Comparative analysis of organophosphorus versus carbamate pesticide poisoning: a case study.

Organophosphorus poisoning is a critical condition that can cause central nervous system depression, respiratory failure, and death early on. As its clinical manifestations closely resemble those of carbamate pesticide poisoning, the aim of this case study is to present a case of misdiagnosis, initially identifying carbofuran poisoning as organophosphate in a patient suspect of a heatstroke. We also present a case of intentional self-poisoning with organophosphate dichlorvos to underline the likelihood of pesticide poisoning in patients exhibiting acute cholinergic symptoms when the ingested substance is not known. In such cases, empirical treatment with atropine and oxime can be started pending timely differential diagnosis to adjust treatment as necessary.

The association between higher cardiac troponin levels and the development of left ventricular diastolic dysfunction in septic patients with diabetes mellitus.

This study was designed to retrospectively analyze the relationship between the levels of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) and the development of left ventricular diastolic dysfunction (LVDD) in septic patients with diabetes mellitus. Furthermore, the predictive value of cTnT and cTnI in the LVDD development in those patients was investigated. The clinical information of 159 septic patients with diabetes mellitus treated in the intensive care unit of Affiliated Hospital of Chengde Medical University from June 2016 to January 2023 were retrospectively analyzed. These patients were separated into LVDD group (LVFP > 15 mmHg) and non-LVDD group (LVFP ≤ 15 mmHg) based on left ventricular filling pressure (LVFP). The differences in clinical data, echocardiographic parameters, as well as cTnT and cTnI levels between the LVDD and non-LVDD groups were compared. The relationship between the cTnT and cTnI levels and the echocardiographic parameters was studied using Pearson correlation analysis. Logistic regression analysis was conducted to explore the factors that influenced the LVDD development in septic patients with diabetes. Receiver operator characteristic (ROC) curves were created to evaluate the predictive value of cTnT and cTnI levels for the LVDD development in septic patients with diabetes. Totally 159 septic patients with diabetes were included in this study, with 97 patients in the LVDD group and 62 in the non-LVDD group. Compared with the non-LVDD group, patients in the LVDD group had much lower left ventricular (LV) early diastolic peak inflow velocity (E), LV advanced diastolic peak inflow velocity (A), E/A, and early diastolic mitral annular velocity (Em) while significantly higher E/Em. The LVDD group showed much higher levels of cTnI and cTnT than the non-LVDD group (P < 0.05). Significant positive correlation between log10cTnI level and E/Em ratio (r = 0.425, P < 0.001) was revealed by the Pearson correlation analysis. Multivariate analysis showed that E/A, E/Em, cTnI and cTnT were independent risk factors for the LVDD development in septic patients with diabetes (P < 0.05). As for ROC curve results, the area under the curve (AUC) of cTnT to predict the development of LVDD in septic patients with diabetes was 0.849 (95% CI 0.788-0.910, P < 0.001); the AUC of cTnI was 0.742 (95% CI 0.666-0.817, P < 0.001). Both cTnT and cTnI are independent risk factors and have predictive value for the LVDD development in septic patients with diabetes mellitus.

Effect of tumor necrosis factor-α on neutralization of ventricular fibrillation in rats with acute myocardial infarction.

The purpose of this study was to explore the effects of tumor necrosis factor-α (TNF-α) on ventricular fibrillation (VF) in rats with acute myocardial infarction (AMI). Rats were randomly classified into AMI group, sham operation group and recombinant human tumor necrosis factor receptor:Fc fusion protein (rhTNFR:Fc) group. Spontaneous and induced VFs were recorded. Monophasic action potentials (MAPs) among different zones of myocardium were recorded at eight time points before and after ligation and MAP duration dispersions (MAPDds) were calculated. Then expression of TNF-α among different myocardial zones was detected. After ligation of the left anterior descending coronary artery, total TNF-α expression in AMI group began to markedly increase at 10 min, reached a climax at 20-30 min, and then gradually decreased. The time-windows of VFs and MAPDds in the border zone performed in a similar way. At the same time-point, the expression of TNF-α in the ischemia zone was greater than that in the border zone, and little in the non-ischemia zone. Although the time windows of TNF-α expression, the MAPDds in the border zone and the occurrence of VFs in the rhTNFR:Fc group were similar to those in the AMI group, they all decreased in the rhTNFR:Fc group. Our findings demonstrate that TNF-α could enlarge the MAPDds in the border zone, and promote the onset of VFs.

Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo.

BACKGROUND: Acute myocardial infarction (AMI) is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-α (TNF-α) on ventricular arrhythmias induced by AMI in rats in vivo. METHODS: Two hundred and forty male Wistar rats were randomized into a sham-operation group, an AMI group, and a recombinant human tumor necrosis factor receptor:Fc fusion protein(rhTNFR:Fc) group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery (LAD), and there was no ligation but operation in the sham-operation group. The rhTNFR:Fc group was treated with rhTNFR:Fc(10 mg/kg), a TNF-α antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-α among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. RESULTS: Expression of TNF-α increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR:Fc group. The time-windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR:Fc group showed a lesser expression of TNF-α protein and a lower incidence of ventricular arrhythmias (P<0.05). There was no obvious change in the sham-operation group. CONCLUSION: The expression of TNF-α induced by AMI could contribute to the onset of ventricular arrhythmias.