2004 Fiscal Year Final Research Report Summary
AUTONOMIC NERVE ACTIVITY AND PLATELET ACTIVATION RELATED TO THE PERIOPERATIVE CORONARY SPASM IN THE PATIENTS WITH ISCHEMIC HEART DISEASE
Grant-in-Aid for Scientific Research (C)
|Allocation Type||Single-year Grants |
|Research Institution||Kurume University |
WATANABE Seiji KURUME UNIVERSITY, MEDICINE, ASSISTANT PROFESSOR, 医学部, 助教授 (10201196)
YAMADA Shinichi KURUME UNIVERSITY, MEDICINE, ASSISTANT, 医学部, 助手 (90258484)
HARA Masato KURUME UNIVERSITY, MEDICINE, ASSISTANT, 医学部, 助手 (15790839)
HIRAKI Teruyuki KURUME UNIVERSITY, MEDICINE, ASSISTANT, 医学部, 助手 (30320237)
KANO Tatsuhiko KURUME UNIVERSITT, MEDICINE, PROFESSOR, 医学部, 教授 (50040605)
|Project Period (FY)
2002 – 2004
|Keywords||Coronary spasm / Autonomic activity / Platelet / Myocardial ischemia / Ischemic heart disease / Anesthesia / 経食道心臓超音波検査|
Etiology of coronary spasm is still unknown. Therefore, we investigated whether the autonomic activity or platelet activity related to the occurrence of the coronary spasm during perioperative period. For this purpose, we carried out the following.
1.We constructed the simultaneous recording system and the particle and dense analysis in the regional area for interest on visual images of the transesophageal echocardiography, ECGs, and analog pressure wave forms on the mobile PC.
2.We examined whether vascular endothelial dilatation was impaired with hypothermia during CPB, which might cause the prolonged hypoperfusion of myocardium after CPB. In conclusion, these results indicated that the blunting of the vascular response to Ach was more prominent than that to TNG in deep hypothermic CPB. This suggests that deep hypothermic CPB caused severe impairment to the endothelial function than to the smooth muscle function.
3.We investigated whether even a smaller production of heparin and protami
n complex(HPC) in patients with off-pump CABG would affect platelet function, by comparing in patients with on-pump CABG. Although a small dose of heparin activated the platelet function, a reduced production of HPC, estimated by smaller doses of hepain and protamin, did inhibit platelet function even in off-pump CABG.
4.Parasympathetic activity augmented, but sympathetic activity did not change during anesthesia induction with using RR-inteirval analysis. Therefore, there was less possibility to induce coronary spasm during anesthesia induction. During the tracheal intubation, parasympathetic activity increased with accompanying augmentation of sympathetic activity. Although myocardial ischemia did not detect either situation, there was a possibility to induce the coronary spasm during tracheal intubation dependent on the balance of sympathetic and parasympathetic activation in the patients with ischemic heart disease. Further investigation is necessary for the determination of the other triggering of coronary spasm except anesthesia induction and tracheal intubation during anesthesia. Less