[Rebound hypertension after controlled hypotension and its prevention by captopril]

In 27 patients undergoing ear, nose and throat surgery, the problem of post-hypotensive hypertension (rebound hypertension) following vasodilator-induced controlled hypotension was studied, together with prevention by the ACE inhibitor captopril. Hypotension was induced by sodium nitroprusside (SNP) in seven patients (group 1) and by nitroglycerin (NTG) in ten patients (group 3). Ten patients (group 2) received 25 mg captopril given orally, together with the preanaesthetic medication, as well as SNP. The degree and duration of the decrease in blood pressure did not differ significantly between groups. After discontinuation of the respective vasodilators, blood pressure had increased to above prehypotensive levels in both group 1 (SNP) and group 3 (NTG) 30 min afterward and, to a more marked extent, 60 min afterward. In these groups plasma renin activity (PRA) increased continuously during the hypotensive period up to 11.4 +/- 2.4 and 19.5 +/- 4.5 ng/ml/h, respectively, and had not yet reached its prehypotensive value 60 min after discontinuation. In group 2 (captopril/SNP) there was no overshoot hypertension on discontinuation of SNP, and the average infusion rate of SNP was reduced. PRA was markedly higher than in groups 1 and 3 (peak level 27.9 +/- 6.5 ng/ml/h) due to inhibition of the feedback mechanism in the renin-angiotensin system. From the results it may be concluded that both SNP and NTG can cause rebound hypertension, the extent of which depends on the level of hypotension previously achieved and the infusion rate of the vasodilator. Pretreatment with captopril prevents the rebound and reduces the dosage of vasodilator required and, therefore, may be considered an alternative to the well-documented beta-adrenergic blockers.