Abstract. "Meconium aspiration syndrome" is a condition resulting in respiratory distress and the occasional death of newborn human beings. A retrospective study was conducted on 52 calves that were submitted for postmortem examination to the Atlantic Veterinary College, Charlottetown, Prince Edward Island, Canada. These calves died of infectious and noninfectious diseases within the first 2 weeks of life due to a variety of causes. The most common cause of death was infectious enteric disease. Histologic examination of lungs revealed that 42.5% of calves had evidence of meconium, squamous cells, or keratin in the lung. There was considerable variation in the magnitude of histologic changes in lungs containing aspirated material. Typically, affected lungs had only a few inconspicuous pieces of meconium, keratin, and squamous cells within bronchoalveolar spaces. Sporadically, the entire lumen of airways was obliterated by aspirated material. Lungs with aspirated material had a mild but diffuse alveolitis characterized by exudation of a few neutrophils, macrophages, and occasional multinucleated giant cells. Obstruction of small airways and focal atelectasis were also observed. Similar lesions have been reported in human meconium aspiration syndrome. It is concluded that histologic changes similar to those of human meconium aspiration syndrome occur commonly in calves that die within 2 weeks of birth. Further studies involving healthy age-matched calves are required to evaluate the clinicopathologic significance of rneconium aspiration in this species.

ABSTRACT:The objective of this review is to integrate clinical findings and laboratory analyses in such a way to improve the welfare of newborn piglets and achieve better prognoses of neonatal viability. Deaths during the intrapartum period account for a significant proportion of pre-weaning mortality in farms worldwide. Piglets which die during parturition generally have normal size and typically lack gross lesions at post-mortem examination. However, circulatory abnormalities in the umbilical cord help in assessing piglet viability. Cord lesions can be classified as normal (adhered), oedematous, congested or haemorrhagic and should always be evaluated in perinatal deaths. The likelihood of neonatal survival decreases rapidly as the severity of umbilical cord lesions increase. The physiometabolic blood profile which includes acid-base balance, degree of dehydration, mineral balance, metabolic expenditure and gas exchange are also useful clinical elements for properly assessing neonatal viability. Neonatal survival is notably reduced when the blood pH falls below 7.0, lactate rises above 90 mg/dl, bicarbonate drops below 10 mmol/l, or the pCO 2 increases above 110 mm/Hg. Blood calcium is also an excellent indicator of neonatal stress when used in combination with the other parameters mentioned above. Trembling due to an imbalance in the movement of calcium in muscle is also a factor involved in neonatal mortality. Neurological function in the newborn piglet could also be evaluated by adapting the Apgar score widely used in human perinatology. Neonates with scores lower than 6 in a 10 point scale have generally lower survival rates. The two most important indicators for this vitality score are breathing latency and bradycardia. If the neonate has apnoea for more than 5 min and the cardiac frequency does not increase to more than 110 beats per minute the prognosis for survival is rather poor.

The present study was carried out to determine the effect of berberine on glucose homeostasis and several biomarkers associated with insulin sensitivity in male Wistar rats with intraperitoneal injection of streptozotocin (STZ)-induced diabetes. Rats with fasting blood glucose 16.7 mmol/L after 2 weeks of STZ injection were divided into two groups. One group was used as the diabetic control and another treated by gavage feeding with 100 mg/kg/d of berberine in water containing 0.5% carboxymethyl cellulose. A group of rats without receiving STZ was used as the normal control. After 7 weeks, berberine supplementation moderately but significantly lowered fasting blood glucose levels and improved oral glucose tolerance. Berberine lowered plasma free fatty acids and C-reactive protein levels without affecting plasma insulin levels. Diabetic rats treated with berberine showed significantly lower plasma triacylglycerol and cholesterol levels. Furthermore, berberine inhibited dipeptidyl peptidase-4 and protein tyrosine phosphatase-1B activities. In conclusion, berberine showed a dramatic effect of lowering blood cholesterol and triacylglycerols and improved moderately glucose homeostasis in STZ-induced diabetic rats in association with multiple factors related to insulin resistance.

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The meconium aspiration syndrome is an important cause of respiratory distress in newborn infants. Alveolar macrophages (AMs) provide a first line of defense in the lower respiratory tract against inhaled pathogens and particles such as meconium. In this study, we examined the effect of meconium on two primary macrophage functions: phagocytosis and respiratory burst. Shortterm exposure of rat NR8383 AMs to sterile meconium from human or equine neonates (1.2-24 mg/mL) produced a dosedependent decrease in phagocytosis of fluorescent latex beads. This effect was not due to decreased cell viability or to an elevation of intracellular cAMP. The effect of short-term exposure to meconium on the respiratory burst response in AMs was quantified using flow cytometry to measure oxidation of dichlorofluorescin diacetate. A robust respiratory burst was triggered when AMs were exposed to 12 or 24 mg/mL meconium. This effect was attenuated but not eliminated by filtration of the meconium. However, subsequent to meconium exposure, AMs had a reduced respiratory burst in response to stimulation with phorbol myristate acetate. In addition, AMs that were exposed to meconium for an extended period (24 h Meconium aspiration syndrome (MAS) is an important cause of respiratory distress in newborn infants (1). Approximately 12-15% of human infants are born through meconiumcontaminated amniotic fluid (2), and these infants are much more likely to develop respiratory distress and require respiratory support (3). When meconium is present in the amniotic fluid,~5% of neonates will develop MAS, and~5% or more of these infants will die (2).The pathophysiology of MAS is complex and involves airway obstruction, surfactant dysfunction, and pulmonary inflammation (4). Alveolar macrophages (AMs) are important in defending the alveolar space against inhaled pathogens and particles. Because the phagocytic activity of AMs is a crucial component of host defense, it is important to know the effect of meconium on phagocytosis. Meconium has been shown to decrease phagocytosis by neutrophils in vitro (5), so it is reasonable to postulate that AM phagocytic activity may also be adversely affected.Once phagocytosis has occurred, macrophages undergo an oxidative metabolic process called respiratory burst, generating reactive oxygen species (ROS) with activity against a wide range of invading organisms. Although production of antimicrobial molecules is essential in host defense, excessive ROS production can also cause injury to surrounding tissue (6,7). For example, ROS generated through respiratory burst activity plays a role in inducing pulmonary injury in diseases such as acute respiratory distress syndrome (8) and may also contribute to the pathophysiology of MAS. The purpose of this study was to investigate the effect of meconium on the phagocytic activity and respiratory burst response of AMs. METHODS Cells.A continuous rat AM cell line, NR8383 (9)

One of the major target organs of hydrogen sulphide gas is the lung. Exfoliation of upper respiratory epithelia and pulmonary edema are prominent efrects. Various neuropeptides contained in afferent C-fibres are intimately associated with the epithelia of the conducting airways and are liberated upon exposure to noxious gases. We sought to determine their role in the pathogenesis ofhydrogen-sulphide-induced pulmonary injury by pretreating rats with the neurotoxin, capsaicin, which is known to ablate a'subpopulation of vagal afferent C-fibres. Groups of capsaicin and saline (control) pretreated Fischer 344 rats were exposed to an edemogenic concentration of hydrogen sulphide (525-559 mg/m3) for 4 hr. Mortality was significantly greater (p < 0.01) in the capsaicin treated rats (12112) compared to the control animals (2112). Pulmonary injury was also more severe in the capsaicin pretreated animals as assessed by lung water content, histological grade of pulmonary edema and protein in the broncho-alveolar fluid. Animals depleted of substance P exhibited a significantly .greater (p c 0.01) degree of bronchial epithelial cell exfoliation and ulceration following exposure to hydrogen sulphide. These experiments indicate that capsaicin sensitive sensory nerves may play a major role in pulmonary defense against the effects of inhaled toxic gases such as hydrogen sulphide.

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