A Study on Left Ventricular Function in Diabetics by Digitized Echocardiography

Echocardiographic evaluation of left ventricular function permits the demonstration of preclinical diabetic cardiomyopathy. In order to define the relationship between diabetic retinopathy and precence of myocardial dysfunction, M-mode echocardiograms were recorded in three groups of diabetics ; group 1, no retinopathy, group 2, background retinopathy, group 3, proliferative retinopathy, and normal controls without evidence fo coronary heart disease. The resultant traces were digitized, and systolic and diastolic parameters were evaluated. None of parameters fo systolic function was modified. however peak velocity of posterior wall thinning was decreased in group 3(p<0.005), peak velocity of left ventricular demension increase was decreased in all three groups(p<0.005, P<0.001, P<0.001 respectively), duration of rapid thinning of posterior wall increased in group 2 and 3(p<0.001, p<0.001 respectively), and duration of rapid inflow of left ventricle was increased in group 3(p<0.005). These results indicate a diminution of myocardial compliance and relaxation in diabetics with retinopathy. It is concluded that abnormalities of left ventricular diastolic function is present in diabetics when left ventricular systolic function is normal and that more severe abnormalities of left ventricular diastolic function in diabetics with proliferative retinopathy reflect a subclinical diabetic cardiomyopathy due to small vessel disease.

Influence of Phenilamine on Pressor Responses of Norepinephrine and Tyramine

The effect of Pheniramine(Avil), a histaminergic-1 receptor blocking agent presently employed in treating various allergic diseases on pressor actions of norepinephring(NE) and tyramine (TR) was studied in the rabbit. Pheniramine, when given into a femoral vein with a dose(3mg/kg) enough to block H1-receptor, potentiated markedly the pressor responses of NE and TR. The pressor action of NE augmented by pheniramine was not affected by additional adminstration of debrisoquin (Drenergic neuron blocker) or phenelzine(monoamine oxidase inhibitor) or desipramine(U1-uptake blocker), or while potentiated by additional treatment with chlorisondamine(ganglionic blocker)or reserpine(catecholamine depleter). The hypertensive response of NE to phenelzine or desipramine was reinforced significantly by addition of pheniramine, but the response of NE in rabbits treated with reserpine or chlorisondamine or debrisoquin was not influenced by pheniramine-addition. Elevation of blood pressure to TR potentiated by pheniramine was attenuated significantly by reserpine treatment with chlorisondamine made the significant augmentation of pressor action to TR after pheniramine. Tyramine-induced response of blood pressure after pheniramine, but the response of blood pressure to TR caused by phenelzine or desipramine was enhanced markedly by pheniramine-treatment. From the above experimental results, it is thought that the pressor effect of NE and TR potentiated by pheniramine is similar to that of debrisoquin, i.e. the sensitization of effector cell, and that central action of pheniramine can not ruled out.