ABSTRACT
There is a paucity of experimental data on the actual mechanism of insulin-induced changes on the myocardial function. In the present study we investigated the myocardial contractile, response to an oral glucose load using echocardiography. Fifteen healthy volunteers were studied after overnight fast and 150 minutes after the oral load of 75 g glucose. Oral glucose load caused an increase in plasma glucose and insulin levels, which was accompained by a significant increase in left ventricular shortening (from 35.2 + 0.7 per cent at baseline, to 38.5 + 0.6 per cent and 39 + 0.9 per cent at 30 and 60 minutes post glucose load, respectively [P<0.05 vs baseline]; ejection faction rose from 0.73 per cent + 0.01 to 0.77 per cent + 0.01 (P<0.05); pressure rate product increased from 7.29 + 0.2 to 8.31 + 0.3 mmHg x beats per min (P<0.007) and heart rate enhanced from 68.3 + 1.9 to 74 + 1.6 (P<0.034) and 75.3 + 1.5 beats per min (P<0.008) at 60 and 90 minutes after glucose, respectively. Meanwhile, mean arterial presure decreased significantly (10+1.5 per cent, P<0.018) when compared to basal values. These results indicate a significant change in the myocardial contractile response to an oral glucose load, probably related to baroreceptor reflex response as well as an overridden by a potent vasodilatador action of insulin. Nevertheless, we could not rule out the cardiac effects may also be due an insulin-induced sympathetic activation or a direct myocardial effect.
Subject(s)
Adult , Female , Humans , Blood Glucose/metabolism , Echocardiography , Glucose/administration & dosage , Insulin/blood , Myocardial Contraction/drug effects , Administration, Oral , Blood Pressure/drug effects , Glucose Oxidase/analysis , Glucose Tolerance Test , Heart Rate/drug effects , Insulin/metabolism , Radioimmunoassay , Regression Analysis , Ventricular Function, Left/drug effectsABSTRACT
Although long recognized, the vasodilator effect of insulin has been relatively neglected over the last few years. Recent reports have focused on the sympathetic and antinatriuretic actions of this hormone. In the first part of the present study we characterized the reduction in blood pressure after a glucose load in hypertensive patients with and without insulin resistance. fourteen hypertensive Caucasian patients and ten Caucasian controls were submitted to a standard oral glucose tolerance test (OGTT) and intravenous insulin tolerance test (15-min ITT). In the hypertensive patients with insulin resistance the reduction in mean arterial presure (MAP) after a glucose load was blunted (6.7 ñ 1.7 per cent (N = 5)) when compared to insulin-sensitive (12.9 ñ 1.1 per cent (N = 9)) and normal subjects (10.1 ñ 0.8 per cent). IN the second part of the study we investigated whether hypertensive patients with myocardial hypertrophy were more insulin resistant than hypertensive individuals with a normal cardiac mass. The glucose disappearance rate (Kitt) was lower in hypertensive patients with myocardial myocardial hypertensive patients with myocardial hypertrophy (6.0 ñ 1.0 (N = 6)) when compared to hypertensive patients without myocardial hypertrophy (8.2 ñ 1.0 per cent/min (N = 8)), suggesting an association between this organomegaly and insulin resistance. In conclusion, our results suggested that 1) insulin resistance, rather than hyperinsulinemia, acts as a risk factor for the development of hypertension, because of insulin's inability to decrease MAP in this situation, and 2) there is an association between left ventricular hypertrophy and insulin resistance in hypertensive patients