Arecoline induces heart injure via Fas/Fas ligand apoptotic pathway in heart of Sprague-Dawley rat.

Habitual chewing of areca nut increases the risk of cardiovascular disease mortality, but less report demonstrate the toxic mechanism of areca nut on heart. To investigate toxicity of areca nut on cardiomyocytes, we induced the heart injury with arecoline to evaluate the acute damage of areca nut on heart. Different concentrations of are coline (lowdosage: 5 mg/kg/day and high dosage 50 mg/kg/day) were injected into Sprague-Dawley rat via intra-peritoneal method for 21 days to create negative effects of arecoline on cardiomyocyte. Themyocardial architecture of the rat heart was observed. The arecoline-induced apoptotic proteins were analysed via western blotting. The myocardialarchitecture of heart was injured with arecoline and TUNEL stain was also shown are coline-induced cardiac apoptosis. Arecoline promoted the protein expression of both Fas dependent snd mitochondrial dependent apoptosis. In summary, arecoline induces cardiac toxicity and apoptosis by inducing both death receptor and mitochondria-dependent apoptotic pathways on heart.

Inducibility of abnormal automaticity and triggered activity in myocardial sleeves of canine pulmonary veins.

BACKGROUND: To study the cellular mechanisms governing cardiac atrial arrhythmias initiated by ectopic focus (or foci) from pulmonary veins (PVs). METHODS: In the present in vitro study, we applied the conventional microelectrode technique to record intracellular action potentials in PV sleeves from dogs. RESULTS: In 80 normal healthy dogs, all action potentials recorded in cardiomyocytes from PV sleeves were fast-response. The pharmacological responses to quinidine, nisoldipine, D-sotalol, 4-aminopyridine, isoproterenol, acetylcholine, and adenosine were characteristic of those in atrial cells. Diastolic depolarization and spontaneous activity could be induced by 1 mmol/L Ba2+ in all the 22 PV specimens being tested, but only in 3 of 11 of left atrial specimens (p<0.0001). In the presence of 1 mmol/L Ba2+, the diastolic slope was only slightly affected by Ni2+ (500 micromol/L), but was significantly suppressed by Cd2+ (200 micromol/L). Ryanodine (2 micromol/L) caused a transient increase, followed by a marked decrease of Ba2+-induced spontaneous activity. Isoproterenol shortened and acetylcholine prolonged the cycle length of the Ba2+-induced automatic activity. In the presence of isoproterenol, washout of acetylcholine induced a rebound phenomenon, which triggered a short period of spontaneous activity. The results suggest an important role of intracellular cytoplasmic Ca2+ loading. Under conditions that mimic ischemia/hypoxia, the resting membrane potential depolarized, upstroke of the action potential became depressed and the action potential duration shortened. In the presence of isoproterenol and elevated external K+, spontaneous activity was generated. CONCLUSIONS: These findings indicate a lack of arrhythmogenic activity in normal healthy PV sleeves. Abnormal automaticity and triggered activity occurred exclusively under simulated pathologic conditions. Ba2+-induced automaticity was more easily induced in PV than in the left atrium. The same conditions might also favor the genesis of reentry in the in vivo condition.

The protective mechanism of magnolol, a Chinese herb drug, against warm ischemia-reperfusion injury of rat liver.

BACKGROUND: Cell apoptosis following warm ischemia-reperfusion injury is a major concern in clinical issues such as organ transplantation, trauma, and cardiogenic shock. The purpose of this study was to evaluate the possible role of magnolol, a Chinese herb drug, in apoptotic injury and the kinetic expression of apoptotic-related genes in rat livers subjected to warm ischemia-reperfusion (WI/R). MATERIALS AND METHODS: Three weeks prior to the experiment 10 rats underwent a portosystemic shunt operation according to Bengmerk's method. The rats were divided into three groups. Group 1 (GI) was the control group, Group 2 (GII) and Group 3 (GIII) the magnolol-treated groups. GI and GII were subjected to 2 h and GIII to 3 h of WI/R by clamping the portal vein and hepatic artery under ether anesthesia. RESULTS: Results show that all the control rats died after 2 h WI/R. Apoptotic cells were detected under microscopy as well as by DNA assay. Magnolol-treated groups tolerated warm ischemia-reperfusion for 2 h and significantly less apoptotic cells were observed (198 +/- 22 vs 42.6 +/- 28). But magnolol-treated rats could not tolerate 3 h warm ischemia-reperfusion. RT-PCR of liver tissue shows that there is an upregulated expression of the anti-apoptotic Bcl-xL gene and suppression of the Bcl-xS gene in GII. CONCLUSION: Magnolol has an anti-apoptotic effect and protects the liver against WI/R for 2 h but not for 3 h through upregulation of the anti-apoptotic Bcl-XL gene and suppression of the Bcl-xS gene.

Ionized calcium changes during living-donor liver transplantation in patients with and without administration of blood-bank products.

Exogenous citrate load from blood transfusion during orthotopic liver transplantation is thought to be the main cause of ionized hypocalcemia, which may result in hemodynamic instability. This implies that if no blood is transfused, chelation of free ionized calcium (Ca(++)) by citrate is avoided and supplemental calcium need not be given. For this study, we divided 39 pediatric living-donor liver transplant patients into two groups according to the blood component replacement given: group I received packed red blood cells and fresh frozen plasma with and without 5% albumin, and group II received 5% albumin alone. The intra-operative serial ionized calcium level was recorded, and the amount of calcium chloride replacement to maintain acceptable blood Ca(++) levels was compared between the groups. The mean serum ionized calcium level changes of both groups could be maintained within lower-to-normal limits intra-operatively. The amount of supplemental calcium chloride required to correct the hypo-ionized calcium was not significantly different between the groups. We can conclude that if an exogenous citrate load is eliminated by the avoidance of blood transfusion and 5% albumin infusion is used, instead, to replace the blood and ascites loss during OLT, the risk of ionic hypocalcemia still persists. Serum Ca(++) monitoring and adequate replacement are, therefore, still required in this setting.