Another unacceptable model of primate septic shock.

The lack of a primate model suitably reproducing clinical septic shock prompted an attempt to adapt a successful canine model to the Rhesus monkey. Animals were sedated wih 2 mg/kg Sernylan. Local anethesia for vascular catheter insertion was produced with 1% lidocaine. After baseline hemodynamic and blood measurements, the abdomen was entered and the cystic artery and duct were ligated and divided. A suspension of E. coli (ATCC 25922) was injected into the gallbladder, and the abdomen was closed. Sequential monitoring was performed every 12-24 hours until the animals expired. The first monkey was given 10(8) E. coli/kg, the dose used in the canine model. This animal expired during the first 24 hours with ATCC 25922 E. coli septicemia. The same outcome was seen in the next monkey with 10(6) E. coli/kg. Neither monkey exhibited a hyperdynamic circulatory status. Autopsies revealed no intraabdominal abscess or peritonitis. Three animals were given 10(4) E. coli/kg. One died within 24 hours, one died after 13 days, and one was a permanent survivor. Two had bacteremia but no abscess. None had a hyperdynamic circulatory status. In three other animals the cystic artery and duct were ligated and divided, but no E. coli was given. Survival varied from 11/2 to 21/2 days. None had a hyperdynamic circulatory status. All had bacteremia. Autopsies revealed no abscesses. In summary, the Rhesus monkey is exquisitely sensitive to endogenous and exogenous sources of bacteremia, which produce a hypodynamic circulatory status and death before peritonitis or intraabdominal abscess can develop. Thus, the ischemic, infected gallbladder preparation is an inadequate septic shock model in the Rhesus monkey.