Medetomidine, an investigational drug indicated for clinical use as a short-term chemical restraint in dogs, was evaluated for its cardiopulmonary effects, in 10 naturally heartworm-infected (HW+) and 10 noninfected (HW-) Beagles. The drug was randomly administered IV (30 microgram/kg of body weight) and IM (40 microgram/kg) in single injections to all dogs. Heart rate, respiratory rate, ECG, blood gas tensions, blood pH, central venous and arterial pressures were measured at 0, 15, 30, 60, 90, 120, and 180 minutes. Medetomidine induced an immediate significant (P less than or equal to 0.001) increase in mean arterial blood pressure followed by decreased blood pressure that remained below normal throughout the study in both groups, irrespective of route of administration. Medetomidine increased central venous pressure, over time, for both groups and both routes of administration. Heart and respiratory rates were significantly (P less than or equal 0.001) decreased after medetomidine administration and remained reduced for the duration of the study in all dogs. The ECG variables were not significantly different between groups or between routes of administration. The HW+ dogs tended to have higher mean PaO2 than did HW- dogs at several postinjection determination times, particularly when the drug was administered IM. The PaO2 decreased during the first 30 minutes in both groups and tended to increase gradually thereafter. The pH decreased over time for both groups and both routes. A significant (P less than or equal to 0.05) decrease in pH was seen in the HW- dogs, compared with HW+ dogs at each measuring time for both routes. The PaCO2 did not significantly change for groups or routes. In general, bradycardia was the predominant cardiovascular effect seen after medetomidine administration in all dogs, irrespective of route. Lowering of blood pressure and heart rate (after a transient blood pressure increase) was synchronized with sedation in these dogs. The overall clinical response with regard to cardiopulmonary effects in HW+ dogs was similar to that in HW- dogs.

Although healthy and diseased bovine respiratory tracts have been intensively studied during the last years, to the authors' knowledge, there have been no attempts to objectively examine the inspiratory drive from the brain to the nerves and muscles and its transformation in pressure. Such technique would be useful in assessing the possibility of altered ventilatory drive or inspiratory muscle fatigue in the context of an animal with ventilatory failure. The relation among ventilation, airway opening occlusion pressure generated 100 milliseconds after onset of inspiration (Pawo100ms) and 6 indexes describing diaphragmatic electromyographic activity (EMGdi) recorded via implanted fishhooks was evaluated during free and impeded CO2, rebreathing in 6 young bulls. The best significant linear correlations (r > 0.8) with inspiratory center afferent stimulation, as judged by end-tidal CO2 concentration in expired air, were found for Pawo100ms, peak moving time average or variance EMGdi, and mean integrated EMGdi, whatever had been the respiratory impedance. However, with an inspiratory load, Pawo100ms responses systematically had greater increase for a given change in the driving EMGdi, implying dependence of the former not only on neural input, but also on configurational factors that determine inspiratory muscle excitation-pressure generation couplings. The reproducibility of EMGdi absolute values and changes was satisfactory up to 10 hours, but could not be repeated from one day to the other. It was concluded that, provided the constancy of the electrical coupling of the recording system to the tissue being studied is ensured, specific EMGdi and Pawo100ms values correlate reliably with amount of CO2 during free and loaded breathing. Simultaneous collection of both values during experimentally induced pulmonary disease in calves could, therefore, produce information to help answer questions about the role of CNS and inspiratory muscle dysfunction in case of ventilatory failure. Careful interpretation, however, requires additional measurements, such as end-expiratory lung volume, and some familiarity with the underlying physiologic processes that link phrenic nerve discharge to generation of negative pressure at the airway opening.

Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the EEG were determined for delta, theta, alpha, and beta frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the delta band. Hypocapnia caused an increase in the absolute power of delta, theta, and alpha frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.