Hyperglycemic and hyperosmolar responses to graded hemorrhage.
Changes of the arterial plasma osmolality and of the glucose concentration were followed during a 30 min period of graded hemorrhagic hypotension (80, 50, and 30 mmHg) in the cat. Bleeding evoked a significant plasma hyperosmolality at all three hypotension levles and the responses were quantitatively related to the degree of hypotension. An approximate steady state increase in the arterial plasma osmolality was reached about 20 min after the start of the bleeding and it then averaged 8. 20, and 25 mOsm/kg H2O at 80, 50, and 30 mmHg, respectively. Bleeding also evoked an increase in the plasma glucose concentration, which almost entirely accounted for the observed hyperosmolality, especially at 80 and 50 mmHg. In late stages of hypotension at 30 mmHg, elevated plasma lactate and potassium concentrations contributed to the overall hyperosmolality. --Previous hemorrhagic hypotension experiments at 50 mmHg (Järhult 1975 b) have shown that hyperosmolality serves as an important regulator of the plasma and extracellular fluid volumes during bleeding. The present results indicate that such an osmolar compensatory mechanism is operating over wide ranges of hemorrhagic hypotension.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002415:Cats; D002712:Chlorides / Q000097:blood; D006470:Hemorrhage / Q000097:blood* / Q000150:complications; D007022:Hypotension / Q000097:blood* / Q000209:etiology; D007773:Lactates / Q000097:blood; D009994:Osmolar Concentration; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood; D013997:Time Factors
D001786:Blood Glucose; D002712:Chlorides; D007773:Lactates; D012964:Sodium; D011188:Potassium