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Objective: To evaluate whether a synthetic analogue of feline facial pheromone (FFP) calms cats before, and reduces struggling during intravenous catheterization., Design: Block-randomized, 'blinded' clinical trial., Animals: Seventy-seven healthy cats presented for elective surgery., Procedure: Cats given glycopyrrolate and oxymorphone were assigned to one of four treatments: acepromazine and exposure to FFP (aceFFP); acepromazine and exposure to a placebo (acePlac); exposure to FFP only (FFP) and exposure to placebo only (Plac). The behaviour of cats was recorded on videotape for evaluation by assessors unaware of treatment group. Cats' veins were then catheterized by veterinary students unaware of the study protocol. Based on each cat's response to catheterization, the student independently decided whether intramuscular ketamine was required., Results: Cats in the aceFFP group appeared to be calmer than acePlac cats on the basis of head position and their location in the cage (suggesting benefit from FFP among cats receiving acepromazine) but appeared to be less sedated. Cats in the aceFFP group also appeared to be calmer than FFP cats on the basis of head position and location in the cage. Feline facial pheromone cats were also calmer than Plac cats when compared using body and leg position. Exposure to FFP did not significantly reduce struggling at catheterization, nevertheless, the students were able to catheterize the veins in all cats., Conclusion and Clinical Relevance: There were no detrimental behavioural effects associated with either FFP or acepromazine. The FFP had additional calming effects in cats given acepromazine and, to a lesser degree, helped to calm cats that were not given acepromazine. Feline facial pheromone helps to calm cats in unfamiliar surroundings.

Objective: To compare plasma colloid osmotic pressure (COP) of both maternal and fetal blood, before and after hemorrhage, and replenishment with Oxyglobin Solution (Biopure Corporation, Cambridge, MA, USA), hetastarch or whole blood in pregnant ewes., Study Design: Prospective, randomized study., Animals: A total of 17 adult Rambouillet ewes at 131 (128-133) [median (minimum, maximum)] days gestation, weighing 56 (46, 63) kg., Methods: Ewes and fetuses were chronically instrumented with catheters in a maternal jugular vein, maternal carotid artery and fetal femoral artery. Twenty milliliters per kilograms of blood were removed from each ewe over 1 hour. The ewes were then given 20 mL kg(-1) of either Oxyglobin Solution (n = 5), hetastarch (n = 6), or autologous whole blood (n = 6) IV. Maternal plasma COP was measured before hemorrhage, after hemorrhage, after replenishment, and 1 and 2 hours later. Fetal plasma COP was measured after maternal hemorrhage and 2 hours after maternal volume replenishment., Results: Median COP of all ewes before hemorrhage was 20 (16, 24) mm Hg and after hemorrhage (p < 0.05), decreased to 16 (11, 19) mm Hg. After volume replenishment, the COP of the Oxyglobin Solution group was 22 (21, 25) mm Hg, the autologous whole blood group was 17 (16, 22) mm Hg and the hetastarch group was 20 (17, 21) mm Hg. The COP of the Oxyglobin Solution group was significantly greater (p < 0.05) than the COP of the hetastarch group immediately and 60 minutes after volume replenishment, and greater (p < 0.05) than that of the autologous whole blood group at 60 minutes after volume replenishment. The COP of all the fetuses after maternal hemorrhage was 16 (12, 19) mm Hg and at 120 minutes after maternal volume replenishment was 15 (11, 18) mm Hg. There were no differences in COP between or within any of the fetal groups., Conclusions: When used to treat blood loss, Oxyglobin Solution increases plasma COP more than an equal volume of hetastarch in the first hour following administration. Maternal administration of Oxyglobin Solution did not alter fetal COP., Clinical Relevance: Oxyglobin Solution is a more potent colloid than hetastarch. Oxyglobin Solution did not appear to translocate fluid from the fetal to maternal circulation.

Unlabelled: We investigated the ability of hemoglobin-based oxygen carrying solutions (HBOCs) to alleviate fetal hypoxemia from maternal hemorrhage. Fifteen pregnant ewes (132-day gestational age) were hemorrhaged 20 mL/kg over 1 h; they were randomized to receive 20 mL/kg IV of HBOC, hetastarch (HTS), or autologous blood (BLD) (n = 5 each) over 30 min and were monitored for 2 h. Hemorrhage significantly (P < or = 0.05) decreased maternal mean blood pressure (from 98 to 48 mm Hg, median), arterial oxygen content (from 12.2 to 11.1 mL/dL), and fetal arterial oxygen content (from 8.1 to 3.9 mL/dL). Fluid replacement restored maternal blood pressure in all groups, although maternal oxygen content immediately returned to baseline only after BLD or HBOC. Maternal oxygen saturation decreased after HBOC (from 98% to 88%). Fetal oxygen content rapidly returned to baseline with either BLD (7.1 mL/dL) or HBOC (8.0 mL/dL) but was never restored with HTS (4.7 mL/dL), and, 60 min after fluid replacement, it was higher with HBOC (8.3 mL/dL) than with HTS (4.7 mL/dL). Fetal plasma-free hemoglobin did not change after HBOC. In conclusion, maternal fluid replacement with HBOC or BLD effectively restored fetal oxygenation, primarily by restoring maternal oxygen content, whereas HTS did not., Implications: Hemoglobin solutions eliminate many limitations of blood transfusions. Our results show that fluid replacement with either blood or a hemoglobin solution, compared with hetastarch, restored fetal oxygenation in pregnant ewes after hemorrhage. If applicable to women, these results suggest a potential for the use of hemoglobin solutions in obstetrics.

Small animal patients may need to be anesthetized in the periparturient period for emergency, nonobstetric reasons, elective ovariohysterectomy, or cesarean section. In each case, the physiologic changes in the dam must be accounted for in designing an anesthetic protocol, but the requirements of the fetuses will be different. Subsequent to birth, the neonatal animal may need to be anesthetized, and the unique physiology and pharmacology at this age is described.

The first few minutes after a neonate's birth may determine the quality of its entire life. Immediate care includes prevention of hypothermia, clearing of nasal and oral passages, stimulation of ventilation and oxygenation, and, in a few cases, advanced life support. Any additional stress during the first weeks of life can also result in neonatal morbidity and mortality. Care of the diseased newborn must focus not only on treatment of the underlying disease but on aggressive supportive care. A safe, warm, clean, proper environment and adequate nutrition are essential.

OBJECTIVE: Magnesium chloride-adenosine triphosphate (MgCl(2)-ATP), advocated as an adjunct treatment in shock resuscitation, might be useful for pregnant women who develop hypovolemia secondary to conditions such as placental abruption. The effects of this treatment on the fetus, however, have never been investigated. This study determined the direct, acute effects of MgCl(2)-ATP on fetal organ blood flow, hemodynamic measurements, and metabolic parameters before and after maternal hemorrhage. DESIGN: Experimental, randomized, nonblinded, control study. SETTING: Animal laboratory at a university research facility. SUBJECTS: This study was performed on 11 chronically instrumented, 123-day gestational age, pregnant ewes (term = 147 days) and their fetuses. INTERVENTIONS: Ewes were randomly allocated to either experimental (Expt, n = 5) or control (Cntl, n = 6) groups. After a 60-min baseline period, Expt fetuses received a 60-min iv infusion of MgCl(2)-ATP (150 &mgr;mole/hr each of MgCl(2) and ATP; at 3 mL/hr), and Cntl fetuses received an equivalent volume of 0.9% NaCl. After this infusion-only period, the infusion was continued, and ewes were intermittently bled over 1 hr for a total blood loss of 20 mL/kg (hemorrhage-plus-infusion period). After this, the infusions were continued, and ewes and fetuses were monitored for 1 additional hr (posthemorrhage period). Measurements: At the end of all periods, fetal and maternal blood pressures, blood gases, oxygen saturation, hemoglobin, serum electrolytes, and serum glucose concentrations were measured. At the end of the baseline, infusion-only, and hemorrhage-plus-infusion periods, fetal organ blood flows were determined using a fluorescent microsphere technique. Nonparametric statistics were used for comparisons (2-tailed, p

Objectives: Even though magnesium sulfate is commonly prescribed for women with preeclampsia as prophylaxis against seizure and for women with preterm labor as a tocolytic agent there is limited information about its effects on the fetus. It is of particular concern that women with preeclampsia or in premature labor are at high risk for abruptio placentae with consequent compromise of fetal oxygenation. Magnesium sulfate is a vasodilator and thus may exert cardiovascular effects on the fetus. The goal of this study was to evaluate the effects of magnesium sulfate on fetal organ blood flow, especially regional cerebral blood flow, during the stressful condition of maternal hemorrhage., Study Design: Studies were performed with 11 long-term instrumented pregnant ewes and their fetuses at 121 to 128 days' gestation (term, 147 days' gestation). Animals were randomly allocated to either the experimental (n = 5) or the control (n = 6) group. After a 60-minute baseline period, experimental fetuses received intravenous magnesium sulfate diluted in 0.9% sodium chloride (0.3 g loading dose, then 0.3 g/h at a rate of 3 mL/h) and control fetuses were infused with an equivalent volume of intravenous 0.9% sodium chloride. After 60 minutes of this infusion-only period, the infusions were continued and ewes were intermittently bled 4 times at a rate of 5 mL/kg for 10 minutes with 5 minutes between hemorrhages. The total blood lost at the end of the hemorrhage-plus-infusion hour was 20 mL/kg. The infusions were continued and the sheep were observed for 1 hour after this period (posthemorrhage period). At the end of baseline, infusion-only, and hemorrhage-plus-infusion periods, fetal and maternal blood pressures and blood gas values were measured and fetal organ blood flows were determined through a fluorescent microsphere technique. Repeated-measures analysis of variance and Wilcoxon tests were used to determine the significance of changes in hemodynamic, blood gas, and organ blood flow parameters between different time points within each group. Comparisons between groups were made with rank sum tests (Mann-Whitney tests)., Results: There were no significant differences between groups or within groups for baseline and infusion-only measurements in any measured hemodynamic or hematologic factor. Mean maternal blood pressure decreased significantly (P <.05) after hemorrhage, with similar median decrements in both control and experimental groups of 41 mm Hg (interquartile range, 24-57 mm Hg) and 41 mm Hg (interquartile range, 12-43 mm Hg), respectively. There were no significant differences between groups in fetal blood gas values or hemodynamic parameters. Fetal arterial PO(2) decreased significantly after hemorrhage plus infusion, with similar mean (+/-SEM) decreases in control and experimental groups of 5.9 +/- 1.4 mm Hg and 4.5 +/- 1.5 mm Hg, respectively. Fetal pH also decreased significantly in both groups. After hemorrhage plus infusion there were significant increases in fetal regional cerebral and myocardial blood flows in both groups. Adrenal blood flow increased significantly from baseline (214%, 183%-294%) in the control group after hemorrhage plus infusion but not in the experimental group. No other difference in organ blood flow between control and experimental groups was observed. Significant regional variations in cerebral blood flow were not observed in either group at any time., Conclusions: In these initially healthy, late-gestation fetal lambs magnesium sulfate exposure did not impair cardiac output redistribution, nor did it cause fetal death in response to maternal hemorrhage.

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.

Objective: To determine pharmacokinetic variables of mivacurium chloride after IV administration in dogs., Animals: 5 healthy Labrador Retrievers., Procedure: Anesthesia was induced with thiopental and maintained with halothane in oxygen. Dogs were ventilated mechanically to an end-tidal P(CO)2 value between 35 and 40 mm Hg. Heart rate, direct blood pressure, and arterial pH were recorded throughout the experiment. Core temperature, end-tidal P(CO)2, and halothane concentration were kept constant throughout the experiment. Paired blood samples for determination of plasma cholinesterase activity were collected prior to administration of a bolus of mivacurium (0.05 mg/kg of body weight), which was administered IV during a 2-second period. Arterial blood samples were obtained for determination of plasma mivacurium concentration 0, 1, 3, 5, 10, 30, 60, 120, 150, and 180 minutes after administration of mivacurium. Blood was collected into tubes containing EDTA and 0.25% echothiophate. Mivacurium concentration was determined, using reversed-phase high-performance liquid chromatography., Results: For the trans-trans isomer, mean +/- SEM volume of distribution was 0.18+/-0.024 L/kg, median half-life was 34.9 minutes (range, 26.7 to 53.5 minutes), and clearance was 12+/-2 ml/min/kg. For the cis-trans isomer, values were 0.31+/-0.05 L/kg, 43.4 minutes (range, 31.5 to 69.3 minutes), and 15+/-2 ml/min/kg, respectively. Values for the cis-cis isomer were not calculated, because it was not detectable in plasma 60 minutes after mivacurium administration in all 5 dogs., Conclusions and Clinical Relevance: The transtrans and cis-trans isomers of mivacurium have a long half-life and slow clearance in healthy dogs anesthetized with halothane.

Objective: To describe dogs undergoing cesarean section in the United States and Canada, to determine perioperative management, and to calculate survival proportions., Design: Multicenter prospective case series., Animals: 3,908 puppies from 808 dams., Results: Survival rates immediately, 2 hours, and 7 days after delivery were 92, 87, and 80%, respectively, for puppies delivered by cesarean section (n = 3,410) and 86, 83, and 75%, respectively, for puppies born naturally (498). For 614 of 807 (76%) litters, all puppies delivered by cesarean section were born alive. Maternal mortality rate was 1% (n = 9). Of 776 surgeries, 453 (58%) were done on an emergency basis. The most common breeds of dogs that underwent emergency surgery were Bulldog, Labrador Retriever, Boxer, Corgis, and Chihuahua. The most common breeds of dogs that underwent elective surgery were Bulldog, Labrador Retriever, Mastiff, Golden Retriever, and Yorkshire Terrier. The most common methods of inducing and maintaining anesthesia were administration of isoflurane for induction and maintenance (n = 266; 34%) and administration of propofol for induction followed by administration of isoflurane for maintenance (237; 30%)., Clinical Implications: Mortality rates of dams and puppies undergoing cesarean section in the United States and Canada are low. Knowledge of mortality rates should be useful to veterinarians when advising clients on the likelihood of puppy and dam survival associated with cesarean section.

Objective: To describe the effects of tromethamine, a putative treatment for metabolic acidosis, and to compare its biochemical effects with those of sodium bicarbonate., Design: Randomized intervention study with repeated measures., Animals: 16 healthy horses, 3 to 17 years old, weighing 391 to 684 kg., Methods: Ten horses received 3 mEq/kg tromethamine and six received 3 mEq/kg sodium bicarbonate. Samples of venous blood and cerebrospinal fluid (CSF) were collected at intervals before and after drug administration. Heart rate and breathing rate were also recorded at intervals., Results: Median standard base excess increased significantly (P < .05) from baseline immediately after both bicarbonate and tromethamine. These increases were not significantly different between treatments. Standard base excess returned toward baseline but remained significantly increased 3 hours after infusion of either treatment. After tromethamine, there was a significant decrease in plasma sodium concentration that lasted for at least 90 minutes. After sodium bicarbonate, no change in plasma sodium concentration was detected. Both sodium bicarbonate and tromethamine increased carbon dioxide tension in venous blood and CSF. Despite venous alkalemia, the pH of CSF decreased after both treatments., Conclusions: Tromethamine and sodium bicarbonate have similar alkalinizing ability. Tromethamine causes hyponatremia, whereas both tromethamine and sodium bicarbonate increase carbon dioxide tension in venous blood and CSF., Clinical Relevance: If hyponatremia, hypercarbia, and acidosis of the CSF occur after tromethamine is given to horses with existing metabolic acidosis, some of the potential advantages of tromethamine may prove theoretical rather than practical.

Objective: To evaluate duration and magnitude of adrenocortical function suppression after administration of etomidate to cats., Animals: 15 purpose-bred, healthy cats., Procedure: Cats were allotted to 2 groups. Anesthesia was induced with etomidate (ET, 2 mg/kg of body weight, i.v.; n = 8) or a mixture (KD, n = 7) of ketamine (5 mg/kg; i.v) and diazepam (0.25 mg/kg, i.v.). Anesthesia was maintained with halothane in all cats for 2 hours. ACTH gel (2.2 U/kg, i.m.) was administered 30 minutes after anesthesia induction. Blood samples for cortisol assay were taken before anesthesia induction (T -30), and before (T0) and at 30, 60, 120, 180, 300, and 420 minutes after ACTH administration. Anesthesia was discontinued after the T120 sample was obtained., Results: After anesthesia induction, median (interquartile range [Q1-Q3]) cortisol values were significantly lower in the ET group (4 [3 to 4] micrograms/dl) at T0, compared with T -30 values and with T0 values in the KD group (5 [3 to 9] micrograms/dl). After ACTH administration, cortisol values in the ET group continued to decrease two- to threefold below T -30 values and remained decreased over the 2-hour anesthesia period. After ACTH administration, cortisol values increased twofold for 2 hours in the KD group, compared with T -30 values. One hour after anesthesia recovery, cortisol values in the ET group (3 [2 to 3] micrograms/dl) remained significantly lower than values in the KD group (9 [7 to 11] micrograms/dl) and preanesthesia values. By T300, both groups had cortisol concentration near 7 micrograms/dl, similar to preanesthesia values., Conclusion: Induction of anesthesia with etomidate caused suppression of adrenocortical function during 2 hours of halothane anesthesia and 1 hour of recovery in cats. Cortisol concentration did not return to baseline until after 2 additional hours., Clinical Relevance: Results from these healthy cats suggest profound suppression of important stress hormones after anesthesia induction with etomidate, use of which could put critically ill cats at further risk.

Objective: To evaluate coagulation variables in 2 groups of dogs after tromethamine administration., Animals: 13 Beagles., Procedures: Both groups of dogs received a 30-minute IV infusion of 10 ml of 0.3M tromethamine/kg of body weight. In unsedated dogs (group 1, n = 8), prothrombin time, activated partial thromboplastin time, normalized ionized calcium concentration, platelet numbers, and platelet function were measured prior to treatment, at the end of the infusion, and 1 hour after the infusion. In xylazine-sedated dogs (group 2, n = 5), buccal mucosal bleeding time and plasma percentage of von Willebrand factor antigen were measured before and 1 hour after infusion, and fibrin degradation products concentration was measured 1 hour after infusion. Platelet function was assessed by determining platelet aggregation and by measuring ATP release from the aggregating platelets over 6 minutes, using a whole blood aggregometer, with 20, 10, and 5 microM ADP and 5 and 10 micrograms of collagen/ml as platelet activation agonists., Results: There was no significant change in any of the variables measured in either group of dogs, compared with baseline values., Conclusions and Clinical Relevance: When administered to healthy dogs, tromethamine does not change the coagulation indices measured.

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.

General anesthesia techniques for swine can be challenging due to the animal's temperament, anatomic traits, physical condition, and the environment in which the clinician may be working. Taking these factors into consideration, this article provides specific information on preanesthetic considerations, venous catheterization, drug selection, monitoring, perioperative complications and therapy, recovery, and analgesia.

This case report describes pneumothorax associated with positive pressure ventilation in two Vietnamese potbellied pigs while under general anesthesia. A discussion of possible causes and barotrauma/volutrauma follows. The cause of pneumothorax in both cases was probably an interaction of intermittent positive pressure ventilation with some factor unique to these two pigs.

Objective: To examine the physiologic effects of inhalation anesthesia in aquatic turtles to improve anesthetic techniques and postanesthetic monitoring., Design: Retrospective case series., Animals: 9 Kemp's ridley sea turtles., Procedure: Isoflurane was used as the general anesthetic during 14 minor surgical procedures. Turtles were orotracheally intubated, and a surgical plane of anesthesia was maintained with 2.7 +/- 0.4% (mean +/- SE) isoflurane. The duration of anesthesia was 131 +/- 12 minutes. Pulse rate, blood pressure, blood gases (PaO2 and PaCO2) and pH, blood lactic acid concentration, and capnography were used to evaluate the physiologic responses of sea turtles to isoflurane., Results: An isoflurane concentration of 3.4 +/- 0.3% provided anesthetic induction in 7 +/- 1 minutes. The mean duration of the recovery phase was 241 +/- 31 minutes. The duration of the recovery phase was not affected by the duration of anesthesia, type of carrier gas, method of ventilatory weaning, or use of selected pharmacologic agents. The recovery phase was characterized by hypoxemia, progressive acidemia, hypercapnia, and lactic acidosis. Awakening in the turtles was preceded by a characteristic tachycardia and tachypnea. All sea turtles recovered from isoflurane anesthesia without apparent adverse effects within 24 hours., Clinical Implications: Isoflurane appears to be safe and effective in providing surgical anesthesia in turtles that require a timely return to an aquatic environment. This study should assist veterinarians in predicting the physiologic responses of aquatic turtles to inhalation agents.

Introduction: Dogs with an inherited predisposition to sudden death display ventricular arrhythmias having certain characteristics, such as pause dependence, that are suggestive of early afterdepolarization-induced triggered activity. We hypothesized that alpha-adrenergic stimulation may facilitate the development of these arrhythmias by inducing a reflex bradycardia and by exerting a direct myocardial effect., Methods and Results: Twenty affected dogs and 7 unaffected dogs were studied. The incidence and severity of ventricular arrhythmias were determined after administration of phenylephrine (0.01 mg/kg IV), with or without pretreatment with propranolol (0.1 to 0.3 mg/kg IV), atropine (0.04 mg/kg IV), or prazosin (0.5 mg/kg IV). Third-degree heart block was induced by AV nodal ablation in 4 affected dogs. Phenylephrine increased ventricular arrhythmias in affected dogs, with or without pretreatment with propranolol, but did not induce ventricular arrhythmias in unaffected dogs. In dogs with intact AV nodal conduction, atropine increased sinus rate, which suppressed baseline and phenylephrine-induced arrhythmias. In dogs with heart block, arrhythmias were increased during baseline and after phenylephrine, with or without pretreatment with atropine. Prazosin and overdrive ventricular pacing suppressed phenylephrine-induced arrhythmias., Conclusion: Phenylephrine increases ventricular arrhythmias in dogs with inherited sudden death via both an induction of reflex bradycardia and a direct myocardial effect. Superimposition of heightened alpha-adrenergic and vagal tone may facilitate the development of sudden death in these animals.

Postresuscitation organ failure may be associated with detrimental changes in body fluid compartments. We measured how shock and resuscitation acutely alters the interstitial, cellular, and plasma compartments in different organs. Nephrectomized, anesthetized rats were bled to 50 mmHg mean arterial pressure for 1 h, followed by 60 min of resuscitation to restore blood pressure using 0.9% normal saline (NS,n = 10), 7.5% hypertonic saline (HS,n = 8), 10% hyperoncotic albumin (HA, n = 8), or 7.5% hypertonic saline and 10% hyperoncotic albumin (HSA, n = 7). A 2-h 51Cr-EDTA distribution space estimated extracellular fluid volume (ECFV), and a 5-min 125I-labeled albumin distribution space measured plasma volume (PV). Total tissue water (TW) was measured from wet and dry weights; interstitial fluid volume (ISFV) and cell water were calculated. NS resuscitation required 7 times more fluid (50.9 +/- 7.7 vs. 8.6 +/- 0.7 for HA, 5.9 +/- 0.4 for HS, and 3.9 +/- 0.5 ml/kg for HSA), but there were no differences between solutions in whole animal PV, ECFV, or ISFV. Fluid shifts within tissues depended on resuscitation solution and type of tissue. TW was significantly reduced by hypertonic saline groups in heart, muscle, and liver (P < 0.05). ISFV was significantly reduced by HA groups in the skin. In all tissues, mean cell water in groups receiving HS was smaller; this was significant for heart, lung, muscle, and skin. In conclusion, 1) HS solutions mobilize fluid from cells while expanding both PV and ISFV, and 2) TW and cellular water increase with both isotonic crystalloids and hyperoncotic colloids in many tissues.

Background: Fentanyl is used in anesthetic protocols for swine, but there are no reports on its potency in this species. This study measured the extent to which fentanyl reduces the minimum alveolar concentration of isoflurane (MACISO) in swine., Methods: Sixteen swine were randomly assigned to four groups. For each group, baseline MACISO was determined, and three groups received two of three fentanyl infusions as follows: 50 micrograms.kg-1.h-1 intravenously followed by 100 micrograms.kg-1.h-1, 50 micrograms.kg-1.h-1 followed by 200 micrograms.kg-1.h-1, or 100 micrograms.kg-1.h-1 followed by 200 micrograms.kg-1.h-1 (n = 8 for each dosage). A loading dose of fentanyl preceded each infusion. Each infusion was maintained for 60 min before initiating minimum alveolar concentration determination. The infusions were maintained throughout the period of minimum alveolar concentration determination. Plasma fentanyl samples were obtained after 30 min of each infusion, and plasma fentanyl and hemodynamic parameters were obtained immediately before stimulating swine for the final isoflurane concentration used in determining minimum alveolar concentration. A fourth group, control animals, received saline infusions. After each infusion, the MACISO was redetermined. Minimum alveolar concentration was determined using incremental changes in isoflurane concentrations until gross purposeful movement resulted when using a hemostat stimulus applied for 1 min to a rear dewclaw., Results: MACISO for controls was 2.19 +/- 0.17% (mean +/- SEM) and changed minimally over time (-0.13 +/- 4.77%). MACISO decreased significantly (P < or = 0.01) 24.5 +/- 3.2%, 29.9 +/- 4.8%, and 45.9 +/- 5.5% with fentanyl dosages of 50, 100, and 200 micrograms.kg-1.h-1, respectively. Corresponding plasma fentanyl concentrations were 14 +/- 1 ng/ml, 26 +/- 3 ng/ml, and 59 +/- 5 ng/ml, respectively. A ceiling effect on reduction of MACISO was not observed. Changes over time or between groups were not observed for arterial blood gas tensions, blood pressure, heart and respiratory rate, or body temperature., Conclusions: These fentanyl dosages are larger than those commonly used in humans and other species. Anesthetic protocols using fentanyl for swine should be designed with the knowledge that a fentanyl infusion of 200 micrograms.kg-1.h-1 contributes approximately a 50% MACISO equivalent.

Objective: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70., Design: Blinded, randomized, control trial., Setting: Laboratory setting., Subjects: Sixteen healthy Yorkshire swine., Interventions: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic acid infusion (1.5 to 2.4 mmol/kg) was given during the last 60 mins of hemorrhage to produce pretreatment acidosis. The pigs were then given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins., Measurements and Main Results: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant but transient decrease in arterial pH (from 7.407 +/- 0.015 to 7.339 +/- 0.025) and base balance (from -6.5 +/- 0.7 to -9.9 +/- 1.0 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline., Conclusions: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

Etomidate, formulated in propylene glycol, was used as the primary anesthetic agent in two dogs (No. 1 and 2) and etomidate, formulated in saline, was used as the primary anesthetic agent in an additional 20 dogs, while developing a canine model for baroreceptor sensitivity testing. Dogs 1 and 2 had signs of acute toxicosis after infusion of etomidate in propylene glycol. Dog 1 received less total etomidate than did dog 2, 5.9 mg/kg vs 15.8 mg/kg, respectively. Average infusion rates were 4.7 and 9 mg/kg/h, respectively. Dog 1 developed clinical signs of mild hemoglobinuria, whereas dog 2 recovered from anesthesia slowly, was obtunded, bradycardic, and hypothermic, with marked hemoglobinuria and intravascular hemolysis. After supportive treatment, dog 2 regained consciousness and hemodynamic variables improved within 12 h. None of the additional 20 dogs that received infusion of etomidate in saline had any clinical adverse effects, suggesting a causal relationship between the etomidate-propylene glycol formulation and the adverse effects in dogs 1 and 2. Although etomidate may be useful in designing cardiovascular models under general anesthesia, such complications may warrant use of a different etomidate formulation in the dog when the agent is administered at these infusion rates.

Redistribution of fluid after isotonic crystalloid resuscitation from hemorrhage may result not only in interstitial edema but also in cellular edema. We measured the extent to which shock and resuscitation altered fluid compartments in different organs. Nephrectomized, anesthetized rats were randomly divided into a Control group (n = 10) and a Hemorrhage plus Resuscitation group (H/R, n = 10). Rats were subjected to 60 min hemorrhagic hypotension (50 mmHg) followed by a 60 min resuscitation period with .9% NaCl infused as needed to maintain mean arterial pressure at 80% of baseline. A 2 h 51Cr-EDTA distribution space was used to estimate extracellular fluid volume (ECFV) and a 5 min 125I-albumin distribution space was used to measure plasma volume (PV). After euthanasia, total tissue water was measured by wet/dry weight analysis and interstitial fluid volume (ISFV) and cell water were calculated for selected organs. Resuscitation volume was two times the shed blood volume, but resulted in a PV equal to that of the Controls. There were no significant differences in whole animal ECFV or ISFV, although the mean values in the H/R group were greater than that of the Control group. The mean values for total tissue water for each tissue in the H/R group were larger than the respective means of the Control tissues but was significantly greater for only the heart (3639 +/- 56 microL/g vs. 3493 +/- 24 microL/g, mean +/- S.E., p < .05). In all H/R tissues, mean values for ISFV were also larger; this difference was significant for only the liver and small intestines (744 +/- 62 vs. 518 +/- 29 microL/g and 1117 +/- 155 vs. 706 +/- 58 microL/g, respectively). Heart cell water was significantly larger in H/R than Controls (2900 +/- 60 microL/g vs. 2738 +/- 27 microL/g). These data suggest that resuscitation of hemorrhage using isotonic crystalloid normalizes overall PV and ECFV but also causes interstitial expansion in selected gut tissues and cellular edema in the heart.

Arterial blood samples were collected from 19 anesthetized pigs before and after hemorrhage was induced. Blood gas tensions and concentrations of sodium, potassium, chloride, lactate, and total protein were measured. Results indicated that hydrogen ion (H+) concentration calculated from a specific formula was a biased and imprecise estimate of measured H+ concentration. The bias was 5.45 nEq/L, with limits of agreement from -7.92 to 18.83 nEq/L. Because albumin is the fraction of plasma protein most important in acid-base balance, the agreement between predicted and measured H+ concentration was reevaluated, using an albumin charge estimate and a reference swine albumin-to-globulin ratio. This improved the ability of the formula to predict H+ concentration; the bias decreased to 1.33 nEq/L with limits of agreement from -12.16 to 9.49 nEq/L. The formula and a simplified approach for clinical application were biased and unacceptably imprecise estimators of lactate (L-) concentration. The formula approach underestimated L- concentration by 2.8 (-12.4, 6.7) mEq/L, whereas the simplified method overestimated L- concentration by 5.0 (-3.8, 13.9) mEq/L.

The caudal border of the last rib was used as a reliable point of orientation while performing paravertebral thoracolumbar anaesthesia (PTLA) on 10 horses undergoing standing flank laparotomy. The local anaesthetic in all horses was 2% lidocaine. The PTLA procedure was completed in 9.8 +/- 1.8 mins (mean +/- sd). Sedation was provided by a combination of intravenous morphine with xylazine or detomidine. Overall analgesia, provided by the combination of PTLA and sedation, was rated as excellent in 2 horses and good in 6 horses. In the remaining 2 horses, overall analgesia was rated as fair because of incomplete analgesia at the ventral portion of the incision. Total time, from start of PTLA to end of surgery was 143.5 +/- 24.2 mins. Five horses responded mildly to suturing of the ventral portion of the incision. Apart from 1 horse which developed transient, unilateral hindlimb weakness intraoperatively, no other complications were noticed. We conclude that PTLA can easily be performed in the horse and, combined with systemic sedation, is an effective and safe method of providing analgesia for standing flank laparotomy.

Surface-induced hypothermia is used to protect tissues from ischemic events during surgery. In a review of 19 clinical cases in dogs, the technique was used to enable intracardiac surgery (4 dogs) and to facilitate removal of extensive thoracic or abdominal masses (15 dogs). For 16 dogs (84%), anesthesia was induced with an opioid/benzodiazepine combination and maintained with a balanced technique by use of an opioid, a neuromuscular blocking agent, and isoflurane in oxygen. Dogs were cooled in an ice bath to a mean esophageal temperature of 27.8 +/- 1.4 C. Mean anesthesia time was 4.04 +/- 1.37 hours. Hypothermic-induced adverse effects, such as increased blood viscosity, increased myocardial irritability, and shivering, were managed by hemodilution, manipulation of acid-base balance, and administration of opioid and neuromuscular blocking agents. Complications requiring treatment included severe hypotension (74%), arrhythmias (47%), hypoxemia (42%), and acidemia (58%). Six dogs (32%) went into cardiac arrest and all were successfully resuscitated once the surgical procedure was completed. One dog was euthanatized during surgery, another died after surgery, and the 17 remaining dogs (90%) were discharged from the hospital to their owners. The technique appears beneficial in selected cases to decrease the morbidity and mortality associated with the risk of prolonged ischemia and life-threatening hemorrhage.

Conventional fluid resuscitation is unsatisfactory in a small percentage of equine emergency surgical cases because the large volumes of fluids required cannot be given rapidly enough to adequately stabilize the horse. In anesthetized horses, the volume expansion and cardiopulmonary effects of a small volume of highly concentrated hypertonic saline-dextran solution were evaluated as an alternative initial fluid choice. Seven halothane-anesthetized, laterally recumbent, spontaneously ventilating, normovolemic horses were treated with a 25% NaCl-24% dextran 70 solution (HSD) at a dosage of 1.0 ml/kg of body weight, IV, infused over 10 minutes, and the effects were measured for 120 minutes after infusion. Plasma volume expansion was rapid and significant (from 36.6 +/- 4.6 ml/kg to 44.9 +/- 4.8 ml/kg), and remained significantly expanded for the duration of the experiment. Packed cell volume, total blood hemoglobin, and plasma protein concentrations significantly decreased, confirming rapid and sustained volume expansion with hemodilution. Cardiac index and stroke index immediately increased and remained high for the entire study (from 69.6 +/- 15.3 ml/min/kg to 106.6 +/- 28.4 ml/min/kg, and from 1.88 +/- 0.49 ml/beat/kg to 2.50 +/- 0.72 ml/beat/kg, respectively). Systemic vascular resistance significantly decreased immediately after HSD infusion and remained decreased for the duration of the study (from 1.41 +/- 0.45 mm of Hg/ml/min/kg to 0.88 +/- 0.22 mm of Hg/ml/min/kg). Arterial and venous blood oxygen content decreased significantly because of hemodilution, but actual oxygen transport transiently increased at the 10-minute measurement before returning toward baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Bipolar electrodes, stereotactically implanted in the hippocampus of adult rats, were used to deliver 10 s trains of suprathreshold tetanic electrical stimuli every few minutes. As indices of seizure intensity, durations of the afterdischarges triggered by these stimuli were measured, and the accompanying behaviors were scored on a 5-point scale. After 2-3 h, prolonged afterdischarges appeared in conjunction with severe limbic seizures, separated by periods of approximately 60 min. After 3-9 h, the stimulation was withheld until the following day. Upon reinstitution of the stimuli, intense seizures were seen at the onset, and the cycle time between them was shortened. Enhanced responsiveness to a fixed stimulus persisted for several months, the longest period tested. In addition, the enhanced epileptogenicity showed transference and was not stimulus-specific. These studies, using stimuli with low intertrain frequency and short interstimulus intervals, establish a robust and rapidly-developing model of epileptogenesis in the hippocampus that is comparable to traditional kindling.