Clinical monitoring of cellular metabolism during
shock, based largely on traditional metabolic indicators, remains unsatisfactory. The purpose of this study was to compare venous
oxygen tension and blood
lactate gradients with blood gradients of
purine nucleotide degradation products which are derived from tissue
ATP catabolism during
hypovolemic shock. Sixteen dogs were instrumented to sample arterial and venous blood. Measurements of arteriovenous
lactate and
PNDP gradients during spontaneous respiration were examined at four tissue sites: gut, kidney, hindlimb, and diaphragm.
Hypovolemic shock (mean arterial blood pressure 35 to 40 mm Hg) was induced and maintained for one hour. The above parameters were remeasured at 30 and 60 minutes after induction of
shock.
Hypoxanthine gradients were greater than that of other
PNDP, and so were used as the primary
indicator of tissue
ATP metabolism. In the hindlimb, the mean AV gradients for
hypoxanthine (1 +/- 1 microM) were not significantly greater than baseline, while the
lactate gradient (700 +/- 300 microM) rose markedly. In contrast, across the kidney there was a significantly greater AV
hypoxanthine gradient (16 +/- 3 microM, p less than 0.002) but no
lactate gradient (-400 +/- 200 microM). Both the
hypoxanthine and
lactate AV gradients were significantly elevated across the diaphragm and gut. Venous PO2 values less than 35 mm Hg predicted an increased
hypoxanthine gradient across the kidney, but not across the hindlimb. We conclude that the metabolic response to
hypovolemic shock as assessed by
PNDP gradients,
lactate gradients, and venous PO2 differs among tissues. Although resting muscle such as the hindlimb may be an important source of blood
lactate, the viscera and working skeletal muscle (the diaphragm) are major contributors to circulating
PNDP.