OBJECTIVE: To investigate the relationship between mean arterial blood pressure and hematocrit in a population of treated diabetic patients and a control population of healthy individuals. RESEARCH DESIGN AND METHODS: Data on hematocrit and blood pressure were obtained from 129 diabetic subjects (87 women and 42 men) and 103 healthy subjects (76 women and 27 men) enrolled in a cross-sectional study. Alcohol consumption, ischemic heart disease, stroke, neoplasia, renal, hepatic, and chronic inflammatory disease were exclusion criteria. RESULTS: The hematocrit of diabetic patients ranged from 0.35 to 0.52, and blood pressure had a bimodal distribution described by a second-order polynomial (P < 0.001), whereby elevated pressures correlated with low and high hematocrit, while the minimum average pressure was at hematocrit 0.43. Hematocrit of normal control subjects (range 0.28-0.55) was uncorrelated to blood pressure (averaged 99.7 +/- 9.7 mmHg). High blood pressure, low hematocrit diabetic subjects up to the minimum average hematocrit of 0.43 had a negative correlation (P < 0.0001) between these variables. CONCLUSIONS: Our findings are compatible with the hypothesis that diabetic patients present normal responses to hematocrit variation and therefore blood viscosity and shear stress in mediating the release of vasodilators and lack the ability to autoregulate blood pressure relative to differences in hematocrit by comparison to nondiabetic subjects. These findings also suggest that the treatment of diabetes should target maintaining an optimal hematocrit in order to lower cardiovascular risk.
OBJECTIVE: To investigate the relationship between mean arterial blood pressure and hematocrit in a population of treated diabeticpatients and a control population of healthy individuals. RESEARCH DESIGN AND METHODS: Data on hematocrit and blood pressure were obtained from 129 diabetic subjects (87 women and 42 men) and 103 healthy subjects (76 women and 27 men) enrolled in a cross-sectional study. Alcohol consumption, ischemic heart disease, stroke, neoplasia, renal, hepatic, and chronic inflammatory disease were exclusion criteria. RESULTS: The hematocrit of diabeticpatients ranged from 0.35 to 0.52, and blood pressure had a bimodal distribution described by a second-order polynomial (P < 0.001), whereby elevated pressures correlated with low and high hematocrit, while the minimum average pressure was at hematocrit 0.43. Hematocrit of normal control subjects (range 0.28-0.55) was uncorrelated to blood pressure (averaged 99.7 +/- 9.7 mmHg). High blood pressure, low hematocrit diabetic subjects up to the minimum average hematocrit of 0.43 had a negative correlation (P < 0.0001) between these variables. CONCLUSIONS: Our findings are compatible with the hypothesis that diabeticpatients present normal responses to hematocrit variation and therefore blood viscosity and shear stress in mediating the release of vasodilators and lack the ability to autoregulate blood pressure relative to differences in hematocrit by comparison to nondiabetic subjects. These findings also suggest that the treatment of diabetes should target maintaining an optimal hematocrit in order to lower cardiovascular risk.
Authors: Beatriz Y Salazar Vázquez; Judith Martini; Amy G Tsai; Paul C Johnson; Pedro Cabrales; Marcos Intaglietta Journal: Am J Physiol Heart Circ Physiol Date: 2010-07-02 Impact factor: 4.733
Authors: Jacob Plange-Rhule; Sally M Kerry; John B Eastwood; Frank B Micah; Sampson Antwi; Francesco P Cappuccio Journal: Int J Hypertens Date: 2018-04-05 Impact factor: 2.420
Authors: Beatriz Y Salazar Vázquez; Miguel A Salazar Vázquez; Marcos Intaglietta; Ulf de Faire; Bengt Fagrell; Pedro Cabrales Journal: Vasc Health Risk Manag Date: 2009-06-07
Authors: Pedro Cabrales; Miguel A Salazar Vázquez; Beatrizy Salazar Vázquez; Martha Rodríguez-Morán; Marcos Intaglietta; Fernando Guerrero-Romeros Journal: Vasc Health Risk Manag Date: 2008