南 浩一郎

BACKGROUND: Feedback devices are used to improve the quality of chest compression (CC). However, reports have noted that accelerometers substantially overestimate depth when cardiopulmonary resuscitation (CPR) is performed on a soft surface. Here, we determined whether a flexible pressure sensor could correctly evaluate the depth CC performed on a mannequin placed on a mattress. METHODS: Chest compression was performed 100 times/min by a compression machine on the floor or a mattress, and the depth of CC was monitored using a flexible pressure sensor (Shinnosukekun) and CPRmeter(™). The depth of machine-performed CC was consistently 5cm. We compared data from the feedback sensor with the true depth of CC using dual real-time auto feedback system that incorporated an infrared camera (CPR evolution(™)). RESULTS: On the floor, the true depth of CC was 5.0±0.0cm (n=100), or identical to the depth of CC performed by the machine. The Shinnosukekun(™) measured a mean (±SD) CC depth of 5.0±0.1cm (n=100), and the CPRmeter(™) measured a depth of 5.0±0.2cm (n=100). On the mattress, the true depth of CC was 4.4±0.0cm (n=100). The Shinnosukekun(™) measured a mean CC depth of 4.4±0.0cm (n=100), and the CPRmeter(™) measured a depth of 4.7±0.1cm (n=100). The data of CPRmeter(™) were overestimated (P<.0001 between the true depth and the CPRmeter(™)-measured depth). CONCLUSION: The Shinnosukekun(™) could correctly measure the depth of CC on a mattress. According to our present results, the flexible pressure sensor could be a useful feedback system for CC performed on a soft surface.

Tramadol is an analgesic that is used worldwide for pain, but its mechanisms of action have not been fully elucidated. The majority of studies to date have focused on activation of the μ-opioid receptor (μOR) and inhibition of monoamine reuptake as mechanisms of tramadol. Although it has been speculated that tramadol acts primarily through activation of the μOR, no evidence has revealed whether tramadol directly activates the μOR. During the past decade, major advances have been made in our understanding of the physiology and pharmacology of ion channels and G protein-coupled receptor (GPCR) signaling. Several studies have shown that GPCRs and ion channels are targets for tramadol. In particular, tramadol has been shown to affect GPCRs. Here, the effects of tramadol on GPCRs, monoamine transporters, and ion channels are presented with a discussion of recent research on the mechanisms of tramadol.