Reallocation of cutaneous and global blood circulation during sauna bathing through a closed-loop model.

OBJECTIVE: Sauna bathing (SB) is an important strategy in cardiovascular protection, but there is no mathematical explanation for the reallocation of blood circulation during heat-induced superficial vasodilation. We sought to reveal such reallocation via a simulated hemodynamic model. METHODS: A closed-loop cardiovascular model with a series of electrical parameters was constructed. The body surface was divided into seven blocks and each block was modeled by a lumped resistance. These resistances were adjusted to increase skin blood flow (SBF), with the aim of reflecting heat-induced vasodilation during SB. Finally, the blood pressure was compared before and after SB, and the blood flow inside the aorta and visceral arteries were also analyzed. RESULTS: With increasing SBF in this model, the systolic, diastolic, and mean blood pressure in the arterial trunk decreased by 13-29, 18-36, and 19-37 mmHg, respectively. Despite the increase in the peak and mean blood flow in the arterial trunk, the diastolic blood flow reversal in the thoracic and abdominal aortas increased significantly. Nevertheless, the blood supply to the heart, liver, stomach, spleen, kidney, and intestine decreased by at least 25%. Moreover, the pulmonary blood flow increased significantly. CONCLUSION: Simulated heat-induced cutaneous vasodilation in this model lowers blood pressure, induces visceral ischemia, and promotes pulmonary circulation, suggesting that the present closed-loop model may be able to describe the effect of sauna bathing on blood circulation. However, the increase of retrograde flow in the aortas found in this model deserves further examination.

Protective Effect of Organic Selenium on Oxidative Damage and Inflammatory Reaction of Rabbit Kidney Induced by T-2 Toxin.

T-2 toxin is a member of a class of mycotoxins produced by a variety of Fusarium species under appropriate temperature and humidity conditions and is a common contaminant in food and feedstuffs of cereal origin. Selenium is an indispensable element in animals, regulates a variety of biological functions of the body, and can antagonize metal and mycotoxin poisoning to a certain extent. However, the effect of selenium on kidney injury induced by T-2 toxin has not been reported. In this study, 50 New Zealand rabbits were divided into 5 groups (the control group, T-2 toxin group, low-dose Se + T-2 toxin group, medium-dose Se + T-2 toxin group, and high-dose Se + T-2 toxin group). Rabbits were examined after oral administration of different doses of selenomethionine (SeMet) for 21 days and after perfusion with 0.4 mg/kg T-2 toxin (or the same dose of olive oil in the control group) for 5 days. We found that T-2 toxin induced kidney function damage and increased the levels of ROS and the contents of inflammatory factors. Renal structure was pathologically damaged. However, we found that after pretreatment with 0.2 mg/kg SeMet, oxidative stress, the inflammatory response, and pathological damage induced by T-2 toxin were attenuated. The results indicate that a low dose (0.2 mg/kg) of SeMet effectively reversed T-2 toxin-induced kidney injury in rabbits.

Protective effect of selenomethionine on intestinal injury induced by T- 2 toxin.

T-2 toxin is the most toxic as a type A trichothecenes, which could contaminate grains, especially in wheat and corn. It can cause immune suppression, neurotoxicity, the apoptosis of cells and even induce tumorigenesis. Recent studies have indicated that selenium (Se) have protective effect against mycotoxins-induced toxicity. The present studies was designed to investigate the protective role of Selenomethionine (SeMet) on T-2 toxin-induced toxicity in rabbit's jejunum. 50 New Zealand rabbits were divided into five group (Control group, T-2 group, low-dose Se + T-2 group, medium-dose + T-2 group and high-dose Se + T-2 group). New Zealand rabbits were orally administered with SeMet (0.2, 0.4 and 0.6 mg/kg, Adding diet) for 21 days. On 17th days, each group began to take 0.4 mg/kg of T-2 toxin orally every day for 5 days. We found that rabbit exposed to T-2 toxin could increase the levels of ROS, and decrease activities of antioxidant enzymes and the expression of Occludin and ZO-1. In addition, T-2 toxin could trigger jejunal inflammatory response and enhance the expression of IL-1ß, IL-6 and TNF-α. After SeMet pretreatment, our results indicated that Se attenuated the T-2 toxin-induced oxidative stress, decreasing the level of ROS, MDA and enhancing the activity of SOD and GSH-Px. Moreover, SeMet can alleviate jejunal inflammatory response, and protect the integrity of the intestinal barrier through up-regulating the expression of ZO-1 and Occludin. In the present research, supplementation of 0.2 mg/kg SeMet in the diet could effectively alleviate the T-2 toxin poisoning in rabbits.