dinoprost and Foot-Diseases

Topics: Apudoma; Diarrhea; Dinoprost; Fever; Fingers; Foot Diseases; Humans; Hypercalcemia; Hypotension; Paraneoplastic Syndromes; Polycythemia; Prostaglandins; Prostaglandins E; Prostaglandins F

To provide insights into the role of prostaglandin F(2 alpha) (PGF(2 alpha)) in the developmental stages of laminitis induced in horses by ingestion of black walnut heartwood extract (BWHE).. 10 adult mixed-breed horses.. Horses were separated into 2 groups and were euthanatized at 12 hours after placebo (water) administration (control horses) or after BWHE administration and development of Obel grade 1 laminitis. Blood samples were obtained to determine plasma PGF(2 alpha) concentrations hourly for the first 4 hours and subsequently every 2 hours after substance administration. Laminar arteries and veins were isolated, and responses to increasing concentrations of PGF(2 alpha) were measured before and after preincubation of blood vessels with prostanoid and thromboxane receptor antagonists SQ 29,548, SC-19220, and AH 6809.. Plasma PGF(2 alpha) concentrations increased in horses given BWHE; the WBC count decreased concurrently. In control horses, PGF(2 alpha) was a potent contractile agonist for laminar veins but not for laminar arteries. In horses given BWHE, PGF(2 alpha) was similarly selective for laminar veins; however, the magnitude of PGF(2 alpha)-induced venoconstriction was less than that in control horses. After preincubation with SQ 29,548, laminar veins from control horses responded to PGF(2 alpha) with a small degree of dilation, whereas laminar veins from horses given BWHE did not.. PGF(2 alpha) may play a role in the inflammatory and vascular dysfunction associated with the prodromal stages of laminitis. Prostanoids such as PGF(2 alpha) may be viable targets for the prevention of acute laminitis in horses.

Topics: Animals; Arteries; Dinoprost; Foot Diseases; Hoof and Claw; Horse Diseases; Horses; Inflammation; Intubation, Gastrointestinal; Juglans; Lameness, Animal; Phenylephrine; Plant Extracts; Veins; Wood

Inflammation and vascular dysfunction occur concurrently during the prodromal stages of equine laminitis. The aim of this study was to provide insights into the role that thromboxane and isoprostanes may play in the development of black walnut heartwood extract (BWHE)-induced laminitis. Horses were divided into two groups, either control or BWHE-administered horses. Plasma concentrations of thromboxane increased transiently after administration of BWHE and coincided with the nadir in white blood cell counts, whereas plasma concentrations of iso-prostaglandin PGF(2alpha) (iso-PGF(2alpha)) did not change in either group. At 12h (for the control group) or Obel grade 1 laminitis (for the BWHE group) the horses were euthanized and laminar tissue collected. Laminar arteries and veins were used in functional studies with vasoconstrictor substances and tissue samples were used for the determination of laminar iso-PGF(2alpha) concentrations. Laminar tissue concentrations of iso-PGF(2alpha) were significantly greater in BWHE horses when compared to control horses. In parallel studies concentrations of iso-PGF(2alpha) in laminar tissue samples obtained 1.5 and 3h after administration of BWHE were indistinguishable from those for control horses at 3 or 12h after administration of an equal volume of water. Laminar vessel constrictor responses to either a thromboxane mimetic (U46619), iso-prostaglandin PGE(2) (iso-PGE(2)) or iso-PGF(2alpha) were determined using small vessel myographs. In some vessels, the effects of putative prostanoid and thromboxane receptor antagonists, SQ 29,548, SC-19220 and AH 6809, upon contractile responses were determined. In control horses, U46619, iso-PGF(2alpha) and iso-PGE(2) more potently and efficaciously constricted laminar veins when compared to laminar arteries. Responses of laminar veins from BWHE horses to iso-PGE(2) were similar to those of laminar veins from control horses, whereas iso-PGF(2alpha) elicited significantly greater responses in laminar veins from BWHE horses when compared to controls. In contrast, responses to U46619 were smaller in laminar veins isolated from BWHE horses when compared to those in laminar veins from control horses. In the presence of SQ 29,548, iso-PGF(2alpha) elicited a small dilation in laminar veins from control horses, which was not apparent in laminar veins from BWHE horses. These results are consistent with both systemic and local inflammatory events occurring during the prodromal stages of BWH

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Animals; Arteries; Dinoprost; Dinoprostone; Foot Diseases; Hoof and Claw; Horse Diseases; Horses; Inflammation; Isoprostanes; Juglans; Plant Extracts; Random Allocation; Thromboxanes; Tissue Culture Techniques; Vasoconstriction; Veins; Wood

Equine laminitis is a crippling condition associated with a variety of systemic diseases. Although it is apparent that the prodromal stages of laminitis involve microvascular dysfunction, little is known regarding the physiology of this vasculature. The aim of the present study was to determine the relative responses of equine laminar arteries and veins to the vasoconstrictor agonists phenylephrine (1 nM-10 microM), 5-HT (1 nM-10 microM), PGF2alpha (1 nM-100 microM), and endothelin-1 (1 pM-1 microM). We have determined that laminar veins were more sensitive, with respect to the concentration of agonist required to initiate a contractile response and to achieve EC(50), for all agonists tested. EC50 values, for veins and arteries, respectively, were 84+/-7 vs. 688+/-42 nM for phenylephrine, 35+/-6 vs. 224+/-13 nM for 5-HT, 496+/-43 nM vs. 3.0+/-0.6 microM for PGF2alpha, and 467+/-38 pM vs. 70.6+/-6.4 nM for endothelin-1. Moreover, when expressed as a percentage of the response to a depolarizing stimulus (80 mM potassium), the maximal contractile response of laminar veins exceeded that for the laminar arteries for each agonist. These results indicate that there may be a predisposition for venoconstriction within the vasculature of the equine digit. While this physiological predisposition for venoconstriction may be important in the regulation of blood flow during exercise, it also may help to explain why laminitis can result from a variety of pathological systemic conditions.

Topics: Animals; Arteries; Causality; Dermis; Dinoprost; Endothelin-1; Foot Diseases; Hoof and Claw; Horse Diseases; Horses; Phenylephrine; Potassium; Regional Blood Flow; Serotonin; Vasoconstriction; Vasoconstrictor Agents; Veins

For the effects of voltages on health and reproduction, 40 cows in second to fifth lactation were divided into four groups of 10. These included a control group that was not subjected to voltages and three treatment groups that were given either 1, 2, or 4 V at the water bowl. Cows in the treatment groups were exposed during the entire lactation to voltage whenever they drank. Voltages did not sufficiently affect milk yield. General health parameters studied were mastitis, hoof problems, and changes in body weight. Reproductive and calving parameters examined were days to first breeding, days open, services per conception, response to PGF2 alpha, calving intervals, visible abortion, and calves born dead. Voltages did not significantly influence cow health or reproductive performance.

Topics: Abortion, Veterinary; Animals; Body Weight; Cattle; Cattle Diseases; Dinoprost; Electricity; Female; Fetal Death; Foot Diseases; Hoof and Claw; Lactation; Mastitis, Bovine; Pregnancy; Reproduction

Carrageenin-induced pedal inflammation in rats, was found to significantly enhance brain levels of prostaglandin (PG) E2 and PGF2 alpha. PG levels increased after 30 min of induction of the inflammation, peaked at 1 h, and attained normal levels by 4 h. Bilateral adrenalectomy had little effect on carrageenin-induced increase in rat brain PGs. The pattern of elevation of central PGs and the time course of carrageenin inflammation were at variance, the latter peaking between 3 and 4 h. The findings lend credence to the postulate that inflammatory hyperalgesia involves participation of central pain circuits, and that fever accompanying inflammation is caused by the central release of PGs. The central nociceptive and hyperthermic actions of PGs are well documented. However, the increase in central PG levels may well be caused by stress induced by the peripheral inflammation, since the pattern of elevation in either case is qualitatively similar.

Topics: Adrenalectomy; Animals; Brain; Carrageenan; Dinoprost; Dinoprostone; Edema; Female; Foot Diseases; Male; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains; Time Factors