A mechanism for shock following stomach rupture in the newborn.
BACKGROUND
Stomach rupture often leads to shock and death within a short period, but the mechanism for this is not well-known. Shock may be due, in part, to endotoxin translocation and endotoxemia.


METHODS
Sterile, endotoxin-free HCl (0.1 mol/L), with or without endotoxin-feeding, was injected intraperitoneally into 10-day-old rats, simulating stomach rupture in the newborn. The plasma endotoxin concentration was measured. Plasma glucose and lactate concentrations were monitored to assess physiologic response to endotoxemia and shock.


RESULTS
Endotoxin feeding alone caused endotoxemia (0.49 +/- 0.12 ng/mL; P < 0.05) in 10-day-old rats, while plasma endotoxin concentration in controls was less than 0.04 ng/mL. However, the endotoxemia did not cause disruption of glucose regulation or death. Injection of HCl alone did not increase plasma endotoxin concentrations and did not alter glucose regulation. However, HCl injection into endotoxin-fed rats induced endotoxemia (211.1 +/- 70.5 ng/mL; P < 0.05), hypoglycemia, lactacidemia and mortality (45%; P < 0.05).


CONCLUSIONS
Early development of shock following stomach rupture may be in part due to endotoxin translocation and endotoxemia.
Goto
M
M
Ronald McDonald Children's Hospital at Loyola, Maywood, Illinois, USA. mgoto@wpo.it.luc.edu
Yoshioka
T
T
Hase
T
T
Tani
T
T
Zeller
W P
WP
D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000032:analysis; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012772:Shock, Septic / Q000097:blood / Q000209:etiology*; D013275:Stomach Rupture / Q000097:blood / Q000150:complications*
D001786:Blood Glucose; D004731:Endotoxins; D019344:Lactic Acid