Pharmacokinetic variables of skeletal muscle creatine kinase (CK) activity after IV administration of a muscle extract; CK bioavailability after IM administration of the muscle extract; and effect of IM administration of saline solution, to appreciate the possible release of CK consecutive to muscle puncture, were determined in 6 cows. A general equation for the quantitative estimation of skeletal muscle damage also was derived. Administration of saline solution IM had no effect on plasma CK activity (ANOVA, P > 0.05) in any of the cows. After IV administration of the muscle extract (150 U/kg of body weight), mean volume of the central compartment, plasma half-life, and plasma clearance of CK were 0.027 +/- 0.007 L/kg, 520 +/- 109 minutes, and 6.43 +/- 2.29 ml/kg/h, respectively. After IM administration (150 U/kg), mean bioavailability of CK was 51 +/- 17% and maximal plasma CK activity (500 +/- 97 U/L) was observed at 454 +/- 131 minutes. The rate of CK activity entry into plasma was determined by use of deconvolution analysis. Two peaks were observed; the first appeared before the 30th minute after IM administration, and the second appeared at 3.3 +/- 1.1 hours. Amplitudes were 6.31 +/- 4.45 and 6.57 +/- 3.08 U/kg/h, for the first and the second peaks, respectively. The quantity of CK liberated from control muscle was 0.69 +/- 0.12 U/kg/h, corresponding to a normal daily catabolism of 5.8 +/- 1.0 mg of muscle/kg. From these results, the following equation can be proposed to determine the corresponding mean equivalent of destroyed muscle (Qmuscle, test article) after IM administration of a test article: Qmuscle, test article (g/kg) = 4.41 X 10(-6) AUC (U/h/L), with AUC being the CK plasma activity area under the curve.

During the hunting season of 1992, 322 black bears from Pennsylvania were examined for Toxoplasma gondii- and Trichinella spp-induced infections. Toxoplasma gondii antibodies were found in 79.8% of 322 bears--titer < 1:25 in 65 (20.2%), 1:25 in 18 (5.6%), 1:50 in 11 (34.5%) and 1:500 in 128 (38.7%) bears--by use of the modified agglutination test. Muscle tissues from 89 of these bears were bioassayed for T gondii parasites. Muscles from 64 bears, including heart from 1 bear, and heart alone from another bear, were digested in pepsin, and the digested samples were bioassayed in mice. Toxoplasma gondii was isolated from 5 bears; from the heart of 1, heart and skeletal muscles of 1, and skeletal muscles of 3. The T gondii antibody titers for the 5 bears with detectable T gondii were: greater than or equal to 1:25 in all 5 bears by use of the modified agglutination test; < 1:10 (3 bears, considered Toxoplasma-negative), 1:20 and 1:320 by use of the Sabin-Feldman dye test; < 1:64 (3 bears, considered Toxoplasma-negative), 1:128, 1:512 by use of the indirect hemagglutination test, and < 1:16 (2 bears, considered Toxoplasma-negative), 1:32, 1:64, and 1:512 by use of the latex agglutination test. Toxoplasma gondii was not isolated from feces of 5 cats fed muscles from the remaining 25 bears with T gondii antibody titer < 1:25. Tissue cysts of the 4 T gondii isolates from bears were rendered noninfective by freezing at -13 C. Antibodies against Trichinella spp were found in 6 (1.8%) of 319 bear sera; Trichinella spp larvae were detected in muscle digests of 2 of 63 bears, and in histologic sections of muscles from 3 of 162 bears. Genetic typing indicated that the 2 Trichinella isolates from bears were a sylvatic genotype and were not the species found in domestic pigs.

Although the respiratory tract of healthy and diseased cattle has been intensively studied during the past few years, only a few attempts to detect dysfunctions of bovine inspiratory muscles have been reported. Such technique would be useful in assessing the possibility of inspiratory muscle fatigue in the context of ventilatory failure. Fatigue in skeletal muscle is associated with characteristic changes in the electromyographic power spectrum. Power spectral analysis was therefore applied to cattle diaphragmatic electromyograms (EMGdi) to precisely determine the exact influence of motion and ECG artifacts, describe its basic frequency content, and extract a spectral index capable of providing an accurate warning of fatigue. The EMGdi was recorded via intramuscularly placed fishhook electrodes in 5 healthy young bulls during resting and stimulated respiration. The EMGdi and EGC signals were analyzed by use of power spectral density analysis after band-pass filtering (20 to 1,800 Hz). The EMGdi spectrum was concentrated in the band width 20 to 530 Hz. Electrode motion artifacts were absent, and it was always possible to find an electrode pair giving ECG-free EMGdi. Of the 12 power and frequency values used to quantitate the spectrum, the most stable was the centroid frequency. It was reproducible within and between calves and was only minimally altered by changing inspiratory, load. Though the clinical relevance of fatigue in the respiratory musculature in case of ventilatory failure is currently unknown, the method described here constitutes a possible approach to detection of such phenomenon in cattle.

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.

Effects of the following treatments on abomasal and duodenal myoelectric activity in yearling cattle were studied: 2 ml of 0.9% sodium chloride solution (NACL); 0.07 mg of bethanechol (BET)/kg of body weight; 0.1 mg of metoclopramide (MET)/kg; and 0.07 mg of bethanechol and 0.1 mg of metoclopramide (BETMET)/kg. All treatments were administered SC during the early part of phase I of the migrating myoelectric complex Myoelectric signals were recorded for 4 hours after administration of the treatments from 1 electrode in the antrum and 3 electrodes in the duodenum. For the antral spike rate (ASR), there was no significant difference among treatments during the first hour, but the ASR was significantly (P < 0.05) greater during hours 2 to 4 after treatment with BETMET, compared with ASR for MET alone. The duodenal spike rate (DSR) was significantly (P < 0.05) greater during the first hour after administration of BETMET than after the other treatments. After administration of BET, DSR was significantly (P < 0.05) greater than after MET or NACL. There was no difference in DSR after MET, compared with DSR after NACL. There was no significant difference in DSR among treatments during the second and third hours. The total antegrade propagating spike (TAPS) count was greater after administration of BETMET in all hours, compared with the other treatments. The ratio of TAPS to total spikes on the orad-most duodenal electrode was significantly (P < 0.05) greater after BETMET during hours 1 and 2.

Repeatability of measurements of peak and mean tracheal and pharyngeal pressures in exercising horses was determined. Five athletically fit horses were subjected to repeated (n = 5) standardized exercise trials. Static pressures in the trachea, nasopharynx, and mask were determined. At least 96% of all mean pressure measurements were within 5 cm of H2O of the mean value for any horse. Peak pressure measurements were less repeatable, but at least 96% of all measurements were within 10 cm of the mean peak measurements for any horse. In 10 horses galloping at 14 m/s, the 95% confidence interval for peak tracheal and pharyngeal inspiratory pressures ranged from -40 to -50 cm of H2O and -20 to -26 cm of H2O, respectively. During expiration, the 95% confidence interval for peak tracheal and pharyngeal pressure at the same speed ranged from 15 to 28 cm of H2O and 10 to 24 cm of H2O respectively. During inspiration, horses with induced laryngeal hemiplegia had static pressure measurements generally outside that range. We conclude that determination of tracheal and pharyngeal pressures is a potentially useful adjunct for assessment of the proximal portion of the respiratory tract.

Seven horses (4 anesthetized and 3 awake) and 2 ponies (anesthetized) were studied to evaluate the high sensitivity of the pulmonary circulation of the horse to various blood-borne particles, and to establish the presence of intravascular macrophages in the lung. Pulmonary and systemic pressures and cardiac output before and during particle injection were measured in some animals. An anesthetized foal had a large increase in pulmonary arterial pressure (32 and 34 mm of Hg) within 1 minute of iv administration of small test doses of radioactively labeled liposomes (2.5 micromoles/kg of body weight) or a 1% suspension of blue pigment (0.3 ml/kg), respectively. Quantitative real-time gamma camera imaging of the foal revealed high retention of the labeled liposomes during the first pass through the lungs; retention persisted throughout the experiment. Postmortem analysis revealed 55 and 47% lung retention of liposomes and blue pigment, respectively. The 2 anesthetized ponies had increased pulmonary artery pressure of 34 +/- 7 mm of Hg, decreased cardiac output, and 42% lung retention after administration of 1% blue pigment (0.2 ml/kg), whereas 3 awake horses had increased pressure of 28 +/- 9 mm of Hg after 1.8 X 10(8) (1.8-micromoles-diameter) latex microspheres/kg. None of the injected particles caused vascular obstruction, and they do not cause pulmonary vascular reactivity in species that lack pulmonary intravascular macrophages. Finally, 3 horses (1 anesthetized and 2 awake) were infused iv with small doses of the blue pigment, and their lungs were perfusion-fixed to identify specific labeling of the pulmonary intravascular macrophages. These cells were fully differentiated macrophages, contained blue pigment in phagocytes, and were tightly adherent to the pulmonary capillary endothelium. At this time, horses (order Perissodactyla) are the only species outside the mammalian order Artiodactyla (sheep, pig, cattle) documented to have reactive intravascular macrophages. Compared with other species, low doses of particles induced marked hemodynamic responses; horses appear to be more sensitive to IV administered particles than are other species studied.

Diamine oxidase (DAO), an enzyme of small intestinal origin, is released from mucosal storage sites by IV administration of heparin, to yield the plasma postheparin DAO (PHD) curve. The PHD curve is diminished when mucosal surface area is lost, and baseline (without heparin) plasma DAO activity increases when mucosal storage sites are damaged. Plasma DAO activity was measured after 2 doses of heparin were administered Iv in healthy, conscious horses. In anesthetized horses, the PHD curve was studied: during sham small intestinal surgery, and during venous strangulation obstruction (VSO) of the distal 50% of the small intestine. In a third group of anesthetized horses, baseline plasma DAO activity (without heparin) was measured during vso of the distal 50% of the small intestine for 90 minutes, followed by reperfusion for 90 minutes. Postheparin plasma DAO curves in conscious horses were similar to those reported in other species Horses with VSO had a similar PHD curve as did sham-operated controls at all times, except at 15 minutes, when plasma DAO activity was significantly (P < 0.05) greater in the vso group. Horses with VSO and reperfusion had no change in baseline plasma DAO activity throughout the study. Peritoneal fluid DAO activity remained low throughout the study, but increased slightly in horses with VSO that received heparin, possibly because of DAO from extravasated blood in the peritoneal fluid. Results indicated that the plasma DAO response to IV administered heparin in horses is similar to that in other mammals, but, unlike other species, baseline and postheparin DAO activities did not change as expected after small intestinal vascular obstruction and mucosal injury. There may be additional sources of DAO in horses, the type of injury induced was not of sufficient magnitude to affect storage sites of DAO, or the circulatory changes induced by vso might have altered tissue delivery of heparin.