Effects of halothane and isoflurane on baroreflex sensitivity in horses

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P less than 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P less than 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P less than 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P less than 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P less than 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sevoflurane anesthesia in desert tortoises (Gopherus agassizii).

The effects of sevoflurane on anesthesia induction, recovery, ventricular pressures, heart rate, ventricular pH, blood gas values, and electrolytes were evaluated in desert tortoises (Gopherus agassizii). Tortoises were orotracheally intubated while awake and ventilated manually with 3-7% sevoflurane in oxygen (1 L/min) to achieve desired expired sevoflurane concentrations. Data, consisting of induction time, recovery time, systolic, diastolic, and mean ventricular pressures, heart rate, ventricular pH, blood gas values, and electrolytes, were collected prior to anesthesia and sequentially at 2.50% and 3.75% expired sevoflurane as measured at the junction of the endotracheal tube and the breathing circuit. Blood pressure was measured and blood samples were collected through a 25-ga needle passed through a cardiac access port that was placed while the tortoises were in dorsal recumbency. Mean (+/-SE) induction time was 2.55+/-0.55 min, recovery time was 27.58+/-7.55 min, and duration of anesthesia was 105+/-12 min. Mean (+/-SD) values for systolic, diastolic, and mean ventricular pressures in awake tortoises were 28+/-3 mm Hg, 22+/-2 mm Hg, and 24+/-2 mm Hg, respectively. Sevoflurane (2.5% expired) significantly decreased systolic (14+/-3 mm Hg), diastolic (12+/-1 mm Hg), and mean (13+/-1 mm Hg) ventricular pressures compared with those of awake tortoises. Ventricular pressures did not decrease further with increasing depth of anesthesia. Heart rate (32+/-4 beats/min) did not change significantly under sevoflurane anesthesia. Sevoflurane administration increased ventricular PO2 but did not change Na+, K+, or iCa++ concentrations. Sevoflurane appears to provide safe and effective anesthesia with rapid induction and recovery.     

Hemodynamics in the guinea pig after anesthetization with ketamine/xylazine

The resting hemodynamics were determined in 8 guinea pigs after they were anesthetized with ketamine/xylazine. Measurements were made of blood pressure, heart rate, cardiac output, arterial blood gases, and pH. These measurements were obtained initially at 4 to 5 hours after an injection (IM) of ketamine HCl (25 mg) and xylazine (0.15 mg) was given to anesthetize the animals for catheterization (period 1), again 5 days after the operation (period 2), and finally 4 to 5 hours after a 2nd injection of ketamine/xylazine (period 3). There were no differences in heart rates, respiratory rates, or cardiac outputs among the 3 study periods. However, arterial blood pressure was slightly, but significantly, lowered after, and presumably due to, instrumentation (62 +/- 4 mm of Hg, P less than 0.05) when compared with the 5-day postoperative period (67 +/- 7 mm of Hg) or after the readministration of anesthetics (66 +/- 7 mm of Hg). The partial pressure of carbon dioxide in the arterial blood was slightly lower (4 mm of Hg, P less than 0.05) in both acutely postanesthetic periods (period 1 and period 3) than in the same animals at postoperative day 5 (period 2). This study has demonstrated that resting hemodynamics measured shortly after this anesthesia with ketamine/xylazine are not largely different from those in chronically instrumented animals.     

Use of halothane to maintain anesthesia induced with etorphine in juvenile African elephants

Sixteen 3- to 5-year-old African elephants were anesthetized one or more times for a total of 27 diagnostic and surgical procedures. Xylazine (0.1 +/- 0.04 mg/kg of body weight, mean +/- SD) and ketamine (0.6 +/- 0.13 mg/kg) administered IM induced good chemical restraint in standing juvenile elephants during a 45-minute transport period before administration of general anesthesia. After IM or IV administration of etorphine (1.9 +/- 0.56 micrograms/kg), the mean time to lateral recumbency was 20 +/- 6.6 and 3 +/- 0.0 minutes, respectively. The mean heart rate, systolic blood pressure, and respiration rate during all procedures was 50 +/- 12 beats/min, 106 +/- 19 mm of Hg, and 10 +/- 3 breaths/min, respectively. Cardiac arrhythmias were detected during 2 procedures. One elephant with hypotension responded to a decrease in the concentration of halothane and IV infusion of dobutamine HCl. Alterations in systolic blood pressure, ear flapping, and trunk muscle tone were useful for monitoring depth of anesthesia. Results indicated that halothane in oxygen was effective for maintenance of surgical anesthesia in juvenile African elephants after induction with etorphine.     

Reference cardiopulmonary physiologic parameters for standing, unrestrained white rhinoceroses (Ceratotherium simum).

Chemical restraint is an important tool for the management and medical care of both captive and free-ranging rhinoceroses. Current anesthetic protocols for the white rhinoceros (Ceratotherium simum) are reported to cause varying degrees of hypertension, tachycardia, muscular stiffness and fasciculation, acidosis, and, most importantly, respiratory depression with resulting hypoventilation, hypoxia, and hypercapnea. To assist in the assessment and development of new and improved anesthetic techniques for the white rhinoceros, the following cardiopulmonary reference parameters for standing, unrestrained white rhinoceroses were generated (mean +/- standard error [minimum maximum]): heart rate = 39 +/- 0.8 beats/min (32-42), respiratory rate = 19 +/- 0.6 breaths/min (16-23), corrected indirect systolic blood pressure = 160 +/- 2.9 mm Hg (146-183), corrected indirect diastolic blood pressure = 104 +/- 2.3 mm Hg (88-117), corrected indirect mean blood pressure = 124 +/- 2.2 mm Hg (108-135), end tidal CO2 = 45.1 +/- 0.7 mm Hg (41.7-48.0), rectal temperature = 36.8 +/- 0.1 degrees C (36.6-37.2), arterial blood pH = 7.391 +/- 0.007 (7.346-7.431), arterial partial pressure of oxygen = 98.2 +/- 1.4 mm Hg (90.2-108.6), arterial partial pressure of CO2 = 49.0 +/- 0.9 mm Hg (44.4-53.7), base excess = 3.5 +/- 0.4 mmol/L (1.9-5.9), bicarbonate = 29.3 +/- 0.4 mmol/L (27.3-32.2), and arterial hemoglobin oxygen saturation (SaO2) = 97.2 +/- 0.1% (96.6-98.0).     

Determination of the minimum anesthetic concentration and cardiovascular dose response for sevoflurane in chickens during controlled ventilation

OBJECTIVE: To determine the minimum anesthetic concentration for sevoflurane and effects of various multiples of minimum anesthetic concentration on arterial pressure and heart rate during controlled ventilation in chickens. STUDY DESIGN: Prospective experimental study. ANIMALS: Seven healthy chickens, 6 to 8 months old, weighing 1.6 to 3.4 kg. METHODS: A rebreathing, semiclosed anesthetic circuit was used. Anesthesia was induced by mask with sevoflurane in oxygen. Each chicken was endotracheally intubated, then controlled ventilation was started and the end-tidal CO2 partial pressure was maintained at 30 to 40 mm Hg. Body temperature was maintained at 39.5 degrees to 41.0 degrees C. The inspired and end-tidal sevoflurane concentration were monitored with a multigas monitor. Minimum anesthetic concentration was determined as the minimal end-tidal sevoflurane concentration which prevented gross purposeful movement in response to clamping a toe for 1 minute. After the determination, the cardiovascular effects of sevoflurane at 1.0, 1.5, and 2.0 times the minimum anesthetic concentration were determined. RESULTS: The minimum anesthetic concentration for sevoflurane was 2.21% + 0.32% (mean +/- SD). Mean arterial pressure and heart rate at minimum anesthetic concentration were 84 +/- 13 mm Hg and 150 +/- 58 beats/min, respectively. There was a dose-dependent decrease in arterial pressure. The heart rate did not change significantly over the range 1 to 2 x minimum anesthetic concentration. No cardiac arrhythmias developed throughout the experiments. CONCLUSIONS AND CLINICAL RELEVANCE: The minimum anesthetic concentration for sevoflurane in chickens was within the range of minimum alveolar concentration reported in mammals. When the concentration of sevoflurane is increased during controlled ventilation in chickens, decrease in arterial pressure should be expected.     

Hypertension in Cats With Chronic Renal Failure or Hyperthyroidism

The Doppler ultrasonic recording technique was used to measure systolic and diastolic blood pressures indirectly in 28 cats with naturally occurring renal failure, 39 cats with hyperthyroidism, and 33 clinically normal cats. The mean systolic and diastolic blood pressures in the normal cats were 118.4 +/- 10.6 mm Hg and 83.8 +/- 12.2 mm Hg, respectively. In the cats with chronic renal failure, both the systolic (146.6 +/- 25.4 mm Hg) and diastolic (96.6 +/- 15.2 mm Hg) blood pressures were significantly higher (P less than 0.0001 and P less than 0.01, respectively) than in the normal cats. Elevations in systolic and/or diastolic blood pressure were recorded in 17 (61%) of the 28 cats with chronic renal failure. In the 39 untreated hyperthyroid cats, both the mean systolic (167.9 +/- 28.9 mm Hg) and diastolic (111.6 +/- 21.5 mm Hg) pressures also were significantly higher (P less than 0.0001) than normal. Increased systolic and/or diastolic blood pressure was recorded in 34 (87%) of the 39 hyperthyroid cats. In seven cats with hyperthyroidism that were reevaluated two to four months after successful treatment of the hyperthyroid state, there was a significant fall in mean systolic pressure (P less than 0.05) from a pretreatment value of 159.5 +/- 15.4 mm Hg to a posttreatment value of 132.0 +/- 1.62 mm Hg. Overall, the results of this study indicate that mild to moderate hypertension is common in cats with chronic renal failure and in cats with untreated hyperthyroidism. In addition, the hypertension appears to be reversible following successful treatment of the hyperthyroid state.     

Variance of indirect blood pressure measurements and prevalence of hypertension in clinically normal dogs

In a series of 3 studies, indirect blood pressure measurements were obtained to define normal variance, identify hypertension, and estimate the prevalence of hypertension in apparently healthy dogs. In part 1, we measured values in 5 clinically normal dogs twice weekly for 5 weeks in a home setting. Mean +/- SD systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) was 150 +/- 16 and 86 +/- 13 mm of Hg, respectively. The DAP significantly (P less than 0.01) decreased with repeated measurements over the 5-week period. In part 2, we assessed the variation between blood pressures measured in a clinic vs those measured in the home. Within a 2-week period, measurements were obtained from 10 clinically normal dogs in a private veterinary clinic and again in their home. Significant differences were not observed between clinic and home measurements of SAP and DAP; however, heart rate was significantly (P less than 0.05) higher in the clinic. In part 3, SD about the SAP and DAP mean values were determined in 102 clinically normal dogs. Canine hypertensive status was determined, using statistical methods and data from 102 clinically normal dogs. Values of SAP greater than 202 mm of Hg and DAP greater than 116 mm of Hg were determined to be 2 SD beyond the mean and, therefore, were interpreted to be hypertensive. Approximately 10% of the 102 apparently healthy dogs measured in this study were considered hypertensive on the basis of these criteria. In addition, a border zone of suspected hypertension was estimated, using the mean + 1.282 SD. The SAP border zone was between 183 and 202 mm of Hg, whereas the DAP border zone was between 102 and 113 mm of Hg. Of the 102 dogs, 12 had values within these zones of suspected hypertension.     

Effect of changes in ionized calcium concentration in arterial blood and metabolic acidosis on the arterial partial pressure of oxygen in dogs

OBJECTIVE: To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca2+) concentration on PaO2 in dogs. ANIMALS: 33 anesthetized dogs receiving assisted ventilation. PROCEDURE: Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO2, Ca2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. RESULTS: In group II, PaO2 increased from baseline value (96 +/- 2 mm Hg) within 10 minutes (pHa, 7.33 +/- 0.001); at 60 minutes (pHa, 7.21 +/- 0.02), PaO2 was 108 +/- 2 mm Hg. For the same pHa decrease, the PaO2 increase was less in group III. In group I, hypocalcemia caused PaO2 to progressively increase (from 95 +/- 2 mm Hg to 104 +/- 3 mm Hg), which correlated (r = -0.66) significantly with a decrease in systolic blood pressure (from 156 +/- 9 mm Hg to 118 +/- 10 mm Hg). Parathyroidectomy did not alter PaO2 values. CONCLUSIONS AND CLINICAL RELEVANCE: Induction of hypocalcemia and metabolic acidosis each increased PaO2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.     

Acute hemodynamic effects of hydralazine in dogs with chronic mitral regurgitation

The hemodynamic response to hydralazine administration was evaluated in 6 conscious small dogs with chronic mitral regurgitation. All dogs underwent invasive and noninvasive hemodynamic monitoring before and after hydralazine administration. Cardiac output and pulmonary capillary wedge pressure were measured with a Swan-Ganz thermodilution catheter. Systemic arterial blood pressure (AP) was measured directly by inserting a needle into the femoral artery. Standard M-mode echocardiograms and thoracic radiographs were obtained. Other hemodynamic variables were calculated. Base-line hemodynamic variables were altered severely in all dogs. Hydralazine decreased mean arterial blood pressure from 104 +/- 18 (mean +/- SD) to 78 +/- 12 mm of Hg (P less than 0.005), total systemic resistance index from 2,946 +/- 625 to 1,261 +/- 420 dynes-s-cm-5m2 (P less than 0.005), and pulmonary capillary wedge pressure from 40 +/- 5 to 26 +/- 3 mm of Hg, (P less than 0.005). Cardiac index increased from 2.92 +/- 0.72 to 5.36 +/- 1.67 L/min/m2 of body surface area (P less than 0.005). Mixed venous oxygen tension (PvO2) increased from 28.4 +/- 4.3 to 41.2 +/- 5.2 mm of Hg (P less than 0.001). Pulmonary edema resolved, as determined on thoracic radiographs. Mixed venous oxygen tension correlated well with the cardiac index (r = 0.92; P less than 0.001). It was concluded that hydralazine administration caused a small decrease in end diastolic diameter (4.8 +/- 0.9 to 4.5 +/- 0.8 cm, P less than 0.05) and end systolic diameter (2.6 +/- 0.8 to 2.3 +/- 0.7 cm, P less than 0.05). Fractional shortening and heart rate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Interand Intraindividual Variation in Doppler Ultrasonic Indirect Blood Pressure Measurements in Healthy Cats

This study was undertaken to evaluate reference ranges for systolic blood pressure (SBP) in cats under conditions mimicking a clinical setting. SBP was measured in 50 healthy adult cats of various ages (range, 1.5-16 years) and body weights (range, 2.2-6.1 kg) by Doppler ultrasonic sphygmomanometry. A cuff width of 2.5 cm was used, placed on the left antebrachium, and this represented a mean cuff width of 35% limb circumference (range, 31-42%). The mean (+/-SD) SBP in the 50 cats was 162 +/- 19 mm Hg (range 124-210), with only 1 cat having a SBP > or = 200 mm Hg. No significant difference (P > .05) in SBP was found between male and female cats, and no significant correlation was found between SBP and age (r(s) = 0.075) or body weight (r(s) = 0.007). Further studies in some of these cats indicated that allowing a period of 10 minutes for acclimatization to the environment where SBP was recorded resulted in a significant decrease in SBP from 176 +/- 17 to 157 +/- 21 mm Hg (n = 7) and that use of a 3.3-cm-width cuff resulted in a significant decrease in measured SBP from 168 +/- 13 to 164 +/- 13 mm Hg (n = 10). Reproducibility of SBP measurements was evaluated in 7 cats by assessing SBP 7 times at intervals of > or = 24 hours over a 10-day period. These 7 cats had a low intraindividual coefficient of variation of SBP measurements (CV < or = 7.9%) although 2 of the 7 cats had SBP values > 200 mm Hg on at least 1 occasion.     

Dynamic baroreflex sensitivity in anesthetized horses, maintained at 1.25 to 1.3 minimal alveolar concentration of halothane.

Dynamic baroreflex sensitivity for increasing arterial pressure (DBSI) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (less than or equal to 2 minutes) pressure changes in the horse. Anesthesia was induced with IV administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (SAP) was increased a minimum of 30 mm of Hg in response to an IV bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the R-R interval/SAP relationship. During dynamic increases in SAP, a significant correlation between R-R interval and SAP was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between R-R interval and SAP were greater than 0.80 in 5 of 8 horses. Mean (+/- SD) DBSI was 4.8 +/- 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between R-R interval and SAP was observed in only 3 of 6 awake horses during dynamic increases in SAP. Lack of correlation between R-R interval and SAP in 3 of 6 awake horses indicated that rapidly increasing SAP with an IV phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (+/- SD) DBSI (3 horses) was 7.3 +/- 3.3 ms/mm of Hg in awake horses.     

Severe hypoxaemia in field-anaesthetised white rhinoceros (Ceratotherium simum) and effects of using tracheal insufflation of oxygen

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (%O2Sa) = 49% +/- 16 (mean +/- SD) and PaO2 = 4.666 +/- 1.200 kPa (35 +/- 9 mm Hg)), hypercapnic (PaCO2 = 8.265 +/- 1.600 kPa (62 +/- 12 mm Hg)) and acidaemic (pHa = 7.171 +/- 0.073 ). Base excess was -6.7 +/- 3.9 mmol/l, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 +/- 5.465 kPa (164 +/- 41 mm Hg)) and tachycardic (HR = 107 +/- 31/min). Following nasal tracheal intubation and insufflation, the %O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged. Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the %O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.     

Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse.

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.     

Duration of action and hemodynamic properties of mivacurium chloride in dogs anesthetized with halothane.

OBJECTIVE: To describe onset and duration of neuromuscular blockade induced by mivacurium chloride and its associated hemodynamic effects at 3 dosages in healthy dogs. ANIMALS: 7 Labrador Retrievers. PROCEDURE: Anesthesia was induced with thiopental and maintained with halothane in oxygen, and dogs were mechanically ventilated to end-tidal P(CO)2 between 35 and 40 mm Hg. Core temperature, end-tidal P(CO)2, and halothane concentration were kept constant throughout the experiment. Neuromuscular function was assessed by evaluation of the train-of-four response to a supramaximal electrical stimulus of 2 Hz applied to the ulnar nerve every 10 seconds. Blood for determination of plasma cholinesterase activity was obtained prior to administration of mivacurium, a bolus of which was administered IV, using a randomized Latin-square design for dosages of 0.01, 0.02, and 0.05 mg/kg of body weight. RESULTS: All dogs had typical plasma cholinesterase activity. After administration of mivacurium, differences were not evident between groups in heart rate, systolic, mean, or diastolic blood pressure, change at any time in heart rate, systolic, mean, or diastolic blood pressure, or pH. Interval from onset to 100% neuromuscular blockade was 3.92+/-1.70, 2.42+/-0.53, and 1.63+/-0.25 minutes at dosages of 0.01, 0.02, and 0.05 mg/kg, respectively. Duration of measurable neuromuscular blockade was 33.72+/-12.73, 65.38+/-12.82, and 151.0+/-38.50 minutes, respectively. Time of onset and duration of effect differed significantly among dosages. CONCLUSIONS AND CLINICAL RELEVANCE: Mivacurium provides good hemodynamic stability at the dosages tested. In dogs, this drug has a rapid onset and long duration of effect.     

Effect of intranasal oxygen administration on blood gas variables and outcome in neonatal calves with respiratory distress syndrome: 20 cases (2004-2006)

OBJECTIVE: To determine the effect of intranasal oxygen administration on blood gas variables and outcome in neonatal calves with respiratory distress syndrome (RDS). DESIGN: Retrospective case series. ANIMALS: 20 neonatal calves with RDS. PROCEDURES: Arterial partial pressure of oxygen (PaO(2)), arterial partial pressure of carbon dioxide, and arterial oxygen saturation (SaO(2)) before and after intranasal administration of oxygen were analyzed. RESULTS: There were significant increases in PaO(2) and SaO(2) in the first 24 hours after oxygen administration was begun, with mean +/- SD PaO(2) increasing from 38.4+/-8.8 mm Hg to 58.7+/-17.8 mm Hg during the first 3 hours of treatment. Calves with PaO(2)>55 mm Hg within the first 12 hours after oxygen administration was begun had a significantly higher survival rate (9/10) than did calves that did not reach this threshold (4/10). CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that intranasal oxygen administration was a simple method of improving blood gas variables in neonatal calves with RDS and that PaO(2) could be used to predict outcome.     

Effects of hypertension and sympathetic denervation on cerebral blood flow in newborn pigs

To investigate the potential role of sympathetic nerves in preventing pronounced increases in cerebral blood flow, we evaluated the effects of abrupt hypertension on the cerebral circulation of newborn pigs with intact cerebral sympathetic innervation and after cerebral sympathetic denervation. Epinephrine infusion was used to induce abrupt increases in mean (+/- SEM) arterial pressure (innervated pigs, 62 +/- 3 mm of Hg to 115 +/- 3 mm of Hg; denervated pigs, 71 +/- 4 mm of Hg to 132 +/- 4 mm of Hg) that remained increased for the 3 minutes of the study. Abrupt hypertension increased blood flow to all brain regions. In denervated pigs, the increased flow to the cerebrum was prolonged, compared with that in pigs with intact sympathetic innervation. Differences between pigs of the innervated and denervated groups were not apparent, with respect to blood flow to any other region (caudate region, brain stem, cerebellum). In newborn pigs, sympathetic nerves may attenuate hypertension-induced increases in blood flow to the cerebrum, but do not appear to affect flow to the rest of the brain.     

Essential hypertension in a dog

Severe hypertension was diagnosed in a dog that initially was referred for evaluation of visual deficits and retinal hemorrhage and eventually was donated for medical treatment of hypertension. Initial blood pressure measured by direct methods was markedly high (systolic, 275 mm of Hg; diastolic, 170 mm of Hg). Measures of renal function were within normal limits, with the exception of hypotonic urine. A test protocol was designed to exclude possible secondary causes of hypertension; negative results of such tests allowed the diagnosis of essential hypertension. The consistency of the hypertension and its response to medical control were studied for 5 years. Blood pressure while the dog was untreated during those years was 240 +/- 24 mm of Hg (systolic) and 146 +/- 14 mm of Hg (diastolic). Plasma renin activity was within normal limits, and the response of the renin-angiotensin system to varied salt intake was normal. The most effective medications used to lower blood pressure were propranolol and captopril, both of which were more effective than salt restriction alone. Five years after the diagnosis of hypertension, the dog was euthanatized because of chronic renal failure secondary to pyelonephritis. Hypertension was less severe as the condition progressed into chronic renal failure. Complete necropsy did not reveal an obvious cause of the hypertension, and histopathologic changes were limited to the cardiovascular system, eyes, and kidneys.     

Effects of atracurium on intraocular pressure, eye position, and blood pressure in eucapnic and hypocapnic isoflurane-anesthetized dogs

OBJECTIVE: To determine effects of atracurium on intraocular pressure (IOP), eye position, and arterial blood pressure in eucapnic and hypocapnic dogs anesthetized with isoflurane. ANIMALS: 16 dogs. PROCEDURE: Ventilation during anesthesia was controlled to maintain Paco2 at 38 to 44 mm Hg in group- I dogs (n = 8) and 26 to 32 mm Hg in group-II dogs (8). Baseline measurements for IOP, systolic, diastolic, and mean arterial blood pressure, central venous pressure (CVP), and heart rate (HR) were recorded. Responses to peroneal nerve stimulation were monitored by use of a force-displacement transducer. Atracurium (0.2 mg/kg) was administered i.v. and measurements were repeated at 1, 2, 3, and 5 minutes and at 5-minute intervals thereafter for 60 minutes. RESULTS: Atracurium did not affect IOP, HR, or CVP Group II had higher CVP than group I, but IOP was not different. There was no immediate effect of atracurium on arterial blood pressure. Arterial blood pressure increased gradually over time in both groups. Thirty seconds after administration of atracurium, the eye rotated from a ventromedial position to a central position and remained centrally positioned until 100% recovery of a train-of-four twitch response. The time to 100% recovery was 53.1 +/- 5.3 minutes for group I and 46.3 +/- 9.2 minutes for group II. CONCLUSIONS AND CLINICAL RELEVANCE: Atracurium did not affect IOP or arterial blood pressure in isoflurane-anesthetized dogs. Hyperventilation did not affect IOP or the duration of effect of atracurium.     

Cardiovascular effects of xylazine recorded with telemetry in the dog

Cardiovascular effects of xylazine have not been studied with telemetry in dogs. In the present study, the effects on cardiovascular parameters after intramuscular (i.m.) administration of 2.0 mg/kg xylazine were studied via telemetry in unrestrained dogs. Telemetry transmitters were implanted subcutaneously (s.c.) with a pressure catheter in the femoral artery. Cardiovascular effects and body temperature effects were assessed after i.m. administration of xylazine. Heart rate decreased for about 10 min and was continuously depressed during 60 min. Thereafter, heart rate slowly increased but had not fully reached pre-dose values 4 h after treatment. Both systolic and diastolic blood pressure increased immediately after administration of xylazine. The systolic blood pressure showed a peak increase for about 5-10 min and then decreased below the baseline value not normalizing within 90 min. The diastolic blood pressure peaked 5-10 min after xylazine administration but did not return to baseline level until 50 min after administration. Body temperature decreased continuously for about 90 min and remained low for more than 4 h after treatment. An additional administration of xylazine to the same individuals after a recovery period of 4 weeks induced exactly the same response in systolic and diastolic blood pressure and in heart rate. By using the telemetric recording system it was possible to continuously evaluate xylazine-induced cardiovascular responses in a way that is not possible with conventional techniques.