Biceps femoris (BF) and masseter muscle (MM) are the mixture of slow oxidative and fast-twitch fibres. Compared with MM, BF had the significantly higher expression of myosin heavy chain (MyHC) fast IIx and IIb isoforms (MyHCIIx and MyHCIIb), but lower expression of MyHC slow isoform (MyHCI) and fast IIa isoform (MyHCIIa). The objective of this study was to investigate the expression pattern of troponin I (TnI) slow-twitch isoform (TNNI1) and fast-twitch isoform (TNNI2) in BF and MM of Yorkshire and Meishan pigs which differed significantly in the growth rate. The expression of the TNNI1 and TNNI2 peaked at the postnatal 35 days in Yorkshire pigs and postnatal 60 days in Meishan pigs. The expression of TNNI1 and TNNI2 in Meishan pigs was significantly higher than that in Yorkshire pigs at the foetal 60 days, while the opposite occurred at postnatal 35 days. The expression ratio of TNNI1 relative to TNNI2 favoured TNNI2 expression in BF and MM regardless of Yorkshire and Meishan pigs. TNNI1 expression in MM was significantly higher than that in BF at 60, 120 and 180 days in Meishan pigs and at 120 and 180 days in Yorkshire pigs. On the contrary, no significant difference of TNNI2 expression in BF and MM was found except for Yorkshire pigs of 180 days. This study provided the foundation for future research on TnI isoforms as the model gene to study mechanisms of muscle fibre-specific gene regulation in pigs.

Summary

Background and objective: Isoflurane has been shown experimentally to protect the myocardium against infarction but the clinical relevance of these findings is not yet well established. We therefore evaluated the effects of isoflurane administration before cardiopulmonary bypass (CPB) on postoperative cardiac troponin I (cTnI) release and clinical outcome in a large group of adult patients scheduled for cardiac surgery.

Methods: Three hundred and fifty-nine consecutive patients were included prospectively in an open observational study and divided into two groups according to whether or not isoflurane was administered before CPB. Postoperative cTnI release, in-hospital mortality, time to discharge from hospital, time to extubation and non-fatal postoperative cardiac events (number of internal cardioversions, need for inotropic support, ischaemic events, dysrhythmias and/or conduction abnormalities) were recorded.

Results: Two hundred and twenty-one (62%) patients did not receive isoflurane and 138 (38%) received isoflurane (1.3% [1.0–1.8%] minimum alveolar concentration over 22 [15–33] min). Postoperative cTnI release was not significantly different between the control and isoflurane groups (5.9 [1.0–336.8] vs. 6.0 [1.5–392.0] ng mL−1, P = 0.88). No significant differences were found in non-fatal cardiac events (63% vs. 57%, P = 0.22) and in-hospital mortality (1.8% vs. 1.4%, P = 0.79) between the control and isoflurane groups.

Conclusions: No significant effect was observed on postoperative cTnI release and in-hospital outcome when isoflurane was added to standardized intravenous anaesthesia before CPB in adult patients undergoing cardiac surgery.