RESUMO
The current study aimed to investigate the effect of sepsis on rat serotonin (5-HT) responses and cardiac action potentials. A total of 20 rats were randomly divided into a sepsis and control group (each, n=10). Rat hearts were harvested and perfused using the Langendorff method 18-h after the induction of sepsis, which was assessed using cecal puncture. Cardiac action potential was subsequently measured using a multichannel electrophysiology instrument. Immunohistochemistry and quantitative analysis were performed to identify the effect of sepsis on myocardial 5-HT expression. The results revealed that mitochondrial changes were present in septic rat hearts. Heart rate (361.10±12.29 bpm vs. 348.60±12.38 bpm; P<0.05) was significantly higher, atrial action potential duration (106.40±2.95 ms vs. 86.60±4.12 ms; P<0.01) was significantly longer and the area (0.62±0.06 µm2 vs. 0.39±0.05 µm2; P<0.05) and number (0.92±0.02/field vs. 0.46±0.01/field; P<0.01) of myocardial cells were significantly higher in the septic compared with the control group. These results demonstrated that 5-HT prolongs the atrial action potential, increases heart rate and aggravates myocardial injury, indicating that it may therefore be one of the factors that leads to cardiac dysfunction in sepsis.
RESUMO
PURPOSE: Although hyperhomocysteinemia (Hhcy) is a risk factor for cerebral infarction, its effect on recurrent cerebral infarction is less-defined. We aimed to investigate the association of Hhcy and increased risk of recurrent cerebral infarct. MATERIALS AND METHODS: From 2011 to 2013, we recruited 231 primary cerebral infarct patients that were divided to a Hhcy group (n = 105) and a control group (n = 126) according to plasma homocysteinemia (Hcy) levels exceeding 15 µmol/L. In this prospective study, risk factors such as gender, age, blood lipid and glucose levels, history of diabetes, high blood pressure, smoking habits and plasma Hhcy levels were determined. A three-year follow-up compared differences in cerebral infarction recurrence rates. Statistical analyses identified whether plasma Hhcy levels were an independent risk factor for recurrent cerebral infarction. RESULTS: Triglyceride and low-density lipoprotein (LDL) levels in the Hhcy group were significantly higher than controls, and cerebral infarct recurrence rates in the Hhcy group exceeded control subject rates through the three-year follow-up (p = .021, p = .036 and p = .025). Cox proportional hazards modeling showed that elevated Hhcy levels (hazard ratio [HR] = 3.062, p < .001), increased age (HR = 1.069, p < .01), circulating triglyceride levels (HR = 1.686, p = .048), and relative National Institutes of Health Stroke (NIHSS) score (HR = 1.068, p = .016) were risk factors for recurrent cerebral infarction. CONCLUSIONS: Level of Hhcy was a risk factor for recurrent cerebral infarction. Further, particular demographic and clinical outcomes including age, relative NIHSS scores, and circulating triglyceride levels were markedly associated with the occurrence of cerebral infarction.
