Role of mitochondrial KATP channels and protein kinase C in ischaemic preconditioning.

1. Activation of mitochondrial KATP (mitoKATP) channels and protein kinase C (PKC) has been implicated in cardioprotective mechanisms of ischaemic preconditioning (IPC). However, the exact role of these events in early IPC remains unclear. 2. Isolated and perfused rat hearts underwent IPC with three cycles of 5 min ischaemia and 5 min reperfusion. The heart was subjected to 30 min global ischaemia followed by 120 min reperfusion. Flavoprotein oxidation was monitored to assess mitoKATP channel activity. Cardioprotection was evaluated by recovery of isovolumic left ventricular (LV) function and infarct size. 3. Diazoxide (50 mgr;mol/L) increased flavoprotein oxidation and conferred cardioprotection in a manner sensitive to the selective mitoKATP channel blocker 5-hydroxydecanoate (5-HD; 0.5 mmol/L). 4. Pretreatment with 0.5 mmol/L 5-HD abrogated IPC-induced flavoprotein oxidation and cardioprotection, whereas late treatment with 5-HD after IPC required a higher dose (2 mmol/L) to abolish flavoprotein oxidation and cardioprotection afforded by IPC. 5. Pretreatment with the PKC inhibitors Ro318425 (1 micro mol/L) and chelerythrine (5 micro mol/L) abolished IPC-induced flavoprotein oxidation and cardioprotection, whereas late treatment with Ro318425 required a higher dose (4 micro mol/L) to abolish flavoprotein oxidation and cardioprotection. 6. In conclusion, these results suggest that activation of mitoKATP channels is the trigger and the mediator of IPC and that PKC plays a crucial role in both phases of mitoKATP channel activation, although mitoKATP channels and PKC may be more activated during the mediator phase.

[Anesthesia for a severe ankylosing spondylitis patient whose posture had been restricted to only sitting for over 20 years].

A 42-year-old woman with an Arnold-Chiari abnormality was scheduled for cervical spine surgery. She had severe ankylosing spondylitis, and all her joints from ankles to occipitocervical joint were fixed except hip joints, which had been replaced with artificial joints 20 years before. She could bend her upper body only in a range from -20 to 70 degree from the sitting position. Her posture had been restricted to only sitting for over 20 years, and she complained vertigo when positioned in supine position. The trachea was intubated with an aid of bronchofiberscopy under sedation in sitting position, and then anesthesia was induced with propofol and fentanyl. When she was turned to prone position, nasal bleeding was noticed and the surgery was performed in a modified sitting position. The intra- and post-operative course was uneventful. The present case indicates that long-term restriction only to sitting position modulates circulatory control in response to changing postures, and that preoperative evaluation for appropriate posture for surgery is mandatory.