Differential effects of propofol, ketamine, and thiopental anaesthesia on the skeletal muscle microcirculation of normotensive and hypertensive rats in vivo.

BACKGROUND

This study utilized the dorsal microcirculatory chamber (DMC) model to determine differential effects of i.v. propofol, ketamine, and thiopental anaesthesia on the skeletal muscle microcirculation (10-180 micro m) of normotensive (Male Wistar Kyoto, WKY) and hypertensive (spontaneously hypertensive Harlan, SHR) rats, importantly, comparing responses to a conscious baseline.

METHODS

Three weeks following implantation of the DMC in WKY (n=8) and SHR (n=6) (130 g) 0.25 ml 100 g(-1) FITC-BSA (i.v.) was administered and the microcirculation viewed using fluorescent in vivo microscopy for a 30 min baseline (t=0-30 min). This was followed by either propofol, thiopental, ketamine, or saline (i.v. bolus induction over 5 min (t=30-35 min)), then maintenance step-up infusion for 60 min (t=45-105 min), so that animals received all four agents 1 week apart (56 experiments).

RESULTS

Dilation of A3 arterioles (15-30 micro m) and V3 venules (20-40 microm) with propofol was greater in SHR (t=95 min, A3 36.7 (12)%, V3 15.5 (2.3)%) than WKY (t=95 min, A3 19.4 (7.4)%, V3 8.0 (2.3)%) (P<0.05). Constriction of A3 with ketamine was greater in SHR (t=95 min, A3 -29.1 (6.4)%) than WKY (A3 -17.5 (8.8)%) (P<0.05). This was accompanied by hypotension with propofol in SHR (-32% decrease in systolic arterial pressure), but not WKY (-6%) and hypertension with ketamine in WKY (-15%) and SHR (-24%) (P<0.05). During thiopental anaesthesia there was dilation of A1 (80-180 microm), A3, and V3 in WKY (P<0.05). Conversely, in SHR dilation of venules (29.2 (8.7)%) was accompanied by constriction of A1 and A3 (t=95 min, A1 -25.1 (5.9)%, A3-45.2 (3.1)%) (P<0.05).

CONCLUSION

Within the skeletal muscle microcirculation of hypertensive rats there is enhanced dilation with propofol and constriction with ketamine, associated with exaggerated changes in arterial pressure. Thus, dysfunctional control mechanisms at the level of the microcirculation alter responses to anaesthesia during hypertension.