Postadulticide pulmonary hypertension mechanisms and treatment with antihistamines and supplemental oxygen were studied in eight dogs with heartworm disease. To ensure severe postadulticide thromboembolism, additional heartworms (either 20 or 40 into 4 dogs each) were transplanted into naturally infected dogs before thiacetarsamide treatment. During pentobarbital anesthesia, 2 pulmonary hemodynamic studies were conducted on each dog with a sequence of baseline, hypoxia with FlO2 = 10%, hyperoxia with FlO2 = 100%, a second baseline, treatment with either diphenhydramine (D) or cimetidine (C), and another hypoxia. All dogs were pulmonary hypertensive, with each dog having a mean pulmonary arterial pressure (PPA) greater than 20 mm of Hg. Mean PPA increased from baseline conditions (25.0 +/- 4.5 SD for D and 24.3 +/- 4.4 for C) to hypoxia (28.5 +/- 4.7 for D and 28.4 +/- 3.7 for C), and decreased during hyperoxia (16.9 +/- 3.0 for D and 17.4 +/-3.0 for C), respectively. Neither antihistamine reduced PPA at normoxia. The degree of pulmonary hypertension when breathing room air increased even more during hypoxia, and this increase was not attenuated by either antihistamine. Histamine did not appear to mediate pulmonary hypertension during postadulticide thromboembolism, nor to modify the hypoxia-mediated pulmonary hypertension at this disease stage. Because baseline PO2 was low (66.6 +/- 11.7 mm of Hg for D and 69.4 +/- 14.2 for C) and because PPA decreased during administration of oxygen, the pulmonary hypertension was mostly hypoxia-induced. In addition to the arterial lesions, much of the pulmonary hypertensive mechanism was an active and reversible vasoconstriction in response to hypoxia caused by the secondary lung disease. Supplemental oxygen to dogs with pulmonary hypertension could reduce PPA and right ventricular afterload. This study supports the use of oxygen, but not antihistamine drugs, in the treatment of postadulticide heartworm disease in dogs that are hypoxic, with signs of congestive heart failure or dyspnea.

Stress is commonly used to describe the detrimental effectsof a variety of conditions surrounding animals on their health performance. Environmental stress causes an increasein oxidative stress and an imbalance in antioxidant status. Oxidative damage increases in stressed poultry when the plasma antioxidant vitamins and minerals such as vitamin C, E, folic acid, and zinclevels declined. Stress factors in birds involve many elements of the transport processes which may be detrimental to the birds. These factors include alteration in atmospheric temperature, poor handlingby man, removal of feed and water (starvation), high ambient temperature (AT) and relative humidity (RH). Other factors incude vaccination, disease conditions such as coccidiosis, novelty,confinement, motion, noise, microthermal core within the vehicle and the use of inappropriate vehicles. Live birds of all ages are being transported mainly by roads to their various destinations and across different ecological zones throughout the year. Mortality increaseswith journey length. The adverse effects of these factors and their combinations may range from mild discomfort and aversion to death. This review was aimed at providing comprehensive information on the role of vitamin C in combating stress factors in poultry with the view of exploring its potentials for future research undertaking.Information compiled in this review were obtained from search engines such as Elsevier, Pubmed, Springer, Medline, Science Direct, Google Scholar, and a library search for articles published in peerreviewedjournals. 100 to 200 mg/kg feed of vitamin C is capable of converting stress factors in poultry and thereby improving the productivity.