Background: Hydrogen sulfide poisoning can cause severe myocardial injury, but the damage is subtle and can be easily misdiagnosed. This report presents the dynamic observation of myocardial injury associated with hydrogen sulfide poisoning. Case report: Two young men presented with symptoms of “lightning-like” death immediately after entering a tank. They were found and rescued in 20 min at a time when they were already in a coma. Case 1 had no spontaneous breathing and pulse, while case 2 had spontaneous breathing and a pulse. Upon transfer to a local hospital, case 1 received continuous cardiopulmonary resuscitation which led to the recovery of his heart rate 3 min after arriving at the hospital. However, the patient remained in a Glasgow coma scale of 3. He was transferred to our hospital where he, unfortunately, died on the seventh day due to multiple organ failure. Case 2 was also transferred to the intensive care unit in our hospital and on the fourth day of hospitalization, the patient presented ST-segment elevation and dynamic changes in markers of myocardial injury. Changes in electrocardiogram and markers of myocardial injury were monitored and examination improved through conventional echocardiography, coronary artery CT, radionuclide myocardial perfusion imaging, and two-dimensional speckle tracking imaging strain. The treatment gradually improved the patient’s myocardial injury and was discharged from the hospital. Conclusion: Hydrogen sulfide poisoning can cause damage to myocardial function and the damage can be more insidious in nature and with a delayed onset. Recovery from myocardial damage can be very slow.
seventy patients with heat-related illness were treated at Jinshan Hospital of Fudan University, and their epidemiological characteristics, laboratory results, treatment and prognosis were retrospectively analyzed. RESULTS:In the 70 patients, 18 patients suffered from heat stroke and 52 patients from nonheat stroke. When the environmnent temperature was above 35 °C, the body temperature of the patients began to increase markedly. The patients with heat stroke were significantly older than those with non-heat stroke (P<0.05). The body temperature, heart rate, blood glucose, blood lactate dehydrogenase and blood creatine kinase in the patients with heat stroke were higher than those in the patients with non-heat stroke (P<0.05). Blood lactate dehydrogenase and blood creatine kinase were positively correlated with body temperature (r=0.801).CONCLUSION: When the environmental temperature goes above 35 °C, heat-related illness should be prevented, especially in the elderly. The body temperature, heart rate, blood glucose, blood lactate dehydrogenase and blood creatine kinase in patients with heat stroke are higher than those in patients with non-heat stroke. Blood lactate dehydrogenase and blood creatine kinase are positively correlated with body temperature, but their relationship with heat-related illness awaits further study.
Ischemia/reperfusion (I/R) damage induced by stroke poses a serious hazard to human life, while mechanism of blood-brain barrier (BBB) dysfunction is still unknown. To imitate stroke induced ischemia conditions in vivo , the rat model of cerebral I/R damage was created by middle cerebral artery occlusion (MCAO). In vitro , the rat microvascular endothelial cell line bEND.3 was subjected to oxygen-glucose deprivation/reperfusion (OGD/R). Evans blue was used to evaluate the permeability of the blood-brain barrier (BBB). To evaluate gene expression at the mRNA and protein levels, researchers used real-time PCR and western blotting. Infarct volume and BBB permeability were considerably higher in cerebral (I/R) animals than in the Sham group. Exosomal miR-370-3p expression was shown to be higher in the brains of I/R injured rats and OGD/R treatment bEND.3. The BBB permeability was considerably increased when miR-370-3p was downregulated in OGD/R pretreated bEND.3. miR-370-3p regulates MAPK1 expression by targeting it. In bEND.3, OGD/R therapy increased BBB permeability substantially. OGD/R was inhibited by miR-370-3p mimic transfection, while miR-370-3p mimic was abolished by co-transfection with MAPK1 overexpression lentivirus. In cerebral I/R damage, exosomal miR-370-3p targets MAPK1 and aggregates BBB permeability.
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