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Biomedical subjects

A Trapp

Publications and source records attributed to A Trapp.

3 recordsLinked to original sources

Interactions of cold stress and Pasteurella haemolytica in the pathogenesis of pneumonic pasteurellosis in calves: method of induction and hematologic and pathologic changes.

Six healthy neonatal calves were chilled with cold water and had focal tracheitis induced by spraying 5% acetic acid into the tracheal lumen. Subsequently, 20 ml of sterile saline solution was injected intratracheally. The effects of these interventions on total and differential white cell counts, plasma cortisol, histamine, and bradykinin, hematocrit, total plasma solids, and indices of the erythrocyte size and hemoglobin content were determined over the subsequent 12 hours. Cold stress increased plasma cortisol levels for less than 1 hour, but did not alter any other variable. This group of calves served as a control group for a second series of neonatal calves which were given 2 X 10(9) organisms of Pasteurella haemolytica intratracheally immediately following an identical period of chilling and acetic acid exposure. Calves given P haemolytica became neutropenic. There were increased numbers of circulating band neutrophils by 12 hours after exposure, and serum cortisol values were maintained at the same or greater than cold stress concentrations for all measurement periods subsequent to exposure. Infected calves had acute fibrinous pneumonia from which P haemolytica was isolated. Contrary to previous reports, these data may indicate a role for the neutrophil in the pathogenesis of early lesions of pasteurellosis. Although the association of circulating corticosteroids with stress and subsequent infection is clear, our data provide no evidence to indicate that circulating histamine or bradykinin are involved in the pathogenesis of the acute lesions of Pasteurella pneumonia.

Animals↗

Aorticopulmonary septal defect in a dog.

A 2-year-old Brittany Spaniel ahd clinical signs of pulmonary diseases and pulmonary hypertension, with cardiac murmur and congestive heart failure. Aorticopulmonary septal defect was detected by means of cardiac catheterization. Attempted surgical correciton was unsuccessful.

Animals↗

Female sex hormones decrease constitutive endothelin-1 release via endothelial sigma-1/cocaine receptors: an action independent of the steroid hormone receptors.

Cardiovascular disease is rare in premenopausal women compared to men. The authors investigate sex hormone-induced endothelin-1 (ET-1) release and the involvement of classic sex hormone receptors as well as the ability of sigma-1/cocaine receptors to respond to sex hormones. ET-1 release was measured in the supernatant of endothelial cells after treatment with beta-estradiol, progesterone, testosterone, or combined with their antagonists, and with the sigma-1 receptor ligand ditolylguanidine (DTG), or haloperidol, a sigma-1 receptor antagonist. Binding assays were performed using 2.5 x 10(-8) M [3H]DTG. Female sex hormones decreased ET-1 release whereas testosterone increased it, sex hormone antagonists only slightly attenuated or had no effect on the respective hormone's effect. DTG totally blocked the female sex hormone-induced inhibition on ET-1 release, whereas testosterone-induced stimulation was not affected. However, haloperidol blocked both. [3H]DTG binding was displaced by beta -estradiol but not by testosterone. DTG-binding sites account for 513 +/- 114 per cell, KD 8.79 nM. These data suggest that besides classic steroid hormone receptors, sigma-1/cocaine receptors mediate the effects of female sex hormones on ET-1 release, an up to now unknown signalling pathway. Results also suggest that female and male sex hormones may bind to different sites on sigma-1 receptors, exerting opposite pharmacological effects.

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