of bFGF might lead to a reduction in infarct size. The application of bFGF might bring about a therapeutic modality for the salvage of infarcted myocardium.

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To elucidate the role of insulin in the control of coronary artery tone, its effects on porcine coronary artery contraction evoked by thromboxane A2 (TXA2) were studied in vitro. Ring preparations of porcine proximal coronary artery were suspended in a Magnus apparatus filled with Tyrode's solution at 370 C and aerated with 100%0 02, and the isometric tension of the contractions was measured. Insulin itself caused neither contraction nor relaxation. Insulin had no significant effect on the coronary artery contractions evoked by 20 mM K', norepinephrine, histamine, and serotonin; however, 120 minutes of preincubation with a physiological concentration of insulin (30-300 ,uunits/ml) significantly accentuated coronary artery contractions evoked by STA2 (10-11 to 10-7 M), a stable analogue of TXA2 that is known to act on TXA2/prostaglandin H2 receptors (141.4+10.9% of the control at 10-M STA2 in the presence of 300 ,uunits/ml insulin; p<0.01). The enhancing effects of insulin on the STA2-induced contractions were affected by extracellular glucose or magnesium ion concentrations. The enhancing effects of insulin were observed only at the glucose concentrations of 100-300 mg/dl and magnesium concentrations of 0.5-1.5 mM. Therefore, insulin was suspected of enhancing TXA2-induced contraction through a process that depends on extracellular glucose and Mg24. (Circulation 1990;81:1654-1659 Although the pathogenesis of coronary vasoconstriction has been studied extensively, its precise mechanisms have not been fully clarified. It is well known that various neurohumoral factors and substances derived from blood cells such as acetylcholine, histamine, serotonin, thromboxane A2 (TXA2), and leukotrienes evoke vasoconstriction in porcine, canine, and human coronary arteries.1-4Several clinical studies have provided evidence that high circulating levels of insulin can promote the development of atherosclerotic vascular diseases like coronary heart disease.5 It has been reported that hypertension is closely related to hyperinsulinemia, and insulin is thought to cause hypertension through its vasoconstricting action.6 8 Other studies have revealed that insulin infusion reduces renal or retinal blood flow in diabetic patients and normal men.9-1' In animal experiments, insulin restored vascular contraction that was attenuated in the diabetic state.12-14 These results suggest that insulin enhances vasoconstriction, although conflicting results have also been reported.'5 In this study, we examined the effect of insulin on porcine coronary artery contraction evoked by TXA2 in vitro and demonstrated that insulin significantly enhanced TXA2-induced coronary artery contraction. Furthermore, we studied the effects of extracellular glucose and magnesium ions on the action of insulin to determine the mechanisms of its action. MethodsCoronary arteries excised from porcine hearts (57 hearts) were studied. The hearts were incubated in ice-cold Tyrode's solution (pH 7.4), containing (mM): NaCl 136.5, KCl 5.4, CaCl2 1.8, MgCl2 0.53, glucose 5.5, ...

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