D. Annane et al., Impaired pressor sensitivity to noradrenaline in septic shock patients with and without impaired adrenal function reserve, BR J CL PH, 46(6), 1998, pp. 589-597
Aims To investigate the relationship between adrenal gland function and pre
sser response to noradrenaline in septic shock.
Methods Basal cortisol level, noradrenaline-mean arterial pressure dose-res
ponse curve and cortisol response to intravenous corticotrophin bolus were
obtained in nine patients fulfilling usual criteria for septic shock and in
six normal volunteers. In patients with septic shock, dose-response curve
to noradrenaline was determined a second time 60 min after a 50 mg intraven
ous hydrocortisone bolus.
Results As compared with controls, patients with septic shock had increased
basal cortisol levels (mean+/-s.d.: 1564+/-818 vs 378+/-104 nmol l(-1) P=0
.002, 95% confidence interval for difference in means: [452, 1920]) and a b
lunted cortisol response to corticotrophin (403+/-461 vs 1132+/-195 nmol l(
-1), P=0.008, [-1163, -295]). Five patients had impaired adrenal function r
eserve. As compared with controls, septic patients displayed a moderate and
non significant decrease in presser sensitivity to noradrenaline (P=0.112)
. As compared with patients with adequate adrenal response, patients with i
mpaired adrenal function reserve showed a significant decrease in presser s
ensitivity to noradrenaline (P=0.038). In septic patients, hydrocortisone i
mproved presser response to noradrenaline (P=0.032). This effect was more m
arked in patients with impaired adrenal function reserve so that, as compar
ed with patients with adequate response, the difference was no longer signi
ficant (P=0.123).
Conclusions In septic shock, impaired adrenal function reserve may partly b
e accounted for by the depressed presser sensitivity to noradrenaline. The
latter may be substantially improved by physiological doses of hydrocortiso
ne.