Guangcai Yu

A case report of acute severe paraquat poisoning and long-term follow-up

In the present study, the successful management of severe paraquat (PQ) poisoning with multiple organ dysfunction syndrome is described. A 42-year-old female ingested >100 ml PQ (20% weight/volume) in an attempted suicide. After 22 h the patient was admitted to hospital with serious liver, kidney and lung damage. Comprehensive therapy that maximized poison elimination was administered, along with appropriate glucocorticoids and medication for anticoagulation and protection of the liver and kidney. The patient was successfully treated and recovered after 40 days. However, pulmonary damage was aggravated when the glucocorticoid treatment was stopped after 2 months; the lungs recovered again following systematic therapy. Subsequent to a 8-month follow-up, the patient was able to look after herself in her daily life. To the best of our knowledge, successful treatment following severe PQ poisoning is rare.

Effect of transforming growth factor-β1 on acute lung injury caused by paraquat

In China, and other Asian countries, numerous patients have succumbed to pulmonary fibrosis induced by paquarat poisoning, but the early pathogenesis remains unclear. In this study the effect of cytokine transforming growth factor (TGF)-β1 was observed in early acute paraquat poisoning and examined the mechanism by which paraquat caused early acute lung injury. It was discovered that the rat serum TGF-β1 levels in the paraquat groups were significant higher than that in the control group (P<0.05) and the rat pulmonary TGF-β1 mRNA expression levels were also higher than that in the control group (P<0.05). Histological examination indicated that the rat lung tissue was broad and congested, and had been infiltrated by inflammatory cells. Massons trichrome staining for collagen showed that the lung tissue appeared fibrotic following paraquat poisoning. Ultramicrostructure observation found that macrophages, red blood cells, lymphocytes and granulocytes infiltrated the alveolar space and there were cytolysosomes in the macrophages. The shape of the type II alveolar epithelial cell nuclei were irregular with karyopyknosis. The heterochromatin migrated to the cell edge and lamellar body vacuolization was also observed. Type I alveolar epithelial cells shrank. In conclusion, the effect of cytokine TGF-β1 on paraquat-induced acute lung tissue injury may be important.

Acute paraquat poisoning with sinus bradycardia: A case report

Paraquat (PQ) is a highly toxic herbicide, which not only leads to acute organ damage, but also to a variety of complications. Patients with severe PQ-induced poisoning may succumb to multiple organ failure involving the circulatory and respiratory systems. Although numerous studies have been performed investigating PQ poisoning, cases of extreme bradycardia caused by acute PQ-induced poisoning are rare. In the present case report, a 59-year-old male who ingested PQ was admitted to the Department of Poisoning and Occupational Disease at Qilu Hospital of Shandong University (Jinan, China) after three days. The patient received treatment known as the ‘Qilu scheme’, which was established in the Department of Poisoning and Occupational Disease. However, the heart rate of the patient remained low following the administration of conventional medicines, until thyroid tablets were administered. To the best of our knowledge, cases of bradycardia following PQ poisoning are rare.

Tetramethylpyrazine can ameliorate hepatocellular mitochondrial dysfunction by decreasing the inflammatory response and increasing AQP8 protein expression in septic rats

Sepsis, which could lead to mitochondrial dysfunction and cellular energy loss, always induces acute liver injury and has a high mortality rate. Tetramethylpyrazine (TMP) is an active extract from the Chinese herb Ligusticum chuanxiong and exhibits anti-sepsis activity. In this study, a rat sepsis model was first established via cecal ligation and puncture (CLP). Then, 48 Sprague Dawley male rats were randomly divided into four groups (12 rats in each group): control group (C), sepsis group (S), TMP treatment group (T), and TMP prevention group (P). Serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), mitochondrial aspartate aminotransferase (mAST), and adenosine triphosphate (ATP) levels and mitochondrial membrane potential (MMP) were measured and used as indicators of hepatic dysfunction severity and mitochondrial function. In addition, the activities of Na+-K+-ATPase, Mg2+-ATPase, Ca2+-ATPase, and Ca2+-Mg2+-ATPase in the mitochondrial membrane, the expression level of AQP8 and some inflammatory factors, and the level of oxidative stress were measured to explore potential mechanisms. We found that AQP8 accepts signals from inflammatory factors upon stimulation and during various infections, and low AQP8 expression levels could result in further downstream mitochondrial dysfunction. In conclusion, our data demonstrated that TMP could ameliorate hepatocellular mitochondrial dysfunction by decreasing the inflammatory response and increasing AQP8 protein expression.