We investigated the levels of nitrosyl hemoglobin (HbNO) in rat jugular blood by electron spin resonance (ESR) spectroscopy during and after middle cerebral artery occlusion. The levels of plasma nitric oxide (NO) end products, nitrate plus nitrate, were compared with the levels of HbNO. Small amounts of HbNO were detected in sham-operated rats (n=4) and those subjected to 2 h of occlusion (n=4), whereas nitrite plus nitrate was increased only in the latter (P<0.01; vs.sham). Upon reperfusion after 2 h of occlusion both HbNO and nitrite plus nitrate clearly increased after 15 min (n=4) and 30 min (n=6) reperfusion (P<0.01; vs.occlusion). Administration of superoxide dismutase (5 mg/kg) significantly increased HbNO (P<0.05) but not plasma nitrate plus nitrate (n=5). The increase in HbNO suppressed by administration of NG-nitro-L-arginine methyl ester (20mg/kg; n=4,P<0.01), and this suppression could be reversed by L-arginine (200 mg/kg) (n=4). The present study clearly showed that the L-arginine-NO synthase pathway was activated during reperfusion after focal cerebral ischemia and indicated the involvement of a reaction between NO and superoxide during early reperfusion.

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Objectives‘Quality Cardiopulmonary Resuscitation (QCPR) Classroom’ was recently introduced to provide higher-quality Cardiopulmonary Resuscitation (CPR) training. This study aimed to examine whether novel QCPR Classroom training can lead to higher chest-compression quality than standard CPR training.DesignA cluster randomised controlled trial was conducted to compare standard CPR training (control) and QCPR Classroom (intervention).SettingLayperson CPR training in Japan.ParticipantsSix hundred forty-two people aged over 15 years were recruited from among CPR trainees.InterventionsCPR performance data were registered without feedback on instrumented Little Anne prototypes for 1 min pretraining and post-training. A large classroom was used in which QCPR Classroom participants could see their CPR performance on a big screen at the front; the control group only received instructor’s subjective feedback.Primary and secondary outcome measuresThe primary outcomes were compression depth (mm), rate (compressions per minute (cpm)), percentage of adequate depth (%) and recoil (%). Survey scores were a secondary outcome. The survey included participants’ confidence regarding CPR parameters and ease of understanding instructor feedback.ResultsIn total, 259 and 238 people in the control and QCPR Classroom groups, respectively, were eligible for analysis. After training, the mean compression depth and rate were 56.1±9.8 mm and 119.2±7.3 cpm in the control group and 59.5±7.9 mm and 116.8±5.5 cpm in the QCPR Classroom group. The QCPR Classroom group showed significantly more adequate depth than the control group (p=0.001). There were 39.0% (95% CI 33.8 to 44.2; p<0.0001) and 20.0% improvements (95% CI 15.4 to 24.7; P<0.0001) in the QCPR Classroom and control groups, respectively. The difference in adequate recoil between pretraining and post-training was 2.7% (95% CI −1.7 to 7.1; pre 64.2±36.5% vs post 66.9%±34.6%; p=0.23) and 22.6% in the control and QCPR Classroom groups (95% CI 17.8 to 27.3; pre 64.8±37.5% vs post 87.4%±22.9%; p<0.0001), respectively.ConclusionsQCPR Classroom helped students achieve high-quality CPR training, especially for proper compression depth and full recoil. For good educational achievement, a novel QCPR Classroom with a metronome sound is recommended.

Excessive levels of reactive oxygen species (ROS) and impaired Ca2+ homeostasis play central roles in the development of multiple cardiac pathologies, including cell death during ischemia-reperfusion (I/R) injury. In several organs, treatment with 2-aminoethoxydiphenyl borate (2-APB) was shown to have protective effects, generally believed to be due to Ca2+ channel inhibition. However, the mechanism of 2-APB-induced cardioprotection has not been fully investigated. Herein we investigated the protective effects of 2-APB treatment against cardiac pathogenesis and deciphered the underlying mechanisms. In neonatal rat cardiomyocytes, treatment with 2-APB was shown to prevent hydrogen peroxide (H2O2) -induced cell death by inhibiting the increase in intracellular Ca2+ levels. However, no 2-APB-sensitive channel blocker inhibited H2O2-induced cell death and a direct reaction between 2-APB and H2O2 was detected by 1H-NMR, suggesting that 2-APB chemically scavenges extracellular ROS and provides cytoprotection. In a mouse I/R model, treatment with 2-APB led to a considerable reduction in the infarct size after I/R, which was accompanied by the reduction in ROS levels and neutrophil infiltration, indicating that the anti-oxidative properties of 2-APB plays an important role in the prevention of I/R injury in vivo as well. Taken together, present results indicate that 2-APB treatment induces cardioprotection and prevents ROS-induced cardiomyocyte death, at least partially, by the direct scavenging of extracellular ROS. Therefore, administration of 2-APB may represent a promising therapeutic strategy for the treatment of ROS-related cardiac pathology including I/R injury.

Pharmacologic activation of delta-opioid receptors affords improvement of functional protection in isolated working rat hearts similar to that conferred by classic ischemic preconditioning. The combination of both pretreatments reduces ischemic cellular damage and further adds to postischemic functional recovery. These changes are reversed by naloxone, an observation providing evidence that ischemic preconditioning involves signaling through opioid receptors.