The occurrence of respiratory alkalosis and potential benefit derived from treatment were examined in thermostressed 4-week-old broiler chicks. Blood pH was greater (P less than .05) in heat-stressed (32 C) panting birds (7.395) than either nonpanting (7.28) or birds raised at 24 C (7.28). Acute thermostress, obtained by elevating ambient temperature from 32 to 41 C over a 20-min period further elevated (P less than .05) blood pH to 7.521. Chronic heat-stressed broiler chicks suffer from intermittent respiratory alkalosis during panting; with acute heat stress, chicks pant continuously and suffer from alkalosis. Including .5% sodium bicarbonate (NaHCO3) in the diet of birds subjected to chronic heat stress enhanced body weight gain by 9% even though it tended (P less than .10) to increase blood pH in nonpanting birds. Adding .3 or 1% ammonium chloride (NH4Cl) to diets decreased blood pH (P less than .01) to 7.194 and increased (P less than .05) body weight gains by 9.5 and 25%, respectively. Effects appeared linear with NH4Cl dose to 1% NH4Cl, but 3% NH4Cl elevated weight gains by only 8% and precipitated blood acidosis (pH 7.09) in nonpanting birds. Supplementing the 1% NH4Cl diet with .5% NaHCO3 increased weight gains an additional 9%. Manipulating sodium: chloride ratios by addition of calcium chloride increased body weight gain 8% and slightly reduced severity of alkalosis. Data indicate that blood alkalosis limits growth rate of broiler chicks reared under chronic thermostress and that the respiratory alkalosis and weight gain depressions attributed to thermostress can be partially alleviated dietarily.

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Cadmium chloride (CdCl2)-induced biochemical changes were characterized in male, CD-1 mouse testes. CdCl2 inhibited the testes microsomal Na+,K(+)-ATPase activity in vitro and in vivo. The inhibitory range was 30-50 microns and the concentration for half maximal inhibition (IC50 value) was 90 microns over 5 min preincubation. CdCl2 (2mg/kg/day, s.c.) for 2 days significantly inhibited testes Na+,K(+)-ATPase (near 90% inhibition). The content of testicular GSH and the ratio of reduced glutathione (GSH)/GSSG (oxidized glutathione) decreased in CdCl2-treated groups. Using salicylate as a trapping agent and high pressure liquid chromatography with electrochemical detection (LCED), we measured the OH production in vivo. 2,5-dihydroxybenzoic acid (2,5-DHBA) and 2,3-dihydroxybenzoic acid (2,3-DHBA) as indices of hydroxyl free radical formation significantly increased after 5 days CdCl2 exposure. Pretreatment with vitamin E (20 mg/kg, s.i.d., i.m., 7d) protected CdCl2-induced increase in OH. generation in testes. From this study, it was demonstrated that CdCl2 induced testicular toxicity could possibly be mediated by a significant increase in hydroxyl free radical formation and a reduction in GSH content and Na+,K(+)-ATPase activity. Vitamin E seems to prevent the CdCl2 induced increase in hydroxyl free radical generation.

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Sprague-Dawley rats were given 42 mg/kg xylazine intramuscularly, and lungs were lavaged with phosphatebuffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from xylazinetreated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with xylazine (0.3, 3, and 30 μg) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in xylazine-induced PE.