EXTRA-ADRENAL SOURCES AND REGULATION OF PLASMA ASCORBIC ACID DURING HEMORRHAGE AND VISCERAL ISCHEMIA12

Abstract

Elevated plasma ascorbic acid (AA) levels were observed in adrenalcctomized rats after acute hemorrhage and after hepatic ischemia induced by clamping afferent vessels to the liver (hepatic artery and portal vein). The AA elevation was proportional to the severity of the circulatory stress. Results were similar in rats adrenalectomized at the time of the experiment or 24 hours earlier. However, hypophysectomy 24 hours prior to acute adrenalectomy resulted in elevated resting levels of plasma AA and a greater response to circulatory stress. In all animals, severe hemorrhage (1.4 to 1.9 ml. blood removed over a 15 minute period) produced higher A A levels in the liver effluent (upper vena cava) than in other vessels sampled simultaneously (lower vena cava, hepatic portal vein, and dorsal aorta), suggesting that the liver was the source of the elevated plasma AA under these conditions. In contrast, the major source of elevated plasma AA during severe hepatic ischemia appeared to be the spleen inasmuch as the highest levels of AA were found in the hepatic portal vein after this circulatory stress. However, evidence was obtained that the liver also contributed to elevated plasma AA levels after severe hepatic ischemia, since exclusion of the spleen from the circulation eliminated the inordinate rise in AA levels in the hepatic portal vein, while AA in the liver effluent was maintained at a higher level than in the systemic circulation. The conclusions may be drawn that the liver and the spleen are major sources of plasma AA during hemorrhage and hepatic ischemia respectively and that AA release from these organs can occur in the absence of pituitary-adrenocortical function.