Affiliations: Faculty of Medicine, Universidad Juárez del Estado de Durango, Durango, México | Department of Bioengineering, University of California, San Diego, La Jolla, CA, USA | Chemical Sciences at Gómez Palacio, Universidad Juárez del Estado de Durango, Durango, Mexico | Intensive Care Therapy, Mexican Social Security Institute (IMSS), Durango, Durango, Mexico | Mexican Social Security Institute (IMSS), México DF, México | La Jolla Bioengineering Institute, La Jolla, CA, USA
Note: [] Corresponding author: Marcos Intaglietta, PhD, Department of Bioengineering University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92037-0412, USA. Tel.: +1 858 534 4275; E-mail: mintagli@ucsd.edu.
Abstract: In this study we determine the effects of reducing blood glucose on mean arterial blood pressure (MAP) and hematocrit (Hct) in patients with type 2 diabetes who are not responding to conventional treatment in an intensive treatment program 1 year after initiation of treatment. Data on MAP, glucose and Hct was obtained from 21 diabetic type 2 individuals subjected to personalized treatment and compared (paired statistics) to pretreatment conditions. Exclusion criteria were severe retinopathy, diabetic nephropathy, amputation of diabetic foot and increased glucose > 50 mg/dl. Treatment was the combined administration of glibenclamide and metformin dosed to obtain a reduction of glucose levels. Exercise and strict adherence to a prescribed diet were prescribed in all cases. One year after initiation of therapy, glucose decreased from 219±87 to 158±51 mg/dl (p<0.002), Hct increased from 41.6±3.2 to 44.7±2.9% (p<0.001) and MAP decreased from 100.6±11.0 to 94.3±7.2 mmHg (p<0.001). There were no statically significant changes in cholesterol and triglyceride concentrations. The patients lost weight (72.5±12.6 to 70.3±13.0 kg, p<0.001) and lowered blood creatinine concentration from 1.04±0.24 to 0.95±0.25 mg/dl, p<0.05. The increase in Hct should correspond to an increase in blood viscosity of about 12%, however blood pressure, and presumably vascular resistance, decreased by 6%. It is proposed that these effects are in part related to improved kidney function resulting in increased Hct and blood viscosity which increases vascular wall shear stress and NO bioavailability leading to a vasodilator effect.
