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2-year-old Quarter Horse stallion was admitted for evaluation of pollakiuria of 6 weeks’ duration. Pollakiuria and hematuria were diagnosed by the referring veterinarian 4 weeks prior to referral. Pseudomonas sp had been cultured from the urine, and the referring veterinarian treated the stallion with amikacin sulfate on the basis of results of susceptibility testing. Hematuria resolved with antimicrobial therapy, but pollakiuria persisted. Initial physical examination revealed no abnormalities. Mild azotemia (BUN, 24 mg/dL [reference range, 14 to 21 mg/dL]; creatinine, 1.9 mg/dL [reference range, 0.6 to 1.7 mg/dL]) was detected. Transrectal evaluation of the bladder revealed normal tone, moderate urine volume, and the absence of cystic calculi. Transabdominal renal ultrasound revealed normal size, shape, and architecture for both kidneys. The stallion was sedated with detomidine (0.02 mg/kg [9 µg/lb], IV) and butorphanol (0.02 mg/kg, IV). The penis was prepared for urethral catheterization and endoscopic examination. The stallion became extremely agitated during handling of the penis, and the agitation escalated to violent kicking. In order to proceed with the endoscopic examination, the stallion was sedated with xylazine (0.45 mg/kg [0.2 mg/lb], IV) and butorphanol tartrate (0.02 mg/kg, IV), and anesthesia was induced with guaifenesin (40 g/kg [18.2 mg/lb], IV) and thiopental sodium (0.3 mg/kg [0.14 mg/lb], IV). General anesthesia was maintained with halothane and oxygen via endotracheal intubation with the horse in right lateral recumbency. The urinary bladder was catheterized, and a urine sample was obtained for urinalysis; results included specific gravity (1.027; reference range, 1.025 to 1.050), glucose (negative), bilirubin (negative), ketones (negative), blood (negative), pH (8.5; reference range, 7.0 to 9.0), protein (negative), casts (negative), WBCs (negative), RBCs (negative), crystals (3+ amorphous phosphate and 3+ calcium carbonate), bacteria (negative), and epithelial cells (negative). Endoscopic examination of the urinary tract was performed. The urethra was found to be normal. The bladder appeared to have a discreet area of discoloration near the apex, but the importance of this finding was not known. Upon recovery from anesthesia, the stallion immediately had signs of anxiety. The dorsal epaxial and gluteal muscles became tense and began to fasciculate, and the horse developed tachypnea and tachycardia. A tentative diagnosis of postanesthetic myopathy was made. The stallion was treated with lactated Ringer’s solution (8.8 mg/kg/h [4 mL/lb/h], IV, continuous), flunixin meglumine (1.0 mg/kg [0.45 mg/lb], IV, q 12

Objective—To characterize the in vitro response of circular and longitudinal myometrial layers of the uterine horn (CMLH and LMLH, respectively) of horses to endothelin (ET)-1 by use of specific ETA (BQ-123) and ETB (IRL-1038) receptor antagonists. Sample Population—Uteruses from 10 nongravid mares in anestrus. Procedure—Muscle strips from the CMLH and LMLH were suspended in tissue baths and connected to force-displacement transducers interfaced with a polygraph. Strips were incubated for 45-minute intervals with no antagonist (control specimens), and 3 concentrations (10–9, 10–7, and 10–5M) of BQ-123, IRL- 1038, or BQ-123 and IRL-1038 before concentrationresponse curves to ET-1 were generated. Contractile response to cumulative concentrations of ET-1 (10–9 to 10–6M) was quantified by measuring change in the area under the curve (AUC) for the 3-minute period after each ET-1 dose. Results—ET-1 caused concentration-dependent contraction of the CMLH and LMLH specimens. Application of BQ-123 decreased AUC values for both layers. Application of IRL-1038 increased the AUC value for LMLH specimens but did not affect the CMLH value. The combination of BQ-123 and IRL-1038 decreased the AUC value for LMLH tissue and increased that for CMLH tissue. Conclusions and Clinical Relevance—ET-1 causes contraction of the CMLH and LMLH in nongravid horses. In both layers, ETA receptors mediate contraction but the role of ETB receptors remains unclear. In the LMLH, ETA receptors have a dominant role; the presence of another receptor or receptor subtype within this layer is suggested. These findings support a physiologic role for ET-1 in uterine contractility. (Am J Vet Res 2005;66:1094–1100)