EFFECTS OF A SUPPLEMENTAL ETORPHINE DOSE ON PULMONARY ARTERY PRESSURE AND CARDIAC OUTPUT IN IMMOBILIZED, BOMA-HABITUATED WHITE RHINOCEROS ( CERATOTHERIUM SIMUM): A PRELIMINARY STUDY.

The effects of etorphine on the pulmonary vascular system of white rhinoceros ( Ceratotherium simum) have not been described and could play a role in the severe hypoxemia that develops after immobilization with etorphine-based drug combinations. Characterization of these effects requires measurement of pulmonary vascular pressures and cardiac output (CO). To refine a technique for pulmonary arterial catheterization, five boma-habituated white rhinoceros (three females and two males weighing 1,012-1,572 kg) were immobilized by remote injection with etorphine plus azaperone followed by butorphanol. This afforded the opportunity to perform a pilot study and acquire preliminary measurements of pulmonary arterial pressure (PAP) and CO before and after supplemental etorphine given intravenously. Ultrasonographic guidance was used to insert a sheath introducer into a linguofacial branch of a jugular vein. A 160-cm-long pulmonary artery catheter with a balloon and thermistor was then passed through the introducer and positioned with its tip in the pulmonary artery. It was not long enough to permit wedging for measurement of pulmonary artery occlusion pressure. Mean PAP was 35 mm Hg (minimum, maximum 32, 47 mm Hg) and increased ( P = 0.031) by 83% (28, 106%) after supplemental etorphine. Thermodilution CO was 120 L/min (92, 145 L/min) and increased 27% (3, 43%) ( P = 0.031). Heart rate was 100 (88, 112) beats/min and increased 20% (4, 45%) ( P = 0.031), whereas arterial partial pressure of oxygen was 35 mm Hg (30, 94 mm Hg) and decreased 47% (20, 72%) ( P = 0.031). The cardiovascular observations could result from etorphine-induced generalized sympathetic outflow, as has been reported in horses. Further studies of etorphine in isolation are needed to test this suggestion and to discern how the changes in pulmonary vascular pressures and blood flow might relate to hypoxemia in etorphine-immobilized white rhinoceros.

Neuromuscular blocking effects of cisatracurium and its antagonism with neostigmine in a canine model of autosomal-recessive centronuclear myopathy.

BACKGROUND: Centronuclear myopathy (CNM) is a rare congenital condition associated with skeletal muscle weakness. Patients with CNM may have decreased acetylcholine receptor expression and a reduced number of releasable quanta. Such perturbations could affect the time-course of neuromuscular blocking agents (NMBAs) and their antagonism with cholinesterase inhibitors. As a result of the rarity of CNM, prospective data regarding NMBA use in this subpopulation is scarce. We evaluated the neuromuscular blocking effects of cisatracurium and its antagonism with neostigmine in a canine model of CNM. METHODS: Six dogs with congenital autosomal-recessive CNM and six controls received cisatracurium 0.15 mg kg(-1) i.v. under general anaesthesia and intermittent positive pressure ventilation. Neuromuscular function was monitored with acceleromyography.When the second response (T2) to train-of-four (TOF) stimulation returned, neostigmine 0.04 mg kg(-1) (with glycopyrrolate) were administered i.v. The onset time, time to spontaneous return of T2, and the time to reach a TOF ratio ≥0.9 after neostigmine administration were recorded. RESULTS: Onset time was no different between groups. Median (interquartile range) time to return of T2 was 27 (24-31) min for control dogs and 26 (22-31) min for CNM dogs (P=0.93).After neostigmine administration, a TOF ratio ≥0.9 was reached in 12 (10-15) min and 17 (16-19) min in control and CNM, respectively (P=0.005). CONCLUSIONS: The spontaneous return of T2 was not different between groups. However, neostigmine-facilitated recovery was significantly slower in dogs with CNM. Canine autosomal-recessive CNM does not preclude the use of cisatracurium or its antagonism with neostigmine.

LABORATORY VALIDATION OF A POINT-OF-CARE CARDIAC TROPONIN I ASSAY FOR USE IN WHITE-TAILED DEER (ODOCOILEUS VIRGINIANUS).

The VetScan® i-STAT® 1 Handheld Analyzer and cardiac troponin I (cTnI) cartridges (i-STAT cTnI assay) measured greater median cTnI concentration [cTnI] in free-ranging white-tailed deer (Odocoileus virginianus) hand-injected with anesthetic drugs after physical restraint in Clover traps than in those ground-darted with the same drugs. This suggested that Clover trapping induces myocardial damage, bringing the use of this capture method under scrutiny. The purpose of this study was to confirm the validity of the i-STAT cTnI assay in deer before recommending changes in capture methods. Median [cTnI] measured by the i-STAT cTnI assay ([cTnI]i) in heparinized whole blood collected from 52 healthy, reproductively mature, female deer physically restrained in a chute was 0.01 ng/ml (10-90% percentiles: 0.00-0.03 ng/ml; minimum, maximum: 0.00, 0.07 ng/ml); [cTnI]i was 0.00 ng/ml in 42% of the deer. There was no association between [cTnI]i and either clotting or hemolytic index. [cTnI]i was 0.00 ng/ml when deer skeletal muscle homogenate was added to deer blood with [cTnI]i of 0.00 ng/ml, confirming the i-STAT cTnI assay does not detect skeletal muscle troponins. When deer cardiac muscle homogenate was serially diluted with 1) deer blood, 2) deer plasma, and 3) cow blood, [cTnI]i was directly proportional (Y intercept=-0.09, 0.7, and -0.08 ng/ml, respectively; r2≥0.97) to the fraction of homogenate in each sample. Deer cardiac muscle homogenate was diluted with deer blood to produce three samples with low, intermediate, and high [cTnI]i; serial measurements (n=10) performed on each sample yielded coefficients of variation (CVs) of 8, 20, and 11%, respectively. Corresponding CVs when plasma was used as diluent were 13, 9, and 7%, respectively. [cTnI]i increased when plasma with a low [cTnI]i was stored at 20-24°C for 9 days. Three freeze-thaw cycles caused no systematic change in plasma [cTnI]i.

Recovery from neuromuscular block in dogs: restoration of spontaneous ventilation does not exclude residual blockade.

OBJECTIVE: To evaluate if return of spontaneous ventilation to pre-relaxation values indicates complete recovery from neuromuscular blockade. STUDY DESIGN: Prospective, with each individual acting as its own control. ANIMALS: Ten healthy adult female Beagle dogs weighing 6.2-9.4 kg. METHODS: Dogs were anesthetized with propofol, dexemedetomidine and isoflurane. Spontaneous ventilation was assessed by measuring end-tidal CO2 , expired tidal volume, peak inspiratory flow, respiratory rate and minute ventilation. Vecuronium 25 µg kg(-1) IV was administered and neuromuscular block was evaluated by measuring the train-of-four (TOF) ratio with acceleromyography in the hind limb. During spontaneous recovery from neuromuscular block, the TOF ratio when each ventilatory variable returned to baseline was recorded. RESULTS: This dose of vecuronium produced moderate neuromuscular block in all dogs, with TOF ratio values of 0-18% at maximal block. Expired tidal volume, peak inspiratory flow and minute ventilation returned to pre-relaxation values when the median TOF ratio was ≤ 20%. The median TOF ratio was 42% when the end-tidal CO2 returned to pre-relaxation values. CONCLUSIONS AND CLINICAL RELEVANCE: Significant residual neuromuscular block could be measured at the hind limb with acceleromyography when ventilation had spontaneously returned to pre-vecuronium values. Monitoring spontaneous ventilation, including end-tidal CO2 , expired tidal volume, peak inspiratory flow or minute ventilation cannot be used as a surrogate for objective neuromuscular monitoring, and this practice may increase the risk of postoperative residual paralysis.

TOF-Watch(R) monitor: failure to calculate the train-of-four ratio in the absence of baseline calibration in anaesthetized dogs.

BACKGROUND: TOF-Watch(®) monitors are designed to display train-of-four (TOF) count when neuromuscular block is intense, and to display TOF ratio when it is less intense. In dogs recovering from non-depolarizing neuromuscular block, when all four twitches are easily visible and apparently of similar magnitude, TOF-Watch(®) monitors often display TOF counts and not TOF ratios, as would be expected. We have never encountered this problem when the monitor was calibrated before neuromuscular blocking agent administration. METHODS: Fourteen healthy female dogs undergoing ovariohysterectomy were investigated. Recovery from neuromuscular block was assessed with a calibrated TOF-Watch SX(®) monitor. When the TOF ratio returned to 90%, the TOF-Watch SX(®) was replaced with an uncalibrated TOF-Watch(®) monitor. The output obtained from the uncalibrated TOF-Watch(®) was compared with that of the calibrated device. RESULTS: The median TOF ratio measured by the calibrated TOF-Watch SX(®) unit at recovery was 91 (86-100)% (n=14). The uncalibrated TOF-Watch(®) monitor displayed TOF counts in six dogs [2 (0, 4)] and TOF ratios in the remaining eight dogs [91 (79, 98)%], that is, the uncalibrated device failed to display appropriately >40% of the time. CONCLUSIONS: TOF-Watch(®) monitors must be calibrated before neuromuscular blocking agents are administered to dogs. When these devices are not so calibrated, they default to a reference value for twitch magnitude that was defined in healthy adult people. Even though neuromuscular transmission was restored in these dogs, we surmise that they did not achieve the default reference value, causing the monitor to display TOF counts rather than TOF ratios.

Unilateral cervical plexus block for prosthetic laryngoplasty in the standing horse.

BACKGROUND: Locoregional anaesthetic techniques can facilitate certain surgeries being performed under standing procedural sedation. The second and third spinal cervical nerves (C2, C3) are part of the cervical plexus and provide sensory innervation to the peri-laryngeal structures in people; block of these nerves might permit laryngeal lateralisation surgery in horses. OBJECTIVES: To describe the anatomical basis for an ultrasound-guided cervical plexus block in horses. To compare this block with conventional local anaesthetic tissue infiltration in horses undergoing standing prosthetic laryngoplasty. STUDY DESIGN: Cadaveric study followed by a double-blinded prospective clinical trial. METHODS: A fresh equine cadaver was dissected to characterise the distribution of C2 and C3 to the perilaryngeal structures on the left side. A second cadaver was utilised to correlate ultrasound images with the previously identified structures; a tissue marker was injected to confirm the feasibility of an ultrasound-guided approach to the cervical plexus. In the clinical study, horses were assigned to two groups, CP (n = 17; cervical plexus block) and INF (n = 17; conventional tissue infiltration). Data collection and analyses included time to completion of surgical procedure, sedation time, surgical field conditions and surgeon's perception of block quality. RESULTS: We confirmed that C2 and C3 provided innervation to the perilaryngeal structures. The nerve root of C2 was identified ultrasonographically located between the longus capitis and the cleidomastoideus muscles, caudal to the parotid gland. The CP group was deemed to provide better (P<0.0002) surgical conditions with no differences in the other variables measured. MAIN LIMITATIONS: Further studies with larger numbers of horses may be necessary to detect smaller differences in surgical procedure completion time based on the improved surgical filed conditions. CONCLUSIONS: For standing unilateral laryngeal surgery, a cervical plexus block is a viable alternative to tissue infiltration and it improves the surgical field conditions.

Accuracy of dilution techniques for access flow measurement during hemodialysis.

Access flow is now widely measured by creating artificial recirculation with the dialysis lines reversed and using dilution methods that sense either ultrasound velocity, electrical impedance, optical, or thermal changes. This study identifies and quantifies factors that influence the accuracy of access flow measurements and recommends ways to reduce these errors. Two major sources of access flow measurement error are identified, arising firstly from the second pass of the indicator by recirculation through the cardiopulmonary system (cardiopulmonary recirculation, CPR), and secondly from changes in venous line blood flow (Qb) and vascular access flow induced by the pressure of venous bolus injections. These errors are considered from theory, by direct measurement of access flow in a sheep model, and by analysis of clinical data. Two extremes for the venous introduction of indicator can be considered in access flow measurements, a slow infusion, which perturbs neither the venous line flow nor access flow but increases the error attributable to the second pass of the indicator by recirculation through cardiopulmonary system, or rapid injection, which eases separation of the second pass of the indicator signal but generates changes in the venous flow and access flow. If CPR is not eliminated, the area added to that of the first pass of indicator ranges up to 40%. Good time resolution could permit the separation of the areas generated by the first and second passage of the indicator. In sheep experiments, injections of 5 or 10 mL into a venous port close to the vascular access caused Qb to change by 20% to 40%. Both the animal experiments and analysis of raw data collected during routine clinical dialysis showed that moving the injection site sufficiently far from the patient, before or into the venous bubble trap, reduced the increase in Qb to only approximately 5% during the critical time when the concentration curve is changing for most tubing brands (Baxter, Belco, Gambro, Hospal, Medisystem, and National Medical Care). Because of the smaller volume of the venous bubble chamber in Cobe tubing (Cobe, Centrysystem 3), this brand showed approximately a 20% increase in Qb. Moving the site of bolus injections to before the bubble trap in the sheep experiments also eliminated the influence of changes in access flow. An additional error in access flow measurement of 20% or more arises from the use of flow reading taken from pump setting rather than a measured flow. The discrepancy between the real flow and pump setting is attributable to needle size, vascular access conditions, or pump calibration. The results show that problems can be minimized by using a dual sensor system that retains the precise timing necessary for separation of access recirculation from CPR; by accurate measurement of dialyzer blood flow; by moving the site of injection to before the venous bubble trap, sufficiently far from the patient, and correcting for any remaining deviations in flow in the venous line concurrent with the dilution curve.

Ventilation in newborn rats after gestation at simulated high altitude.

Pregnant rats were kept at a simulated altitude of 4,500 m (PO2 91 Torr) for the whole of gestation and returned to sea level 1 day after giving birth. During pregnancy, body weight gain and food intake were approximately 30% less than in controls at sea level. Measurements were made on the 1-day-old (HYPO) pups after a few hours at sea level. In normoxia, ventilation (VE) measured by flow plethysmography was more (+17%) and O2 consumption (VO2) measured by a manometric method was less (-19%) than in control (CONT) pups; in HYPO pups VE/VO2 was 44% greater than in CONT pups. In acute hyperoxia, VE/VO2 of HYPO and CONT pups decreased by a similar amount (15-20%), indicating some limitation in O2 availability for both groups of pups in normoxia. However, VE/VO2 of HYPO pups, even in hyperoxia, remained above (+34%) that of CONT pups. HYPO pups weighed slightly less than CONT pups, their lungs were hypoplastic, and their hearts were a larger fraction of body weight. An additional group of female rats was acclimatized (8 days) to high altitude before insemination. During pregnancy, body weight gain and food intake of these females were similar to those of pregnant rats at sea level. Measurements on the 1-day-old pups of this group were similar to those of HYPO pups. We conclude that newborn rats born after hypoxic gestation present metabolic adaptation (low VO2) and acclimatization (high VE/VO2), possibly because of hypoxemia. Maternal acclimatization before insemination substantially alters maternal growth in hypoxia but does not affect neonatal outcome.

Respiratory mechanics in adult rats hypercapnic in the neonatal period.

Because chronic hypoxia in the neonatal period has long-term effects on the mechanical properties of the respiratory system (S. Okubo and J. P. Mortola, J. Appl. Physiol. 66: 1772-1778, 1989), we asked whether similar effects would occur after neonatal exposure to hypercapnia. Three groups of rats were used. The first was exposed to 7% CO2 in normoxia from day 1 to 7 after birth and then returned to normocapnia (NB-CO2). The second was exposed to the same level and duration of hypercapnia from day 36 to 42, i.e., approximately 2 wk after weaning (AD-CO2). The third was raised in normoxia and normocapnia (control). At approximately 50 days, i.e., 1-2 wk after puberty, the passive mechanical properties of the respiratory system, lung, and chest were measured during artificial ventilation in the anesthetized and paralyzed animal. No differences were observed between AD-CO2 and control. NB-CO2 had higher compliance of the lung (approximately +40%) and respiratory system (+32%) than control or AD-CO2. Average values of resistance of the total respiratory system, lung, and chest wall were consistently lower in NB-CO2 than in control and AD-CO2, although the magnitude and statistical significance of the decrease depended on the method of measurement. In a separate group of NB-CO2, lung compliance was measured during spontaneous breathing, and it averaged 34% more than in control. The exponential constant of the deflation quasi-static pressure-volume curve of the liquid-filled lungs was also significantly higher than in control.(ABSTRACT TRUNCATED AT 250 WORDS)

Extravascular lung water in the exercising horse.

Seven Standardbred horses were exercised on a treadmill at speeds (approximately 12 m/s) producing maximal heart rate, hypoxemia, and a mean pulmonary arterial pressure of approximately 75 mmHg. Extravascular lung water was measured by using transients in temperature and electrical impedance of the blood caused by a bolus injection of cold saline solution. Lung water was approximately 3 ml/kg body wt when standing but did not increase significantly with exertion. We conclude that any increase in fluid extravasation from the pulmonary hypertension accumulates in the lung at a level that is less than that detectable by this method. At maximal exertion, the volume of blood measured between the jugular vein and the carotid artery increased by approximately 8 ml/kg, and the actively circulating component of the systemic blood volume increased by approximately 17 ml/kg with respect to corresponding values obtained when walking before exertion. These volume increases, reflecting recruitment and dilatation of capillaries, increase the area for respiratory gas exchange and offset the reduced transit times that would otherwise be imposed by the approximately eightfold increase in cardiac output at maximal exertion.

Pulmonary capillary pressure during exercise in horses.

The object of this study was to relate pulmonary capillary pressure to arterial and wedge pressures during exercise. Pulmonary vascular pressures were measured in six standardbred horses exercising at speeds equivalent to 75, 90, and 100% of maximal heart rate. Vascular pressures were measured with transducer-tip catheters and expressed relative to esophageal pressure. Pulmonary capillary pressure was estimated by the arterial-occlusion technique modified for exercise. Mean pulmonary arterial, capillary and wedge pressures increased from 30.5 +/- 6.3, 17.8 +/- 4.3, and 13.4 +/- 1.6 mmHg, respectively, at rest, to 70.5 +/- 5.2, 42.1 +/- 5.3, and 38.4 +/- 5.6 mmHg, respectively, at maximal exercise. The largest part of the increase occurred during the first level of exertion. With exercise, the pressure across the lung barely doubled at a time when the cardiac output would have increased at least fivefold. Thus the absolute resistance in both pre- and postcapillary segments must have decreased. The capillary and wedge pressures rose similarly, whereas the difference between them did not change with exertion. The fractional resistance of the precapillary segment increased with exercise. The postcapillary resistance, initially 28% of the total pulmonary vascular resistance, fell to 9% at maximal exercise. The rise (to approximately 45 mmHg) in pulmonary capillary pressure with exertion is consistent with an increase in transvascular filtration.

Volume of extravascular lung fluid determined by blood ultrasound velocity and electrical impedance dilution.

A hypertonic sodium chloride bolus passing through the lung has a sound velocity transient that is biphasic when it reaches the carotid artery. This transient is compatible with water moving into the hypertonic bolus from the lung parenchyma, thereby leaving the lung parenchyma hypertonic. Subsequently, as the bolus leaves the lung vasculature, water passes from the blood into the tissue to return the lung tonicity to baseline, giving a moment when net movement is zero, an instant of osmotic equilibrium. Concurrent measurements of impedance track the sodium chloride transient. A theoretic basis for the calculation of extravascular lung water is derived from the water transferred to the blood, the amount of sodium chloride moved from blood to the lung, and the increase in blood osmolarity measured at the moment of equilibrium. Examples from measurements on sheep suggest that two intravenous injections of hypertonic and isotonic sodium chloride, with observations of sound velocity and electrical impedance in the systemic arterial circulation (which could also provide the cardiac output), provide a basis for calculation of lung permeability, water and salt movements, and extravascular lung water estimation.

Effect of clenbuterol on arterial oxygen tension in the anaesthetised horse.

In horses in dorsal recumbency, spontaneously breathing oxygen, with halothane at a constant end-tidal concentration, the arterial oxygen tension (PO2) increased from 9.9 +/- 0.3 SEM kPa to 21.7 +/- 4.0 kPa with 0.8 micrograms kg-1 clenbuterol and to 29.1 +/- 3.8 kPa with 2.4 micrograms kg-1 clenbuterol. In horses initially in dorsal recumbency then turned to sternal recumbency the PaO2 rose to 54.0 +/- 3.0 kPa, but this rise was unaffected by clenbuterol administration. The response in dorsal recumbency was consistent with clenbuterol counteracting the factor postulated to direct the pulmonary blood flow caudodorsally, but the response to clenbuterol in sternal recumbency was not. Although these results do not unequivocally characterise the postulated factor, the effect of the clenbuterol itself is of interest because of its potential as a treatment for the low PaO2 often observed in anaesthetised horses.

Effect of prior administration of suxamethonium on non-depolarising muscle relaxants in the dog.

The depolarising muscle relaxant suxamethonium (0.3 mg kg-1) was administered to six dogs. At 50 per cent return of the neuromuscular activity, as measured by the train-of-four technique, a non-depolarising muscle relaxant was administered. Three drugs, alcuronium (0.1 mg kg-1), gallamine (1.0 mg kg-1) and pancuronium (0.06 mg kg-1) were injected intravenously. At the 50 per cent return of neuromuscular activity, atropine and neostigmine were administered to reverse the neuromuscular block. The duration of action of the three non-depolarising relaxants was reduced by the prior administration of suxamethonium.

Effect of prior administration of a non-depolarising muscle relaxant on the action of suxamethonium in the dog.

The non-depolarising muscle relaxants alcuronium (0.1 mg kg-1), gallamine (1 mg kg-1) and pancuronium (0.06 mg kg-1) were administered to six dogs. At 50 per cent return of neuromuscular activity, as measured by the train-of-four technique, the depolarising muscle relaxant suxamethonium (0.3 mg kg-1) was injected intravenously. At 50 per cent return of neuromuscular activity, atropine and neostigmine were administered to reverse the neuromuscular block. The duration of action of suxamethonium was reduced by each of the non-depolarising muscle relaxants.

Improvement in arterial oxygen tension with change in posture in anaesthetised horses.

Observations were made on horses spontaneously breathing oxygen, with halothane at a constant end tidal concentration. The horses were positioned in dorsal recumbency for the first 45 minutes of each anaesthetic episode during which the arterial oxygen tension (PaO2) was found to peak and then decline. The remaining 60 minutes of each anaesthesia was used to test the effect of various manoeuvres on PaO2. The PaO2 of horses decreased further both when remaining in dorsal recumbency and when repositioned in right or left recumbency. In contrast, placing the horses in sternal recumbency for these remaining 60 minutes caused the PaO2 to rise rapidly providing evidence for redistribution of ventilation. Replacing some inspired oxygen with less absorbable nitrogen did not improve PaO2 in dorsal recumbency. Thus there was no evidence that the low PaO2 of dorsal recumbency was associated with alveoli that had collapsed because of gas absorption.

Do Thoroughbred and Standardbred horses have similar increases in pulmonary vascular pressures during exertion?

To test the hypothesis that the pulmonary vascular pressures of Thoroughbred and Standardbred horses behave similarly during exertion. Measurements were made on 5 Thoroughbred and 5 Standardbred horses on a treadmill at rest and during 3-minute exercise intervals at speeds predicted to produce 75%, 90%, and 100% maximal heart rate. Left forelimb acceleration, heart rate, esophageal pressure, and pulmonary artery pressure were measured continuously. Pulmonary capillary and wedge pressures were measured during intermittent occlusion of the pulmonary artery. Breathing rate and gait frequency were the fundamental frequencies of the esophageal pressure and limb acceleration signals respectively. The ratio of speed:gait frequency gave stride length. The effects of exertion and breed were evaluated using two-way analysis of variance. Exertion produced significant increases in pulmonary artery (P = 0.001), capillary (P = 0.002), and wedge (P = 0.005) pressures. No significant effect of breed was detected on pulmonary artery pressure, but at exertion pulmonary capillary and wedge pressures were 15% (P = 0.03) and 23% (P = 0.04) greater in Thoroughbreds, respectively. Treadmill speed was approximately 12% greater (P = 0.04), stride length was approximately 25% greater (P = 0.0003), gait frequency was approximately 10% less (P = 0.006), breathing rate was approximately 10% less (P = 0.001), and heart rate was approximately 6% less (P = 0.06) for Thoroughbreds. There was no effect of breed on inspiratory or expiratory esophageal pressure although mean esophageal pressure was approximately 2 mmHg greater (P = 0.03) in exercising Standardbreds. In conclusion, pulmonary capillary and wedge pressures are greater in Thoroughbreds than in Standardbreds at similar fractions of maximal heart rate. This is compatible with the higher incidence of exercise-induced pulmonary hemorrhage observed in Thoroughbreds.

Cardiovascular and pharmacokinetic effects of isoxsuprine in the horse.

Isoxsuprine (0.6 mg/kg) administered IV to 6 standing horses produced substantial, transient decreases in systemic blood pressure, systemic vascular resistance, and stroke volume. It also produced substantial, transient increases in heart rate, cardiac output, and purposeful movement. Plasma concentrations of isoxsuprine peaked soon after the drug was administered IV and then decreased over a 12-hour period in a biexponential manner, with distribution and elimination half-lives of 14 minutes and 2.67 hours, respectively. Total body clearance and steady-state volume of distribution were calculated to be 53.8 ml/min/kg and 10.5 L/kg, respectively. When a recommended therapeutic dosage regimen (0.6 mg/kg 2 times a day, per os) was used in 4 of these horses, changes were not detected. Isoxsuprine was not detected in plasma after the drug was given orally. We conclude that 0.6 mg of isoxsuprine/kg given orally every 12 hours is not likely to produce cardiovascular changes in the resting horse and that this is probably because plasma concentrations are not high enough to do so.

Acid-base, metabolic, and hemodynamic effects of sodium bicarbonate or tromethamine administration in anesthetized dogs with experimentally induced metabolic acidosis.

OBJECTIVE: To evaluate buffering capacity and side effects of equivalent doses of tromethamine (THAM) and sodium bicarbonate (BIC). ANIMALS: 18 purebred dogs. PROCEDURE: Acidosis was induced by having dogs breathe a hypoxic gas mixture (FIO2 = 0.10) until arterial base balance < or = -7.5 mEq/L was reached. Dogs then received a 30-minute infusion of 5% BIC (n = 6) or 0.3M THAM (n = 8), and FIO2 increased to 0.30. Drug doses were calculated to correct base balance to zero. RESULTS: During hypoxia, for BIC- and THAM-treated groups, median (interquartile range [Q1, Q3]) pHa and arterial base balance decreased to 7.16 (7.07, 7.38) and 7.19 (7.11, 7.31), -14 (-16, 9) and -12 (-16, -11) mEq/L, respectively, and mixed venous lactate concentration increased to 7 (2, 15) and 6 (3, 13) mmol/L, respectively. Immediately after each infusion, acid-base and cardiopulmonary variables returned toward baseline. For respective BIC- and THAM-treated groups, pHa increased to 7.37 (7.26, 7.44) and 7.40 (7.33, 7.49) and base balance increased to 0 (-4, 7) and 0 (-4, 2) mEq/L. Lactate concentration decreased only slightly to 5 (2, 6) and 5 (2, 9) mmol/L, but continued to decrease throughout the study. The only significant (P < or = 0.05) difference between groups was hypernatremia after BIC administration that persisted for 60 minutes. The PaCO2 in BIC-treated dogs increased immediately after infusion, compared with values during hypoxia. Standardized ionized calcium values initially decreased in both groups, but returned to baseline by 60 minutes. CONCLUSION: The buffering capacity of THAM is equal to that of BIC, although THAM does not cause the transient hypernatremia or hypercapnia observed after BIC administration. Hypocalcemia may be transient after administration of either solution. Thus, THAM is an acceptable alternative to BIC for treatment of metabolic acidosis in selected anesthetized dogs.

Cardiac dysrhythmias during anesthesia for cervical decompression in the dog.

In a retrospective study, the risk for cardiac dysrhythmias was evaluated in dogs undergoing ventral decompression and/or fenestration of the cervical spine (CERV) and compared with that for dogs undergoing dorsal laminectomy for decompression of the thoracic or lumbar spine (TL). The dogs in the CERV subset (48 dogs) tended to be heavier and older than the dogs in the TL subset (111 dogs). There was no apparent bias detected in treatment before anesthesia and surgery. The risk for dysrhythmias was 2.5 times greater in the CERV subset, compared with that in the TL subset (P less than 0.01). The risk for ventricular premature contraction was 3.5 times higher in the CERV group (P less than 0.05). Bradycardia was found in 6 dogs from the CERV subset and was not found in any dogs from the TL subset. A logistic model was derived from the data and may be used to evaluate the risk for dysrhythmias in similar patients undergoing similar surgery and anesthesia. This model uses age, preoperative heart rate, and site of surgery (CERV or TL) to estimate the risk.