Effect of polymorphism of angiotensin Ⅱ type Ⅰreceptor gene A1166C on arterial Mood pressure during cardiopulmonary bypass
- VernacularTitle:血管紧张素Ⅱ受体A1166C基因多态性对体外循环中血压的影响
- Author:
Shouyong WANG
;
Shirhai ZHANG
;
Shanglong YAO
- Publication Type:Journal Article
- Keywords:
Receptors,angiotensin;
Polymorphism (genetics);
Cardiopulmonary bypass;
Blood pressure
- From:
Chinese Journal of Anesthesiology
1994;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of polymorphism of angiotensin Ⅱtype Ⅰ receptor (AT1R) gene A1166C on arterial blood pressure during cardiopulmonary bypass (CPB).Methods Eighty-two patients (46 male, 36 female) aged 17-55 yr undergoing surgical correction of congenital heart disease or valve replacement under moderate hypothermic CPB were studied. Blood sample was taken from each patient and gene type was identified by polymerase chain reaction and restriction fragment length polymorphism (PCR-RLFP) method. The patients were divided into mutation group and normai group according to whether there was an A→C replacement in 1166 position of the AT1R gene code. MAP was continuously recorded at 1 min intervals during CPB. The plasma level of angiotensin Ⅱ was measured before and 40 min after CPB was started. The relationship between the AT1R polymorphism and the fluctuation in MAP was analyzed. Results There were 7 heterozygote patients with AC gene type (mutation group) and 75 homozygote patients with AA gene type ( normal group) . The average MAP in mutation group ( n = 7) was 64 ?5 mm Hg, significantly higher than that in normal group [ (58 ? 8) mm Hg] . The amount of phentolamine given was significantly larger in mutation group. The plasma level of angiotensin Ⅱ was significantly increased during CPB as compared with the baseline level before CPB. There was no significant difference in plasma angiotensin Ⅱ level between the two groups either before or during CPB. Conclusion AT1R A1166C polymorphism results in significant increase in MAP during CPB and may be partly responsible for hyperperfusion.
