Effects of furosemide, exercise, and atropine on tracheal mucus transport rate (TMTR) in horses were investigated. Atropine (0.02 mg/kg of body weight) administered IV or by aerosolization significantly (P < 0.05) decreased TMTR at 60, but not at 30 minutes after its administration in standing horses. Furosemide (1.0 mg/kg, IV) did not have any significant effect on TMTR when measured at 2 or 4 hours after its administration in standing horses. Exercise alone or furosemide (1.0 mg/kg, IV) administration followed 4 hours later by exercise did not alter TMTR, compared with values for standing control or exercised horses administered saline solution. Atropine (0.02 mg/kg, IV) administered after exercise significantly (P < 0.05) decreased TMTR, compared with values for no exercise standing controls, for exercise after administration of saline solution, and for furosemide and exercise.

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. Ventricular beats were clearly evident in 8 of the 12 arrhythmias meeting the criteria for establishing the ADD. These results indicate that atropine may lower the arrhythmogenic threshold.

In vitro effects of a mixture of Escherichia coli heat-stable enterotoxins (STa and STb) on isolated jejunum of 3-week-old male pigs were studied, using everted intestinal sac techniques. Heat-stable enterotoxins increased chloride secretion and chloride absorption in everted intestinal sacs. The increase of secretory flux was greater than that for absorptive flux. Vasoactive intestinal peptide (6 x 10-9M) increased chloride secretion, but had no effect on chloride absorption. Neither vasoactive intestinal peptide nor pilocarpine (10-5M) had additive effect to ST. Secretory effects of ST were not blocked by atropine 2 x 10-5M), clonidine (10-6M), or morphine (4.2 X 10-6M).

Organophosphates (OP) and carbamates are widely utilized insecticides, but they also pose significant risks as sources ofintoxicationfor both humans and animals. A male non-descript dog, seven years old was presented with a chronic respiratory distress, dysphonia, exercise intolerance, and neurologic signs to Veterinary Clinical Complex, VCRI, Orathanadu on April 2023. Physical examination revealed elevated rectal temperature and congested mucous membrane with elevated heart beat and respiratory rate. Thoracic auscultation revealed muffled heart sound. The dog's medical history indicated a potential case of organophosphate poisoning. Treatment involved administering atropine sulfate, normal saline, ceftriaxone, and furosemide. However, throughout the treatment process, the dog continued to experience upper respiratory stridor and dyspnoea. Clinical examination and radiographic observations confirmed the diagnosis of laryngeal paralysis. This case highlights the occurrence of laryngeal paralysis polyneuropathy complex in a canine affected by organophosphate poisoning.

Organophosphates (OP) and carbamates are widely utilized insecticides, but they also pose significant risks as sources ofintoxicationfor both humans and animals. A male non-descript dog, seven years old was presented with a chronic respiratory distress, dysphonia, exercise intolerance, and neurologic signs to Veterinary Clinical Complex, VCRI, Orathanadu on April 2023. Physical examination revealed elevated rectal temperature and congested mucous membrane with elevated heart beat and respiratory rate. Thoracic auscultation revealed muffled heart sound. The dog's medical history indicated a potential case of organophosphate poisoning. Treatment involved administering atropine sulfate, normal saline, ceftriaxone, and furosemide. However, throughout the treatment process, the dog continued to experience upper respiratory stridor and dyspnoea. Clinical examination and radiographic observations confirmed the diagnosis of laryngeal paralysis. This case highlights the occurrence of laryngeal paralysis polyneuropathy complex in a canine affected by organophosphate poisoning.

Objective—To evaluate the ability of atropine sulfate, butylscopolammonium bromide combined with metamizole sodium, and flunixin meglumine to ameliorate the clinical adverse effects of imidocarb dipropionate in horses. Animals—28 horses with piroplasmosis. Procedures—28 horses were randomly assigned to 4 equal groups according to the pretreatment administered. Fifteen minutes before administration of 2.4 mg of imidocarb dipropionate/kg IM, horses in the first group were pretreated with 0.02 mg of atropine sulfate/kg IV, the second group with a combination of 0.2 mg of butylscopolammonium bromide/kg IV and 25 mg of metamizole sodium/kg IV, the third group with 1.1 mg of flunixin meglumine/kg IV, and the fourth (control) group with 1 mL of saline (0.9% NaCl) solution/50 kg IV. Physical examination, including evaluation of rectal temperature, heart and respiratory rates, capillary refill time, mucous membrane color, hydration status, abdominal sounds, signs of abdominal pain, salivation, diarrhea, and number of defecations, was performed. Results—Imidocarb dipropionate use in the control group was associated with serious adverse effects including signs of abdominal pain (4/7 horses) and diarrhea (2/7). Horses pretreated with atropine had no diarrhea, but 6 had signs of abdominal pain. Only 1 horse that received butylscopolammonium-metamizole pretreatment had signs of abdominal pain and 3 had diarrhea, which was numerically but not significantly different than the control group. Of horses pretreated with flunixin, 3 had signs of abdominal pain and 3 had diarrhea. Conclusions and Clinical Relevance—A combination of butylscopolammonium bromide and metamizole sodium may be useful to ameliorate the adverse effects of imidocarb dipropionate in horses, although group size was small and significant differences from the control group were not found.

During acute bouts of recurrent airway obstruction (heaves) in horses, neutrophils that are capable of increased production of reactive oxygen species accumulate in the airways. In the study reported here, the effect of hydrogen peroxide (H2O2; 1 micromolar to 0.1M), one of these reactive oxygen species products, on the responses of isolated trachealis muscle of horses was determined. Before and after incubation with H2O2, contractile responses to acetylcholine, electrical field stimulation (EFS), 127 mM KCl, and relaxation responses to isoproterenol and activation of the nonadrenergic noncholinergic inhibitory response (iNANC) were evaluated. Beginning at 1 mM, H2O2 contracted trachealis muscle in a concentration-dependent manner. This contraction was unaffected by atropine (1 micromolar), tetrodotoxin (1 micromolar), or 1 micromolar meclofenamate. Contraction of trachealis muscle in response to H2O2 is, therefore, not attributable to release of prostaglandins, acetylcholine, or other neurotransmitters. Above a concentration of 0.1 mM, H2O2 depressed the responses to EFS. acetylcholine, and KCl in a concentration-dependent manner. At 0.1M, H2O2 decreased the maximal responses to EFS, acetylcholine, and KCl by 62.7 +/- 7.2, 60.58 +/- 6.12, and 37.8 +/- 9.54%, respectively. In the presence of meclofenamate (1 micromolar), partial but significant protection against 1 to 100 mM H2O2 was observed. In tracheal strips contracted with 0.3 micromolar methacholine, H2O2 had no effect on the isoproterenol concentration-response curve. Up to a concentration of 100 mM, H2O2 had no effect on iNANC response. However, in the presence of 100 mM H2O2, this response was abolished in 2 of 4 horses. We conclude that high concentrations of H2O2 affected the responses of airway smooth muscle by actions on neurotransmission, muscarinic receptors, and downstream from receptors; some of the H2O2 effects were in part mediated by cyclooxygenase products; and H2O2 had no effect on beta-adrenergic- or iNANC-induced relaxation.

Hemodynamic and analgesic effects of medetomidine (15 microgram/kg of body weight, IM) and etomidate (0.5 mg/kg, IV, loading dose; 50 micrograms/kg/min, constant infusion) were evaluated in 6 healthy adult Beagles. Instrumentation was performed during isoflurane/ oxygen-maintained anesthesia. Before initiation of the study, isoflurane was allowed to reach end-tidal concentration less than or equal to 0.5%, when baseline measurements were recorded. Medetomidine and atropine (0.044 mg/kg) were given IM after recording of baseline values. Ten minutes later, the loading dose of etomidate was given IM, and constant infusion was begun and continued for 60 minutes. Oxygen was administered via endotracheal tube throughout the study. Analgesia was evaluated by use of the standard tail clamp technique and a direct-current nerve stimulator. Sinoatrial and atrial-ventricular blocks occurred in 4 of 6 dogs within 2 minutes after administration of a medetomidine-atropine combination, but disappeared within 8 minutes. Apnea did not occur after administration of the etomidate loading dose. Analgesia was complete and consistent throughout 60 minutes of etomidate infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output. Etomidate infusion caused a decrease in respiratory function, but minimal changes in hemodynamic values. Time from termination of etomidate infusion to extubation, sternal recumbency, standing normally, and walking normally were 17.3 +/- 9.4, 43.8 +/- 14.2, 53.7 +/- 11.9, and 61.0 +/- 10.9 minutes, respectively. All recoveries were smooth and unremarkable. We concluded that this anesthetic drug combination, at the dosages used, is a safe technique in healthy Beagles.

Distal airway segments (ID, 3 to 4 mm; length, 5 mm) from 2 groups of horses were isolated and suspended in tissue baths filled with Krebs solution, aerated with 5% CO2 in oxygen and maintained at 37 C. Responses to exogenous acetylcholine, isoproterenol, or electrical field stimulation were compared. Control horses (n = 30) had no history of recurrent airway obstruction, whereas principal horses (n = 15) had recurrent airway obstruction and were studied during an acute episode of airway obstruction. Although the distal airways contracted in response to the cumulative half-logarithmic addition of acetylcholine (10(-10)M to 10(-3)M) in both groups, bronchi obtained from principals were less sensitive to acetylcholine than were bronchi obtained from controls. Tetrodotoxin-sensitive electrical field stimulation-induced contractions were observed in both groups of airways, but the tension achieved in principal bronchi was less than in controls. All electrical field stimulation-induced contractions were abolished by atropine, indicating that the only excitatory innervation of equine distal airways is through the parasympathetic system. To examine the effect of isoproterenol and determine inhibitory innervation, bronchi were precontracted with histamine. Electrical field stimulation did not cause relaxation of precontracted bronchi in either group, thus indicating that distal airways lack inhibitory innervation. Isoproterenol caused similar, dose-dependent relaxation in both groups.