Manifestations of and risk factors for acute myocardial injury after acute organophosphorus pesticide poisoning.

This study aimed to explore the risk factors for acute myocardial injury (AMI) caused by acute organophosphorus pesticide poisoning (AOPP).The clinical data of 98 patients, who were treated in our hospital due to oral AOPP from April 2013 to April 2017, were retrospectively analyzed. These patients were divided into two groups: AMI group and control group. The incidence of AMI was analyzed. Furthermore, the dosage forms and dose of the pesticide, and the interval between pesticide taking and doctor visit were compared between these two groups. Moreover, their clinical symptoms were observed; the serum cholinesterase levels, myocardial injury, and heart failure markers were detected, and the occurrence of arrhythmia and the structure and function of the heart were investigated through continuous electrocardiographic monitoring and transthoracic echocardiography.Among these 98 AOPP patients, 51 patients were complicated with AMI, and the incidence was 52.0%. The main manifestations of these 51 patients with AMI were as follows: the serum levels of myocardial injury markers (creatine kinase-Mb [CK-Mb] and cardiac troponin I [cTnI]) and heart failure markers (N-terminal pro B-type natriuretic peptide [NT-pro BNP]) were significantly higher, when compared with the control group (P < .001), and the incidence of arrhythmia (FVPB, P = .02; RAA, P = .03; RVA, P = .02; ST-T changes, P = .01) and heart failure (P = .04) was also significantly higher when compared with the control group. With regard to dosage forms of the pesticides, the number of patients taking the pesticides with solvents containing aromatic hydrocarbons was significantly higher in the AMI group than in the control group (P = .001). And the number of patients taking over 100 mL of pesticides was also significantly higher in the AMI group than in the control group (P < .001). Significantly more patients in the AMI group had an interval of over 1 h between pesticide taking and doctor visit than in the control group (P < .001).Risk factors for AMI after AOPP may include the dose and dosage form of the pesticide, and the interval between pesticide taking and doctor visit.

[Effects of telmisartan and pyridoxamine on abdominal aorta vascular remodeling in spontaneously hypertensive rats].

OBJECTIVE: To investigate the effects of telmisartan and pyridoxamine on vascular smooth muscle cells (VSMCs) proliferation and apoptosis as well as abdominal aorta vascular remodeling in spontaneously hypertensive rats (SHRs). METHODS: SHRs randomly received placebo, telmisartan (6 mg kg(-1) x d(-1)), pyridoxamine (200 mg x kg(-1) x d(-1)) or telmisartan (6 mg x kg(-1) x d(-1)) plus pyridoxamine (200 mg x kg(-1) x d(-1), n = 12 each) for 16 weeks. Wistar-Kyoto (WKY, n = 12) rats serve as normotensive control. The systolic blood pressure (SBP) of rat was measured before and weekly thereafter. The serum advanced glycation end-products (AGEs) were detected by competitive ELISA. The serum super oxide dismutase (SOD) and nitric oxide (NO) were measured. The abdominal aorta were assessed by image analysis in HE stained sections. The VSMCs apoptosis and proliferation in abdominal aorta were detected with in situ end labeling technique and proliferating cell nuclear antigen (PCNA) immunohistochemistry staining respectively. RESULTS: SBP were significantly lower in telmisartan and telmisartan plus pyridoxamine therapy group than in placebo treated hypertensive rats while not affected by pyridoxamine (P > 0.05). Activity of SOD and NO were significantly higher and AGEs significantly lower in telmisartan, pyridoxamine and combination therapy treated SHRs than in placebo treated hypertensive rats (P < 0.01). The telmisartan, pyridoxamine and combination therapy can significantly inhibit the PCNA expression and significantly enhance the apoptosis value in abdominal aorta (P < 0.01). The efficacy of combined treatment was significantly higher than telmisartan and pyridoxamine alone (P < 0.05). CONCLUSION: Telmisartan and pyridoxamine could attenuate abdominal aorta vascular remodeling via reducing oxidative stress and AGEs production as well as restoring the balance of VSMCs proliferation and apoptosis in SHRs abdominal aorta.