Effects of nicardipine-induced hypotension on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus under sevoflurane anesthesia.
OBJECTIVE
The purpose of this study was to examine the effects of nicardipine-induced hypotension on cerebrovascular CO2 reactivity in patients with diabetes mellitus under sevoflurane anesthesia.


METHODS
Nineteen diabetic patients, and 11 nondiabetic patients (serving as controls), undergoing elective orthopedic, cardiovascular, or thoracic surgery were included in the study. The diabetic patients were divided into three groups according to the antidiabetic therapy they were receiving, i.e., diet therapy (n = 6), oral antidiabetic drugs (n = 7), and insulin (n = 6). Anesthesia was maintained with 1.0 minimum alveolar concentration of sevoflurane. Absolute and relative cerebrovascular CO2 reactivity was calculated using a 2.5-MHz pulsed transcranial Doppler (TCD) probe for the continuous measurement of mean blood flow velocity in the middle cerebral artery (Vmca). The cerebrovascular CO2 reactivity was measured both at baseline and during hypotension by increasing the ventilatory frequency by 4 to 7 breaths.min(-1). Nicardipine was used to induce hypotension.


RESULTS
We found that values for the Bispectral index (BSI), baseline mean blood pressure, endtidal CO2 (Pet(CO2)), and Vmca were essentially identical in all patients, irrespective of the type of antidiabetic treatment being taken. Values for absolute and relative CO2 reactivity in insulin-dependent patients, at both baseline blood pressure and during hypotension, were lower than those in patients in the antidiabetic drug, diet, and control groups (during hypotension, absolute CO2 reactivity: diet group: 3.2 +/- 0.9; oral antidiabetic drug group: 3.2 +/- 0.7; insulin group: 1.5 +/- 0.6; control group: 3.4 +/- 0.8 cm.s(-1).mmHg(-1), [P < 0.05 insulin group vs the other groups]; relative CO2 reactivity: diet group, 6.3 +/- 1.0; oral antidiabetic drug group, 6.5 +/- 0.8; insulin group, 3.5 +/- 0.8; control group, 6.5 +/- 0.7%.mmHg(-1), [P < 0.05 insulin group vs the other groups].


CONCLUSIONS
We concluded that cerebrovascular CO2 reactivity in insulin-dependent patients is impaired during nicardipine-induced hypotension under sevoflurane anesthesia.
Kadoi
Yuji
Y
Department of Anesthesiology, Gunma University, Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
Goto
Fumio
F
D000368:Aged; D018685:Anesthetics, Inhalation; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D003920:Diabetes Mellitus / Q000097:blood / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology; D017558:Elective Surgical Procedures; D006801:Humans; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology*; D008738:Methyl Ethers; D008875:Middle Aged; D016343:Monitoring, Intraoperative; D009529:Nicardipine / Q000494:pharmacology*; D000077149:Sevoflurane
D018685:Anesthetics, Inhalation; D000959:Antihypertensive Agents; D008738:Methyl Ethers; D002245:Carbon Dioxide; D000077149:Sevoflurane; D009529:Nicardipine