Blood oxygen transport and endothelial dysfunction in patients with arterial hypertension.

Abstract

Disturbed nitric oxide (NO) synthesis leads to development of endothelial dysfunction that plays a significant role in the pathogenesis of arterial hypertension. The presence of various compounds of haemoglobin with NO can affect haemoglobin-oxygen affinity of the whole blood. Methaemoglobin and S-nitrosohaemoglobin increase it, whereas nitrosyl-haemoglobin decreases. The aim of this study was to investigate the blood oxygen transport indices and to assess the endothelial function in patients with arterial hypertension. The patients with mild hypertension had a 4.47% increased actual p50 (the blood pO(2) corresponding to its 50% oxygen saturation) (P<0.05), a diminished pO(2) (P<0.05), and a raised pCO(2) (P<0.01) as compared with the controls. The patients with severe hypertension had decreased pO(2) and pH, and actual p50 was reduced by 3.03% (P<0.05), which reflects a more pronounced oxyhaemoglobin dissociation curve shift leftwards. These changes can be assessed as a blood oxygen transport decompensation that enhanced tissue hypoxia. The results of our studies indicate that the endothelial dysfunction in patients with arterial hypertension leads to significant impairments in blood oxygen transport indices. The endothelium may be involved in development of the above blood oxygen transport impairments, since only sufficient amounts of NO maintain a normal blood flow and oxygen transport to tissues. The endothelial dysfunction leads to a disturbed production of different haemoglobin NO derivatives, which not only affects NO release at different sites of the arterial bed, but also haemoglobin-oxygen affinity and optimal blood oxygenation and deoxygenation in capillaries. These data support the notion that endothelial dysfunction may alter haemoglobin-oxygen affinity and tissue oxygen supply in vivo. Alternation of haemoglobin-oxygen supply may be involved in the pathogenesis of hypertension.