The uterine hemodynamic response to maternal positioning in dorsal recumbency was evaluated in 7 conscious pregnant cows during the third trimester. Anesthetic or sedative drugs were not administered. Uterine artery flow was measured, using a previously implanted ultrasonic flow probe. Catheters implanted in the uterine artery and vein were used for measurement of blood pressure and for blood sample collections. Heart rate, systemic arterial pressure, uterine arterial blood flow, arterial and venous oxygen and carbon dioxide tensions, and pH were measured in cows in standing position. Cows were cast with ropes and positioned in dorsal recumbency, then measurements were repeated at 15 and 30 minutes. Compared with standing measurements, dorsal recumbency caused 50% increase in heart rate and 44% increase in arterial blood pressure. Uterine artery flow did not change significantly. Despite increased ventilation, arterial oxygenation was reduced during dorsal recumbency. There were minimal differences between measurements at 15 and 30 minutes of dorsal recumbency.

Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, Paco2 and Pao2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, Paco2, and Pao2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and Pao2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration. In ducks of the KET + XYL group, pHa and Pa02 were significantly (P less than or equal to 0.05) decreased at all time points up to and including 45 and 15 minutes, respectively, after administration of the drugs. In ducks of the XYL group, Paco2 increased significantly (P less than 0.05) during the first 15 min. after drug administration, and for 45 min. after administration of KET + XYL. Results indicated that ketamine when given alone to ducks, was not associated with pulmonary depression.

Cardiovascular and at accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2, and PaCO2, did not significantly change during the 12 hours of study, PVO2 increased significantly P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-ketoprostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, an alpha 2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of CNS, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered IV. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.

OBJECTIVE To fluoroscopically evaluate the effects of head posture and sedation on the laryngopharyngeal anatomic structures in dogs. ANIMALS 6 clinically normal Beagles (mean age, 6.2 years; mean weight, 10.4 kg). PROCEDURES Each dog was sedated and placed in right lateral recumbency, and fluoroscopic examinations were performed with flexed, neutral, and extended head postures (FHP, NHP, and EHP, respectively). During 3 respiratory cycles, the angle between the basisphenoid bone and nasopharyngeal dorsal border (ABN), thickness of the soft palate, diameter of the nasopharyngeal lumen (DNL), overlapping length between the epiglottis and soft palate, and distance between the epiglottis and tympanic bulla (DET) were measured and percentage difference in the DNL (PDNLD) during a respiratory cycle was calculated. RESULTS For the FHP, NHP, and EHP, median ABN was 91.50° (interquartile range [IQR], 86.75° to 95.00°), 125.00° (IQR, 124.50° to 125.50°), and 160.00° (IQR, 160.00° to 163.50°), respectively, with no significant differences between ABN and posture angle. For the FHP, median DNL and DET significantly decreased, compared with values for the NHP, and median thickness of the soft palette significantly increased. For the EHP, the minimal DNL and DET significantly increased, and the median overlapping length between the epiglottis and soft palate significantly decreased, compared with values for the NHP. The PDNLD significantly increased and decreased with FHP and EHP, respectively, compared with the PDNLD with NHP. Sedation did not affect upper airway structure changes. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that head posture significantly affected the laryngopharyngeal structures in dogs. Fluoroscopic examination of the upper respiratory tract of a dog should be performed with an NHP to minimize posture-induced changes in measurements.