Acidosis induced by lactate, pyruvate, or HCl increases blood viscosity

Serum lactate correlates with the severity of disease and the mortality in shock. It is not clear if lactate is only a marker or a mediator of disease. We tested the hypothesis that acidosis induced by lactate and pyruvate affects blood flow properties.

Human blood was incubated with additional lactate (0-50 mmol/L) or pyruvate (0-25 mmol/L) for 1 hour at 37 degrees C. Blood viscosity was measured at high (94.5 s(-1)) and low (0.1 s(-1)) shear rate. Hematocrit was measured with an electronic particle counter as well as centrifugation.

A total of 50 mmol/L additional lactate produced acidosis (pH 6.4) and increased whole-blood viscosity at high shear rate (94.5 s(-1): 6.53 +/- 0.51 mPa.s vs 4.94 +/- 0.18 mPa.s for control, n = 5, P <.001) and low shear rate (0.1 s(-1): 93.9 +/- 18.6 mPa.s vs 53.5 +/- 7.7 mPa.s, n = 5, P <.001). Simultaneously, an increased centrifuged hematocrit was observed (about 7% with 50 mmol/L lactate, P <.001), indicating eryth-rocyte swelling. These changes were reversible on removal of lactate. The addition of 25 mmol/L pyruvate also induced acidosis and increased blood viscosity and centrifuged hematocrit. When HCl was used to induce a comparable pH level decrease, a similar increase in blood viscosity and hematocrit were observed.

Pronounced acidosis induced by either lactate, pyruvate, or HCl impairs blood flow properties, which may contribute to the understanding of the pathophysiology of critical illness.