No abstract

Mortality in piglets during the perinatal period, especially the first days after birth, is frequently caused by noninfectious conditions, such as hypoglucemia or low birth weight, which can be associated with hypothermia experienced at birth. The thermal stability of newborn piglets is a fundamental aspect of neonatal care, so maintaining a constant, ideal temperature will substantially reduce newborn mortality. Species-specific characteristics, such as a limited capacity for thermoregulation, low energy reserves, a lack of brown adipose tissue (BAT) (-, and environmental conditions that are adverse for the piglet around the time of birth, including the absence of a microclimate, all of them contribute to difficulties in reaching thermal homeostasis in the first hours post-birth. Shivering thermogenesis and behavioral modifications to regulate body temperature through innate mechanisms allow animals to reduce their energy expenditures. Some body postures are effective in reducing contact with the floor and also nestling are useful to avoid heat loss, and also decreases heat dissipation. Achieving optimal development of thermoregulation is a challenge that newborns must confront to successfully adapt to extrauterine life. The objectives of this review, are to discuss the adverse factors that can lead to a death event due to hypothermia by analyzing the thermoregulation mechanisms at the central and cutaneous levels, also to analyze the harmful impacts that surviving neonate piglets confront in an unfavorable thermal environment, and to describe the pathophysiological mechanisms of death caused by hypothermia.

No abstract

It is thought that the degeneration of germ cells associated with an increase in the temperature due to cryptorchidism involves oxidative stress. α-Tocopherol is a powerful antioxidant that prevents oxidation of polyunsaturated fats found in membranes and stabilizes peroxyl radicals. For this reason we were interested in determining the role of α-Tocopherol using experimental cryptorchidism, followed by orchidopexia in neonatal rats. Eighty-four, 10-day-postpartum (dpp) male rats (Wistar strain) were used and divided into 7 groups: healthy control, sham with α-Tocopherol treated with 30 or 100 mg/kg doses, sham vehicle, cryptorchidism treated with α-Tocopherol at 30 or 100 mg/kg doses and cryptorchidism vehicle. Cryptorchidism was surgically induced at 10 dpp. At 25 dpp the animals were treated with α-Tocopherol and the vitamin vehicle. Lipoperoxidation and testicular morphology was determined in half of the animals at 40 dpp (short term). The remaining animals underwent orchidopexia and fertility was determined at 90 dpp. Testicular morphology was determined at 120 dpp (long term) in these animals. A significant reduction of lipoperoxidation was observed in the cryptorchid group treated with α-Tocopherol compared to the untreated cryptorchid group, in addition to short-term histological alterations. At long term, we observed an increase in the area and maturation of the seminiferous epithelium, a decrease in apoptosis and histological alterations and an increase in fertility from α-Tocopherol treatment. α-Tocopherol treatment decreased lipoperoxidation, possibly stabilizing free radicals produced during cryptorchidism, reducing morphological testicular alterations and favoring fertility.