Health and ruminal variables were intensively measured during adaptation to grain-based diets in 6 beef cattle with fistulated rumens. The cows had been maintained on prairie grass hay-supplemented diets, and were converted to a grain-based finishing ration by feeding each successive diet (diets 1-4, respectively) for a period of 7 days. Each cow was evaluated and samples were obtained 3 times each day for the first 5 days that each diet was fed. Health variables monitored were rectal temperature, pulse, respiratory and rumen motility rates, fecal consistency, demeanor, blood pH, and blood glucose and L(+) lactate concentrations. Ruminal variables monitored were pH and glucose, DL-lactate, and volatile fatty acid concentrations of rumen contents. Data were analyzed by use of a multivariate ANOVA. We determined that most of the health variables were within reference rang limits throughout the adaptation period; however, analysis of pulse and respiratory rates indicated that diets 2 and 4 were stressful. Although blood pH continually decreased during feeding of the 4 diets (7.38 to 7.30), blood L(+) lactate and glucose concentrations had large increases only within diet 4. The pH of ruminal contents decreased progressively from 6.8 to 5.3. Rumen glucose concentration was low (< 1 micromole/ml), except with diet 4 in which values were 8 times higher than for other diets. By the end of the study, the ruminal contents of all animals were acidic (pH < 5.5), and, on the basis of higher than background amounts of ruminal glucose and DL-lactate, it was determined that rumen microbial equilibrium had not yet been achieved. Analysis of results of this study suggested that ruminal imbalance could be evaluated by monitoring pulse and respiratory rates, blood pH, and blood glucose concentrations. Assessment of the rumen alone could be accomplished by monitoring the variables of rumen pH, rumen glucose, and DL-lactate concentrations.

We compared the ability of 2 alpha2-adrenergic receptor antagonists, atipamezole and yohimbine, to reverse medetomidine-induced CNS depression and cardiorespiratory changes in lambs. Twenty lambs (7.8 +/- 2.6 kg) were randomly allotted to 4 treatment groups (n = 5). Each lamb was given medetomidine (30 micrograms/kg of body weight, IV), followed in 15 minutes by IV administration of atipamezole (30 or 60 micrograms/kg), yohimbine (1 mg/kg), or 0.9% NaCl (saline) solution. Medetomidine caused lateral recumbency in 1 to 2 minutes in all treated lambs. Medetomidine significantly (P < 0.05) decreased heart rate at 5 and 10 minutes after its administration. Heart rate remained above 120 beats/min, and severe bradycardia (< 70 beats/min) and other arrhythmias did not occur throughout the study. Medetomidine also induced tachypnea in all treated lambs. The tachypnea was abolished by atipamezole and yohimbine, but not by saline solution administration. The medetomidine-induced tachypnea did not significantly affect arterial pH and PaCO2. Arterial oxygen tension was within acceptable range (PaO2 = 71 to 62 mm of Hg), but was lower than expected. Administration of atipamezole, yohimbine, or saline solution did not change PaO2 significantly. Lambs treated with 30 or 60 micrograms of atipamezole/kg were able to walk unassisted in 2.4 +/- 0.4 and 2.3 +/- 0.7 minutes, respectively, whereas yohimbine-and saline-treated lambs did not walk unassisted until 15.6 +/- 2.7 and 73.0 +/- 6.8 minutes later, respectively. Results of this study indicated that medetomidine is a potent CNS depressant in lambs. Atipamezole at dosage of 30 or 60 micrograms/kg was equally effective, and was more effective in antagonizing medetomidine-induced CNS depression than was yohimbine.

Cardiorespiratory effects of abdominal insufflation were evaluated in 8 dogs during isoflurane anesthesia. Each dog was studied 3 times, in 1 of the following orders of insufflation pressures: 10-20-30, 20-30-10, 30-20-10, 10-30-20, 20-10-30, and 30-10-20 mm of Hg. Anesthesia was induced by use of a mask, dogs were intubated, and anesthesia was maintained by isoflurane in 100% oxygen. After instrumentation, baseline values were recorded (time 0), and the abdomen was insufflated with nitrous oxide. Data were recorded at 5, 10, 15, 20, 25, and 30 minutes after insufflation. The abdomen was then desufflated, with recording of data continuing at 35 and 40 minutes. Mean arterial pressure increased at 5 minutes during 20 mm of Hg insufflation pressure, and from 20 to 30 minutes during 30 mm of Hg pressure. Tidal volume decreased from 5 to 30 minutes during 10 and 20 mm of Hg pressures, and from 5 to 40 minutes during 30 mm of Hg pressure. Minute ventilation decreased at 10 and 20 minutes during 20 mm of Hg pressure. End-tidal CO2 concentration increased from 5 to 30 minutes during 20 and 30 mm of Hg pressure. The PaCO2 decreased at 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Values for pH decreased from 10 to 30 minutes during 20 and 30 mm of Hg pressures. The PaO2 decreased from 20 to 40 minutes during 10 mm of Hg pressure, at 30 minutes during 20 mm of Hg pressure, and from 10 to 40 minutes during 30 mm of Hg pressure. Percentage decrease in tidal volume was greater at 5 and 15 minutes with 30 mm of Hg pressure. Differences in percentage increase in end tidal CO2 concentration were observed among the 3 pressures from 5 to 30 minutes. Although significant, these changes do not preclude use of laparoscopy if insufflation pressure > 20 mm of Hg is avoided.

Tidal breathing flow-volume (TBFV) loops were determined in a group of control horses and in horses affected with recurrent airway obstruction (heaves). The latter group was studied when the condition was in remission and under increasing amounts of airway obstruction as reflected by measurements of change in pleural pressure, pulmonary resistance, and dynamic compliance. The TBFV loops of control horses had biphasic inspiratory and expiratory patterns; peak inspiratory and peak expiratory flows were detected early in inspiration and expiration, respectively. Tidal volume was unaffected by heaves, but at all stages of heaves, respiratory frequency was increased principally because of shorter inspiratory time, and therefore, inspiratory flow rate was increased. In horses with heaves, TBFV loops did not have a biphasic pattern; peak inspiratory flow was observed late in inspiration, and peak expiratory flow was observed early in expiration. As airway obstruction became more severe, peak expiratory flow increased as pulmonary resistance increased so that, during severe airway obstruction, TBFV loops had a characteristic appearance with high peak expiratory flow early in expiration followed by low flow rate.

Effects of IV and aerosol administration of 5-hydroxytryptamine (5-HT) on ventilation, pulmonary mechanics values, pulmonary arterial pressure, and heart rate were investigated in healthy unsedated Friesian calves. Minute volume increased significantly, mainly because of an increase in respiratory rate. Except for total pulmonary resistance after bolus injection, continuous administration of 5-HT given by either route caused significant alterations of lung dynamic compliance and total pulmonary resistance, the former decreasing to one-fifth of its baseline value and the latter increasing twofold. Pulmonary arterial pressure increased significantly, whatever the speed or route of administration. Administration of a bolus did not affect heart rate, whereas continuous iv administration of 5-HT as well by perfusion or by aerosol resulted in sustained tachycardia. It was concluded that 5-HT induces reversible bronchoconstriction and pulmonary vasoconstriction in healthy unsedated calves, 5-HT-induced functional alterations depend on the speed of administration, and excess of 5-HT production or depression in uptake by the lungs during bovine respiratory tract diseases could contribute to pulmonary dysfunction.

To determine whether abnormal airway pressures have a role in development of dorsal displacement of the soft palate (DDSP), measurements of tracheal and pharyngeal pressures were correlated with nasopharyngeal morphology in exercising horses. Exercising videoendoscopy and measurement of tracheal and pharyngeal pressures were used in 14 clinically normal horses and 19 horses with intermittent DDSP. The pressure signals were superimposed on the videoendoscope image, and both images were saved simultaneously on a videocassette for slow motion analysis to determine the instant displacement occurred in the respiratory cycle. Horses were submitted to an escalating 8-minute high-speed test with a maximal speed of 14 m/s. Compared with clinically normal horses, horses with intermittent DDSP did not have excessively negative inspiratory pressures during exercise. Eight horses displaced the soft palate during inspiration, 4 horses displaced it during expiration, and 7 displaced it by swallowing. Some horses displaced the soft palate at the beginning of the exercise trial, before reaching maximal speed, some horses displaced it at the peak speed, and some horses displaced it when slowing down. Epiglottic size in horses with DDSP was within normal limits, ruling out epiglottic hypoplasia as a cause of DDSP during exercise. Airway pressures were significantly (P < 0.002) altered after DDSP. Pharyngeal and tracheal inspiratory pressures were less negative, whereas pharyngeal expiratory pressure became less positive and tracheal expiratory pressure became more positive after displacement, suggesting a decrease in airflow and an increase in expiratory resistance in the upper airway.

Eighteen dogs undergoing lateral thoracotomy at the left fifth intercostal space were randomly assigned to 1 of 3 postoperative analgesic treatment groups of 6 dogs each as follows: group A, morphine, 1.0 mg/kg of body weight, IM; group B, 0.5% bupivacaine, 1.5 mg/kg given interpleurally; and group C, morphine, 1.0 mg/kg given interpleurally. Heart rate, respiratory rate, arterial blood pressure, arterial blood gas tensions, alveolar-arterial oxygen differences, rectal temperature, pain score, and pulmonary mechanics were recorded hourly for the first 8 hours after surgery, and at postoperative hours 12, 24, and 48. These values were compared with preoperative (control) values for each dog. Serum morphine and cortisol concentrations were measured at 10, 20, and 30 minutes, hours 1 to 8, and 12 hours after treatment administration . All dogs had significant decreases in pHa, PaO2, and oxygen saturation of hemoglobin, and significant increases in PaCO2 and alveolar-arterial oxygen differences in the postoperative period, but these changes were less severe in group-B dogs. Decreases of 50% in lung compliance, and increases of 100 to 200% in work of breathing and of 185 to 383% in pulmonary resistance were observed in all dogs after surgery. Increases in work of breathing were lower, and returned to preoperative values earlier in group-B dogs. The inspiratory time-to-total respiratory time ratio was significantly higher in group-B dogs during postoperative hours 5 to 8, suggesting improved analgesia. Blood pressure was significantly lower in group-A dogs for the first postoperative hour. Significant decreases in rectal temperature were observed in all dogs after surgery, and hypothermia was prolonged in dogs of groups A and C. Significant differences in pain score were not observed between treatment groups. Cortisol concentration was high in all dogs after anesthesia and surgery, and was significantly increased in group-B dogs at hours 4 and 8. Significant differences in serum morphine concentration between groups A and C were only observed 10 minutes after treatment administration. In general, significant differences in physiologic variables between groups A and C were not observed. Results of the study indicate that anesthesia and thoracotomy are associated with significant alterations in pulmonary function and lung mechanics. Interpleurally administered bupivacaine appears to be associated with fewer blood gas alterations and earlier return to normal of certain pulmonary function values. Interpleural administration of morphine does not appear to provide any advantages, in terms of analgesia or pulmonary function, compared with its IM administration.

Owing to technical and ethical limitations, a substantial part of the knowledge about the pathophysiologic mechanism of the human diaphragm has been obtained from studies in which phrenic nerve activation was usually carried out by direct surgical exposure of the nerves in the neck of deeply anesthetized, mechanically ventilated animals. Novel information has been gleaned from such studies, but the restrictive conditions under which it was collected preclude reliable extrapolation. We, therefore, addressed the question of whether accurate electrophysiologic evaluation of the phrenic nerve-diaphragm pathway can be performed in intact, nonanesthetized calves. Transjugular phrenic activation was well tolerated, safe, specific, and able to achieve constant symmetric and supramaximal phrenic stimulations during prolonged periods. Eighteen noninvasive cutaneous and esophageal reception circuits were tested for their ability to record the diaphragmatic evoked potential. In addition, they were compared for specificity and reproducibility of the recorded potentials during prolonged periods of tidal or stimulated respiration. The best diaphragmatic potential was recorded from surface electrodes attached to the skin of the ninth and tenth intercostal spaces, using a xyphoidian reference. We describe a method that allows easy, long-term, and reliable electrophysiologic evaluation of the phrenic nerve-diaphragm pathway in intact, conscious calves. It is hoped that such a model will produce relevant novel information regarding pathophysiology of the diaphragm.