Menguy R, Masters Y F
Adv Shock Res. 1978;1:43-54.
Terms such as "insulin resistance" and "glucose intolerance" applied to shock-induced hyperglycemia suggest that this state may prejudice survival. However, our data indicate that posthemorrhage hyperglycemia improves short-term survival. Rabbits, either fed until the experiment or fasted for 24 hours, were shocked by rapid removal of 25% of their blood volume (BV) measured by 131IHSA. During the next 60 minutes, blood pressure (BP) was recorded, and the following variables were measured every 10 minutes: plasma volume (PV); arterial and venous plasma osmolality (PO), glucose, lactate, Na, K and hematocrit. Other fasted animals studied similarly received short intravenous pulses of hypertonic xylose after bleeding. The PO of fed animals, who all survived for 60 minutes rose to an extent accounted for by rises in glucose and lactate. A significant PV fluid gain was maintained for 60 minutes. The fasted animals, 42% of whom died before 60 minutes, had a flat glucose curve with a correspondingly small rise in PO. The PV fluid balance, after an initial small gain, became negative. Although a lower blood pressure in fasted rabbits was probably due to lack of PV refill, death resulted from hyperkalemia. Poor tolerance of fasted animals to shock is not attributable only to less glucose for energy metabolism, because when they received xylose, homeostatic features of fed animals were restored. The data suggest that, immediately after hemorrhage, glucose acts as a nonpermeant solute drawing fluid into the circulation. This study also shows that control of the nutritional status of animals used for shock models is important.
