In a group of eight brim patients with a mean of 65.3 +/- 17.4 per cen
t TBSA burn injury (range 50-90 per cent TBSA), accompanied by a mean
of 43.5 +/- 18.9 per cent TBSA full-thickness injury, it was shown tha
t the evidence of global hypovolaemia had disappeared at 12 h after th
e injury following aggressive fluid resuscitation, while there was sti
ll a subnormal pHi of stomach at 48 h. As a prolonged period of inadeq
uacy of oxygen delivery to the intestine might result in impairment of
the intestinal mucosal barrier function, and then endogenous endotoxa
emia might ensue, ii seems to be important to correct intestinal hypox
ia as early as possible. Since the inadequate perfusion to the gut wal
l is due to selective vasoconstriction? of the mesenteric vasculature,
logic dictates that the use of a vasodilator is in order. Anisodamine
, an anticholinergic drug, was then given in six burn patients with co
mparable burn size and amount of fluid replenishment with the eight pa
tients in the control group. It was clearly demonstrated that gastric
pHi returned to normal before 48 h after injury. Plasma endotoxin and
TNF contents were measured, and they were significantly lower than con
trol values after 72 h. In conclusion, it is believed that anisodamine
might be a valuable adjunct to the resuscitation regime of burn shock
, anti, therefore, a promising drug to abate endogenous endotoxaemia s
ubsequent to splanchnic vasoconstriction due to hypovolaemia. The shor
t-comings of the drug were a mild abdominal distention and tachycardia
after its administration. (C) 1997 Elsevier Science Lid for ISBI.