Diabetic patients have an impaired cerebral vasodilatory response to hypercapnia under propofol anesthesia.

Abstract

The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO2 increased and remained stable for 5 to 10 minutes. Significant differences were observed in absolute and relative CO2 reactivity between the diabetes and control groups (absolute CO2 reactivity: control, 2.8+/-0.7; diabetes mellitus, 2.1+/-1.3; P<0.01; relative CO2 reactivity: control, 6.3+/-1.4; diabetes mellitus, 4.5+/-2.7; P<0.01, Mann-Whitney U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute (P=0.002) and relative (P=0.002) CO2 reactivity, glycosylated hemoglobin (P=0.0034), and fasting blood sugar (P=0.01) (Scheffé's test, Mann-Whitney U test). There was an inverse correlation between absolute CO2 reactivity and glycosylated hemoglobin (r=0.69, P<0.001). Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.