In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (HWD), pulmonary hemodynamic measurements were obtained from 7 experimentally infected, anesthetized dogs before and after hydralazine administration (mean dose, 1.96 mg/kg of body weight). Five dogs were maintained on room air, while 2 were maintained on 100% oxygen during the hydralazine study. The hemodynamic effect of hydralazine in dogs with HWD was evaluated, using heart rate, cardiac index, mean pulmonary artery pressure, mean arterial pressure, total pulmonary resistance, total systemic resistance, total systemic resistance/total pulmonary resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure X heart rate] and [mean pulmonary artery pressure X heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased greater than or equal to 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was less than or equal to 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test. Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders. However, pretreatment right ventricular end diastolic pressure was significantly less in responders than in nonresponders. Two dogs sustained hypotension after hydralazine administration, but no dogs had significant tachycardia. In dogs with experimentally induced HWD, treatment with hydralazine had significantly greater effect on cardiac index and mean pulmonary and systemic arterial pressures and resistance than did administration of 100% oxygen. These data indicate that further study of vasodilators for treatment of HWD-induced pulmonary hypertension may be warranted.

Six Jersey cows were implanted with 8 pairs of bipolar electrodes: 1 in the jejunum, 1 in the ileum, 3 in the cecum, and 3 in the proximal loop of the ascending colon (PLAC). Myoelectric activity was recorded at 2- to 3-day intervals, 3 times for 8 hours or 4 times for 6 hours, using a computer-based oscillograph and data-acquisition program. Mean (+/- SD) duration of the migrating myoelectric complex (MMC) in the ileum was 84.52 +/- 4.87 minutes. Phases I and II of the MMC lasted significantly (P < 0.05) longer than phase III. Two types (A and B) of cyclic activity were found in the cecum and PLAC. Cyclic activity type A was observed predominantly in the cecum, and type B was observed exclusively in the PLAC. Phase III of the MMC in the ileum was accompanied by hyperactivity type A at the level of the ileocecocolic junction in 60.90 +/- 12.65% of the MMC. Twenty-seven types of orally and aborally propagated spike sequences, involving the cecum and PLAC, were found. They were most frequent when an MMC phase III was observed in the ileum, and least frequent when an MMC phase I was observed in the ileum (P < 0.05). All electrode sites of the cecum and PLAC served as pacemaker areas. Propagated and nonpropagated spikes were found at all electrode sites of the cecum and PLAC. Although propagated spikes lasted significantly (P < 0.05) longer than nonpropagated spikes, a clear distinction on the basis of duration could not be defined between the 2 spike types because broad overlapping of duration existed. Duration of cecocolic spiking activity per electrode (expressed as percentage of time) was significantly (P < 0.05) greater during MMC phase III in the ileum than during MMC phase I. It can be concluded that myoelectric activity of the cecum is well coordinated with the ileum and the PLAC. Phases of reduced and increased myoelectric activity in the cecum and PLAC are simultaneous with phases I and III of the MMC in the ileum.

The effects of 2 drugs, xylazine and propofol, on the urethral pressure profile were compared. Seven female dogs were sedated by administration of one drug, then the other, and urethral variables were measured. In the dogs sedated with propofol, the mean +/- SD, maximal urethral closure pressure (51 +/- 7.4 cm of H2O) was significantly (P < 0.05) higher than the value when dogs were sedated with xylazine (23.3 +/- 7.6 cm of H2O). Results were compared with those obtained by various authors, in particular for nonsedated dogs. It is concluded that propofol is a good drug for investigation of the urethral pressure profile, whatever its effect on maximal urethral closure pressure.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.

Strips of trachealis muscle were dissected from the mid-cervical portion of the trachea from horses that were free of respiratory tract disease. The epithelium and mucosa were removed from one group of tissues and were left intact in a second group of tissues. Each tissue was suspended in a bath filled with Krebs-bicarbonate solution that was aerated with 5% CO2 in oxygen and maintained at 37 C. Isometric tension was continuously recorded. The contractile response to square-wave electrical stimulations increased as frequency (3, 5, 10, 15, 20, 25, and 30 Hz), voltage (10, 15, 18, and 25 V), and pulse duration (0.2, 0.5, 1.0, 1.5, and 2.0 ms) increased in tissues with the epithelium and mucosa intact. A stimulus of 18 V, 20 Hz, and 0.5 ms induced maximal contraction. Atropine (10(-6) M) abolished the response to 18 V and 0.5 ms at all frequencies. The increase in active isometric tension was concentration dependent when acetylcholine (10(-9) to 10(-4) M) was added to the baths in 0.5-logarithmic increments. Tissues that were contracted in response to acetylcholine (10(-5) M) had a concentration-dependent decrease in active isometric tension when isoproterenol was added to the baths in 0.5-logarithmic increments (10(-9) to 10(-4) M). The contraction and relaxation curves were qualitatively similar, but quantitatively different in tissues with and without the epithelium and mucosa. Removing the epithelium and mucosa increased the contractile response to acetylcholine at bath concentrations of 3.1 X 10(-7) M and 10(-6) M. The presence of epithelium and mucosa enhanced the magnitude of isoproterenol-induced relaxations. We concluded that electrical stimulation released acetylcholine from isolated equine trachealis muscle, that isoproterenol induced relaxation of the trachealis muscle, and that the magnitude of the responses to exogenous agonists depended on the presence of epithelium and mucosa.

Strips of trachealis muscle were dissected from the mid-cervical portion of the trachea of horses that were free of respiratory tract disease, and the overlying epithelium and mucosa were removed. Muscle strips were suspended in tissue baths that were filled with Krebs-bicarbonate solution, aerated with 5% CO2 in oxygen and maintained at 37 C. Isometric tension was continuously recorded. The increase in active isometric tension was concentration dependent when acetylcholine (10(-9) to 10(-4) M) or histamine (10(-9) to 10(-4) M) was added to the tissue baths in 0.5-logarithmic increments. When the tissues were contracted with acetylcholine (3.1 X 10(-6) M) or histamine (10(-4) M), the decrease in active isometric tension was concentration dependent when isoproterenol (10(-9) to 10(-4) M) or salbutamol (10(-9) to 10(-4) M) was added to the tissue baths in 0.5-logarithmic increments. There was no difference between the response to isoproterenol and salbutamol when tissues from the same horses were compared whether the tissues were contracted in response to acetylcholine (3.1 X 10(-6) M) or histamine (10(-4) M). Relaxation was antagonized by 10(-6) M) propranolol. The degree of relaxation obtained in these muscle strips was considerably less than that reported from other species' tracheal muscle strips that had the epithelium and mucosa intact. We concluded that equine tracheal smooth muscle contains beta-adrenoceptors that can be stimulated by either a mixed beta-1, beta-2 agonist or a selective beta-2 agonist.

Smooth muscle strips from the midcervical portion of the trachea and bronchial smooth muscle strips from third-generation airways of horses were placed in tissue baths, and isometric contractile force was measured. Active force was measured in response to electrical stimulation and exogenous acetylcholine. Square-wave electrical stimuli were applied at various voltages (10, 12, 15, 18, 20, 25 V), frequencies (3, 5, 10, 15, 20, 25, 30 Hz), and pulse durations (0.2, 0.5, 1.0, 1.5, 2.0 ms). Isometric contractile force increased as voltage, frequency, and pulse duration increased. Maximal contractile response to electrical stimulation was obtained at 18 V, 25 Hz, and 0.5 ms. Atropine (10-6M) or tetrodotoxin (3 X 10-6M) blocked the contraction, indicating that the contractile response was attributable to the release of neurotransmitter from cholinergic nerves. Cumulative concentration-response curves to acetylcholine (10-9M through 10-4M) were determined. Isometric contractile force increased as acetylcholine concentration increased. There was a significant (P less than 0.05) difference in the 50% effective dose for acetylcholine in tracheal smooth muscle and bronchial smooth muscle. The mean (+/- SD) contractile response to maximal electrical stimulus was 89% (+/- 7.4%) of that in response to 10-4M acetylcholine in tracheal smooth muscle and was 68% (+/- 10.4%) of the response to 10-4M acetylcholine in bronchial smooth muscle.

Eosinophilic myositis lesions are characterized by severe eosinophil infiltration along muscles of affected animals. The exact cause of the lesion remains controversial and the carcass is condemned once this lesion is seen during meat inspection. A cow slaughtered in Chonbuk province, Korea was observed to have disseminated pale foci throughout the musculature; meat samples were obtained and macroscopically investigated. Cut ends of neck and thigh muscle tissues showed variably sized, multifocal pale white-grayish nodular lesions. Histopathological examination consistently revealed inflammatory lesions with adjacent infiltration of eosinophilic granulocytes and focal necrotic calcification. However, no parasites, including Sarcocystis sp., could be discerned in the affected carcass. This case was diagnosed as idiopathic eosinophilic myositis in cattle.

The effects of hypertonic saline solution (HSS) and hyperosmotic dextrose (HD; 2,400 mosm/L, 4 ml/kg of body weight) on left ventricular afterload were determined in normovolumic, chloralose-anesthetized, autonomically blocked dogs (n = 8). Solutions were infused IV over 3 minutes. Left ventricular afterload was assessed by use of a dual-tipped micromanometer catheter with an electromagnetic fluid-velocity sensor located in the ascending aorta, and the impedance spectrum was calculated after Fourier analysis of signal-averaged aortic pressure and flow signals. Hypertonic saline solution and HD decreased peripheral resistance, reflection coefficient at zero frequency, and frequency of the first zero crossing of the phase angle for 3 to 5 minutes after either fluid was administered. Characteristic impedance was not altered by HSS or HD. These impedance spectrum changes indicate transient vasodilatation and afterload reduction. We conclude that the vascular effect of an ionic hyperosmotic solution (HSS) is similar to that of a nonionic hyperosmotic solution (HD), and that HSS and HD transiently decrease afterload in normovolumic dogs. The duration of the afterload reduction after HSS administration appeared to be too short to be of great clinical benefit.

The effect of xylazine, cisapride, and naloxone on myoelectric activity of the ileum, cecum, and proximal loop of the ascending colon (PLAC) was determined in 4 healthy Jersey cows implanted with 8 pairs of bipolar electrodes. A 4 X 4 Latin square design was used. The treatments included xylazine (0.04 mg/kg of body weight), cisapride (0.08 mg/kg), naloxone (0.05 mg/kg), and 0.9% sodium chloride solution (20 ml). All treatments were administered IV during early phase I of the migrating myoelectric complex in the ileum. Myoelectric activity was recorded for 4 hours after treatment, and data were analyzed for each hour separately. Xylazine significantly (P < 0.05) increased the duration of phase I of the first migrating myoelectric complex in the ileum to 220.72 +/- 26.89 minutes, compared with 30.91 +/- 10.11 minutes after administration of 0.9% sodium chloride solution. The number of cecocolic spikes per minute per electrode and the duration of cecocolic spike activity (percentage of recording time) were significantly (P < 0.05) decreased for the first 3 hours, and the number of propagated spike sequences in the cecum and PLAC was significantly (P < 0.05) decreased for the first 2 hours after administration of xylazine. Significant difference was not found between control and either,cisapride or naloxone treatment of healthy cows. However, during hour 1 after treatment with cisapride, number of spikes per minute, duration of spike activity, and number of propagated spike sequences were highest, compared with the other treatments. It was concluded that naloxone at the dosage used in this study was not suitable for medical treatment of cecal dilatation in cattle, when hypomotility of the cecum and PLAC must be reversed. Xylazine should not be used for relief of signs of pain in cases of cecal dilatation, because it significantly reduced myoelectric activity of the cecum and PLAC for at least 2 hours after treatment. Furthermore, results of this study indicated a trend (P > 0.05) toward increase of cecocolic myoelectric activity after administration of cisapride. It is the authors' opinion that the potential benefit of cisapride for medical treatment of cecal dilatation in cattle needs further evaluation.