Cardioprotective effect of nicorandil against myocardial injury following cardiac arrest in swine.

INTRODUCTION: Nicorandil, a vasodilatory drug used to treat angina, was reported to protect against myocardial ischemia-reperfusion injury in various animal models. However, its cardioprotective action following cardiac arrest is unknown. We examined the cardioprotective effects of nicorandil in a porcine model of cardiac arrest and resuscitation. METHODS: Ventricular fibrillation was induced electrically for 4min in anesthetized domestic swine, followed by cardiopulmonary resuscitation. Sixteen successfully resuscitated animals were randomized to saline control (n=8) or nicorandil (n=8) groups. Nicorandil (150µg/kg) was administered by central intravenous injection at onset of restoration of spontaneous circulation (ROSC), followed by 3µg/kg/min infusion until reperfusion end. Sham-operated animals received surgery only (n=4). Hemodynamic parameters were monitored continuously. Blood samples were taken at baseline, 5, 30, 180, and 360min after ROSC. Left ventricular ejection fraction was assessed by echocardiography at baseline and 6h after ROSC. The animals were euthanized 6h after ROSC, and the cardiac tissue was removed for analysis. RESULTS: 6 h after ROSC, nicorandil had significantly improved all hemodynamic variables (all P<0.05) except the maximum rate of left ventricular pressure decline and heart rate (P>0.05) compared with the control group. Control animals showed elevated cardiac troponin I and lactate levels compared with sham animals, which were significantly decreased following nicorandil treatment (P<0.05). In the saline control group, the adenosine triphosphate (ATP) content was largely reduced but subsequently rescued by nicorandil (P<0.05). Histopathologic injury was reduced with nicorandil treatment. Nicorandil reduced cardiomyocyte apoptosis as evidenced by reduced terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells, decreased Bax and caspase-3 expression, and increased Bcl-2 expression in the myocardium (all P<0.05). CONCLUSION: Nicorandil exhibited cardioprotective effects on myocardial injury following cardiac arrest via improvement in post-resuscitation myocardial dysfunction and energy metabolism, reduction in myocardial histopathologic injury, and antiapoptotic effects.

[MRI diagnosis of multiple cerebral sclerosis].

OBJECTIVE: To investigate the magnetic resonance imaging (MRI) feature of multiple cerebral sclerosis (MS) for better understanding and diagnosis of this disease. METHODS: The MRI data of 32 patients with MS were reviewed. Conventional scanning with T1WI, T2WI, Flair sequence was performed, and 26 patients underwent Gd-DTPA enhanced scanning. The MS plaques were analyzed for their locations, sizes, shapes, MR signals and enhanced features, space-occupying signs, and the related corpus callosum changes and brain atrophy. Descriptive statistical method was used for all the data. RESULTS: MRI identified MS lesions in the brain in 30 cases, with the sensitivity of 93.75%. All the MS patients had multiple lesions with predilection sites of the cortical/juxtacortical and periventricle areas, the centrum semiovale, and the corpus callosum. Most of the MS plaques were round or oval of different sizes. Bilateral lesions were almost symmetrical in distribution. Twenty patients had "rectangular demyelination" and 12 had "dirty white matter" signs, and 11 had both manifestations. The lesions were isointense, slightly hypointense or hypointense on T1WI, and hyperintense on T2WI and Flair sequences. Most of the MS plaques presented no enhancement, with occasional nodular or circular enhancement. No or slight space-occupying effect was found in the plaques. Of the 28 MS patients undergoing sagittal scanning of the corpus callosum, 17 presented with abnormal signals, with the sensitivity of 60.71% (17/28). Five patients had corpus callosum atrophy, and 10 had brain atrophy of different degrees. CONCLUSION: These results suggest that the corpus callosum is often compromised by the MS lesions to present diffusive, nodular, radiating signal abnormalities and irregular ependymal thickening, which can be most obvious with sagittal FLAIR imaging.