Open AccessThe Differential Effects of Prostaglandin E1 and Nitroglycerin on Regional Cerebral Oxygenation in Anesthetized Patients
Author(s) -
Yuji Kikuchi,
Shigeru Saito,
Toshihiro Morita,
Takasuke Imai,
Huminori Kawahara,
Nao Fujita,
Fumio Goto
Publication year - 1997
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1097/00000539-199711000-00017
Subject(s) - medicine , nitroglycerin (drug) , oxygenation , anesthesia , prostaglandin e1 , differential (mechanical device) , differential effects , cardiology , engineering , aerospace engineering
We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS). Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P < 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P < 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values.