Effects of repeated atropine injection on heart rate variability in Thoroughbred horses.

To investigate the effects of repeated atropine injection on heart rate (HR) variability in resting Thoroughbred horses, two microg/ kg of atropine as parasympathetic nervous blockade was injected intravenously every 6 min to a total of 8 microg/kg after intravenous administration of 0.2 mg/kg of propranolol as sympathetic nervous blockade. We recorded electrocardiograms and obtained the HR, then evaluated variation in HR from the power spectrum in terms of low frequency (LF, 0.01-0.07 Hz) power and high frequency (HF, 0.07-0.6 Hz) power. Administration of atropine decreased parasympathetic nervous activity in a dose-dependent manner, affecting first the LF power, then the HF power and finally HR. These responses may provide valuable information for evaluating autonomic nervous activity in Thoroughbred horses.     

Frequency domain analysis of heart rate variability in horses at rest and during exercise

The pattern of variation in heart rate on a beat-to-beat basis contains information concerning sympathetic (SNS) and parasympathetic (PNS) contributions to autonomic nervous system (ANS) modulation of heart rate (HR). In the present study, heart period (RR interval) time series data were collected at rest and during 3 different treadmill exercise protocols from 6 Thoroughbred horses. Frequency and spectral power were determined in 3 frequency bands: very low (VLF) 0-< or = 0.01, low (LO) >0.01-< or = 0.07 and high (HI) >0.07-< or = 0.5 cycles/beat. Indicators of sympathetic (SNSI = LO/HI) and parasympathetic (PNSI = HI/TOTAL) activity were calculated. Power in all bands fell progressively with increasing exercise intensity from rest to trot. At the gallop VLF and LO power continued to fall but HI power rose. SNSI rose from rest to walk, then fell with increasing effort and was lowest at the gallop. PNSI fell from rest to walk, then rose and was highest at the gallop. Normalised HI power exceeded combined VLF and LO power at all gaits, with the ratio HI to LO power being lowest at the walk and highest at the gallop. ANS indicators showed considerable inter-horse variation, and varied less consistently than raw power with increasing physical effort. In the horses studied, the relationship between power and HR changed at exercise intensities associated with heart rates above approximately 120-130 beats/min. At this level, humoral and other non-neural mechanisms may become more important than autonomic modulation in influencing heart rate and heart rate variability (HRV). HRV at intense effort may be influenced by respiratory-gait entrainment, energetics of locomotion and work of breathing. HRV analysis in the frequency domain would appear to be of potential value as a noninvasive means of assessing autonomic modulation of heart rate at low exercise intensities, only. The technique may be a sensitive method for assessing exercise response to experimental manipulations and disease states.     

Impaired baroreflex control of arterial pressure in WHHL rabbits.

The present study was designed to investigate baroreflex control capacity of arterial pressure (AP) in the conscious Watanabe heritable hyperlipidemic (WHHL) rabbit. The control capacity of the baroreflex system was assessed with overall open-loop gain (G). Seven WHHL and 14 normal Japanese white rabbits were chronically implanted two catheters in the aortic arch through the left subclavian and common carotid arteries. A small amount of blood (2 ml/kg, body weight) was rapidly extracted into a syringe via the left common carotid artery in the conscious state. Mean arterial pressure (MAP) was monitored with a catheter-transducer system through the left subclavian artery. The MAP responses to the rapid hemorrhage were averaged 8 times by a computer. G was calculated as G = delta API/delta APS-1, where delta API was an immediate MAP fall after the hemorrhage and delta APS was a steady-state error 1-2 min after the hemorrhage. The values of G in the conscious normal and WHHL rabbits were 7.35 +/- 0.24 and 1.91 +/- 0.29 (mean +/- SE, p < 0.01), respectively. To investigate effects of pentobarbital anesthesia on baroreflex system, the hemorrhage experiment was repeated several times under pentobarbital anesthesia (20 mg/kg, i.v.). The values of G in the anesthetized normal and WHHL rabbits were 6.69 +/- 0.23 and 1.68 +/- 0.34 (mean +/- SE, p < 0.01), respectively. G in the normal and WHHL rabbits did not show any significant change in the presence and absence of pentobarbital anesthesia (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Influence of gastrointestinal tract disease on pharmacokinetics of lidocaine after intravenous infusion in anesthetized horses

OBJECTIVE: To determine the disposition of lidocaine after IV infusion in anesthetized horses undergoing exploratory laparotomy because of gastrointestinal tract disease. ANIMALS: 11 horses (mean +/- SD, 10.3 +/- 7.4 years; 526 +/- 40 kg). PROCEDURE: Lidocaine hydrochloride (loading infusion, 1.3 mg/kg during a 15-minute period [87.5 microg/kg/min]; maintenance infusion, 50 microg/kg/min for 60 to 90 minutes) was administered IV to dorsally recumbent anesthetized horses. Blood samples were collected before and at fixed time points during and after lidocaine infusion for analysis of serum drug concentrations by use of liquid chromatography-mass spectrometry. Serum lidocaine concentrations were evaluated by use of standard noncompartmental analysis. Selected cardiopulmonary variables, including heart rate (HR), mean arterial pressure (MAP), arterial pH, PaCO2, and PaO2, were recorded. Recovery quality was assessed and recorded. RESULTS: Serum lidocaine concentrations paralleled administration, increasing rapidly with the initiation of the loading infusion and decreasing rapidly following discontinuation of the maintenance infusion. Mean +/- SD volume of distribution at steady state, total body clearance, and terminal half-life were 0.70 +/- 0.39 L/kg, 25 +/- 3 mL/kg/min, and 65 +/- 33 minutes, respectively. Cardiopulmonary variables were within reference ranges for horses anesthetized with inhalation anesthetics. Mean HR ranged from 36 +/- 1 beats/min to 43 +/- 9 beats/min, and mean MAP ranged from 74 +/- 18 mm Hg to 89 +/- 10 mm Hg. Recovery quality ranged from poor to excellent. CONCLUSIONS AND CLINICAL RELEVANCE: Availability of pharmacokinetic data for horses with gastrointestinal tract disease will facilitate appropriate clinical dosing of lidocaine.     

Effects of Fosinopril on Renal Function,Baroreflex Response and Noradrenaline Pressor Response in Conscious Normotensive Dogs

The blood pressure, renal function, baroreflex response of heart rate and noradrenaline (norepinephrine) pressor response were determined in conscious, normotensive, sodium-replete dogs that had received fosinopril. Oral administration of fosinopril at a dose of 1 mg/kg per day for 5 days decreased the systolic arterial pressure from 147.1±3 to 131.8±4.3 mmHg (p<0.05) and the mean arterial pressure from 99.7±3.9 to 87.5±2.8 mmHg (p<0.05), while heart rate was unchanged. A study of the noradrenaline pressor response showed a tendency to alleviate the increased MAP by fosinopril treatment, although this was not significant. There were no significant changes in the sensitivity of the baroreflex response in HR, although the setpoint was reduced. After 7 days of fosinopril treatment, the glomerular filtration rate had increased by 18.5% (p<0.05). The effective renal plasma flow tended to increase, leaving the filtration fraction unchanged. The renal vascular resistance was reduced by 11.3% (p<0.05). Fosinopril caused a significant 41.5% increase in urinary excretion of Na⁺ (p<0.05), along with an elevation of urinary excretion of K⁺ and Cl^–. It is concluded that fosinopril can lower the blood pressure, reduce the noradrenaline pressor response and lower the cardiac baroreflex setpoint to noradrenaline. Oral administration of fosinopril for 7 days affects both the renal haemodynamics and electrolyte excretions in conscious, normotensive, sodium-replete dogs.     

Inotropic mechanisms of dopexamine hydrochloride in horses.

Mechanisms responsible for the positive inotropic effects of dopexamine were investigated in 8 halothane-anesthetized horses. The hemodynamic effects of increasing infusions of dopexamine (5, 10, 15 micrograms/kg of body weight/min) were determined before and after sequential administration of specific antagonists. Using glycopyrrolate and chlorisondamine, and atenolol and ICI 118,551, muscarinic and nicotinic ganglionic, and beta 1, and beta 2-adrenergic receptor blockade, respectively, was induced. Dopexamine infusions induced increase in heart rate, cardiac output, systolic and mean arterial blood pressure, and maximal rate of left ventricular pressure development (+dP/dtmax). Right atrial pressure and systemic vascular resistance decreased. Parasympathetic and ganglionic blockade attenuated cardiac output, systolic and mean aortic blood pressures, and +dP/dtmax responses to dopexamine infusion. Dopexamine-induced increase in heart rate was potentiated by parasympathetic and ganglionic blockade. beta 1-Adrenergic receptor blockade decreased heart rate, cardiac output, arterial blood pressure, and +dP/dtmax from baseline values and markedly reduced the response to dopexamine infusion. beta 2-Adrenergic receptor blockade induced further decrease in hemodynamic variables from baseline values and completely abolished the cardiostimulatory effects of dopexamine on +dP/dtmax. These data indicate that baroreflex activity, beta 1- and beta 2-adrenergic receptor stimulation may be an important cause of dopexamine's positive inotropic effects in horses.     

Cervicothoracic (stellate) ganglion block in conscious horses

Seven adult horses were used to compare the cardiovascular and respiratory effects of unilateral (right side) and bilateral cervicothoracic ganglion (CTG) blockade. An 18-gauge, 25-cm needle was placed midventrally between articulations of the 1st and 2nd ribs from a cranial and paratracheal site. One gram of lidocaine HCl in aqueous solution (100 ml) was used to infiltrate the CTG. Cervicothoracic sympathetic blockade was characterized by Horner's syndrome, increased skin temperature and profuse sweating over the face, neck, and thoracic limb. Comparison of base-line data with data obtained during unilateral and bilateral CTG blockades indicated a significant (P less than 0.05) decrease in respiratory rate, significant (P less than 0.05) increases in arterial oxygen, and carbon dioxide tensions, and a significant increase in subcutaneous temperature at the neck and shoulder. Systolic, diastolic, and mean aortic blood pressures, pulse pressure, rectal temperature, arterial pH, bicarbonate, PVC, and total solid concentration did not change significantly from base-line values. Arterial O2 tension was significantly (P less than 0.05) less in horses with bilateral CTG blockade than in horses with unilateral CTG blockade. In 4 horses without cervicothoracic sympathetic blockade that were given lidocaine (1 g in 100 ml) in the right cervicothoracic region, cardiovascular and respiratory values did not change significantly from base-line values. The nonsedated healthy horse tolerated unilateral CTG blockade well. Bilateral and unilateral injections of 100 ml of 1% lidocaine into the CTG at intervals of less than 2 hours induced bilateral recurrent nerve paralysis and airway obstruction.     

Effect of butorphanol administration on cardiovascular parameters in isoflurane-anesthetized horses - a retrospective clinical evaluation.

OBJECTIVE: To determine cardiovascular responses to administration of butorphanol in isoflurane-anesthetized horses. STUDY DESIGN: Retrospective evaluation of anesthetic records. ANIMALS: Seventy-six horses anesthetized for a variety of clinical surgical procedures. METHODS: Anesthetic records of clinical equine patients anesthetized between January 1999 and December 2003 were searched. The records were reviewed for horses in which anesthesia was induced with ketamine and a benzodiazepine and maintained with isoflurane, and horses that received butorphanol intraoperatively. Exclusion criteria included horses in which the rate of infusion of an inotrope or end-tidal isoflurane concentration was changed 10 minutes before or after the butorphanol bolus. The horses were separated into two groups: group 1 horses received butorphanol at intervals as part of a balanced protocol, group 2 horses had > or = 10% increase in heart rate (HR) or blood pressure within 10 minutes prior to butorphanol administration. RESULTS: Eighty-nine butorphanol administration events matched the criteria for inclusion, 49 in group 1 and 40 in group 2. There were no significant changes after butorphanol administration in systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), and heart rate (HR) in group 1, or in end-tidal carbon dioxide concentration or hemoglobin oxygen saturation in either group. There were significant decreases in SAP (p < 0.0001), MAP (p < 0.0005), and DAP (p < 0.0008) after butorphanol administration in group 2. CONCLUSIONS AND CLINICAL RELEVANCE: The results presented here confirm that butorphanol can be administered to horses during isoflurane anesthesia without adverse effects on HR and arterial blood pressure. The results imply that butorphanol can deepen the plane of anesthesia and obtund sympathetic stimulation from a surgical procedure.     

Cardiopulmonary effects of desflurane in horses

OBJECTIVE: To determine the cardiopulmonary effects of desflurane (DES) in horses. ANIMALS: Six healthy adult horses, three males and three females, aged 9 +/- 4 (mean +/- SD) years and weighing 370 +/- 36 kg. MATERIALS AND METHODS: Anaesthesia was induced with an O2 (10 L minute(-1)) and DES mixture (vaporizer setting 18%). After oro-tracheal intubation, horses were positioned in right lateral recumbency. Anaesthesia was maintained with DES in O2 (20 mL kg(-1) minute(-1)) delivered through a large animal circle breathing system. The minimum alveolar concentration of DES (MAC(DES)) that prevented purposeful movement in response to 60 seconds of electrical stimulation of the oral mucous membranes was determined for each horse. The delivered concentration of DES was then increased to achieve end-tidal concentrations corresponding to 1.5 x MAC(DES), 1.75 x MAC(DES), and 2.0 x MAC(DES). Heart rate (HR), mean arterial blood pressure (MAP), respiratory rate (fr), tidal volume (VT), minute volume (VM) and core temperature were determined, and blood samples for arterial blood gas analysis taken at each DES concentration. All data were analysed by two-way anova for repeated measures and Fisher's test for multiple comparisons. A probability level of p < 0.05 was applied. RESULTS: Desflurane concentrations of 2.0 x MAC(DES) increased HR whereas lower concentrations did not. Mean arterial pressure was not affected by 1.0 x MAC(DES) 1.5 x MAC(DES) or 1.75 x MAC(DES), whereas it decreased at 2.0 x MAC(DES). All concentrations of DES examined significantly depressed fr, VT and VM. CONCLUSIONS AND CLINICAL RELEVANCE: Desflurane concentrations between 1.0 and 1.75 x MAC(DES) reduces fr and VM but does not affect HR or MAP in horses.     

Plasma lidocaine concentrations in conscious horses after cervicothoracic (stellate) ganglion block with 1% lidocaine HCl solution

Arterial and/or central venous plasma concentrations of lidocaine were determined in 12 nonmedicated adult horses (422 +/- 59 kg of body weight, mean +/- SD) after injecting a 1% lidocaine HCl solution into the cervicothoracic ganglion (CTG). A mean dosage of 2.9 +/- 0.5 mg of lidocaine/kg of body weight was used to induce unilateral CTG blockade in 8 horses and 4.8 +/- 0.8 mg was used to induce bilateral CTG blockade in 4 horses. Blood samples were collected before and at 5, 15, 30, 45, 60, 75, 90, 105, and 120 minutes after injection. The plasma lidocaine concentrations were determined by use of gas chromatography (sensitivity less than 0.01 microgram/ml). Cervicothoracic sympathetic blockade was characterized by Horner's syndrome and by profuse sweating over the face, neck, and thoracic limbs. Mean maximal venous concentrations of lidocaine were 0.86 +/- 0.33 microgram/ml at 26.3 +/- 6.9 minutes after unilateral CTG blockade, and 1.14 +/- 0.25 micrograms/ml at 31.2 +/- 18.9 minutes after bilateral CTG blockade. The mean venous and arterial concentrations of lidocaine were not significantly different at 45 and 120 minutes after injection. Venous concentrations of lidocaine were consistently higher than were concentrations in simultaneously collected arterial blood samples in 2 horses in which the right CTG and brachial plexus were temporarily anesthetized after repeated administration of 100 ml of lidocaine into the right CTG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Canadian veterinarians' use of analgesics in cattle, pigs, and horses in 2004 and 2005

Anecdotal evidence suggests that many veterinarians may not use analgesics in livestock for routine surgical procedures or painful disease states. To investigate this, we conducted a national mail survey of a random sample of 1431 Canadian veterinarians (response rate, 50.1%). Questions primarily concerned veterinarians' analgesic usage for common surgeries and medical conditions in beef and dairy cattle, pigs, and horses, and attitudes toward pain management. More than 90% of veterinarians used analgesic drugs for equine surgeries, for cesarean section in sows and cows, and for bovine claw amputation and omentopexy. However, in these and other categories, the analgesics used were often inadequate, and many veterinarians did not give analgesics to young animals. When castrated, < 0.001% of piglets received analgesia, compared with 6.9% of beef calves and 18.7% of dairy calves < or = 6 mo of age, 19.9% of beef calves and 33.2% of dairy calves > 6 mo of age, and 95.8% of horses. Respondents largely agreed that there are no long-acting, cost-effective analgesics available for use in livestock (median rating 8/10; interquartile range 4-9), and that the long or unknown withdrawal periods of some drugs outweighed the benefits of using them (median rating 7/10; interquartile range 4-9). The results indicate an urgent need for veterinarians to manage pain in livestock better. Continuing education would help, as would an increase in the number of approved, cost-effective analgesic drugs with known withdrawal periods.     

Intraoperative nociception-antinociception monitors: A review from the veterinary perspective

ObjectiveTo review monitors currently available for the assessment of nociception-antinociception in veterinary medicine.Databases usedPubMed, Web of Science and Google Scholar. The results were initially filtered manually based on the title and the abstract.ConclusionsThe provision of adequate antinociception is difficult to achieve in veterinary anaesthesia. Currently, heart rate and arterial blood pressure are used to monitor the response to a noxious stimulus during anaesthesia, with minimum alveolar concentration-sparing effect and stress-related hormones used for this purpose in research studies. However, since none of these variables truly assess intraoperative nociception, several alternative monitoring devices have been developed for use in humans. These nociceptive-antinociceptive monitoring systems derive information from variables, such as electroencephalography, parasympathetic nervous system (PNS) response, sympathetic nervous system response and electromyography. Several of these monitoring systems have been investigated in veterinary medicine, although few have been used to assess intraoperative nociception in animals. There is controversy regarding their effectiveness and clinical use in animals. A nociceptive-antinociceptive monitoring system based on the PNS response has been developed for use in cats, dogs and horses. It uses the parasympathetic tone activity index, which is believed to detect inadequate intraoperative nociception-antinociception balance in veterinary anaesthesia. Nonetheless, there are limited published studies to date, and cardiovascular variables remain the gold standard. Consequently, further studies in this area are warranted.     

Effects of ventriculectomy, prosthetic laryngoplasty, and exercise on upper airway function in horses with induced left laryngeal hemiplegia

Effects of ventriculectomy and prosthetic laryngoplasty on upper airway flow mechanics and blood gas tensions in exercising horses with induced left laryngeal hemiplegia were assessed. Five adult horses were trained to stand, trot (4.5 m/s), and gallop (7.2 m/s) on a treadmill (6.38 degrees incline). Inspiratory and expiratory airflows (VImax, VEmax, respectively) were measured using a 15.2-cm diameter pneumotachograph in a face mask. Inspiratory and expiratory transupper airway pressures (PuI, PuE, respectively) were determined as pressure differences between barometric pressure and lateral tracheal pressure. Blood collected from exteriorized carotid arteries was analyzed for PaO2, PaCO2, pH, hemoglobin (Hb) content, and HCO3- values. Heart rate (HR) was determined with an HR monitor. Measurements were made with horses standing, trotting, and galloping before left recurrent laryngeal neurectomy (LRLN; base line), 14 days after LRLN, 30 days after ventriculectomy (44 days after LRLN), and 14 days after prosthetic laryngoplasty (58 days after LRLN). Before LRLN (base line), increasing treadmill speed for horses from standing to the trot and gallop progressively increased HR, respiratory frequency, VImax, VEmax, PuI, PuE, Hb, and PaCO2 values and decreased PaO2, pH, and HCO3- values; inspiratory and expiratory impedances were unchanged. After LRLN, inspiratory impedance and PuI were significantly (P less than 0.05) increased in horses at the trot and gallop, and PaCO2 was significantly increased in horses at the gallop. The VImax and respiratory frequency were significantly (P less than 0.05) decreased in horses at the gallop. Left recurrent laryngeal neurectomy had no effect on PuE, VEmax, HR, PaO2, pH, Hb, or expiratory impedance values.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electroencephalographic and cardiovascular indicators of nociception during isoflurane anaesthesia in pigs

Objective To evaluate electroencephalographic indices, invasive arterial blood pressure and pulse rate as indicators of nociception during isoflurane anaesthesia in pigs. Animals Ten Norwegian Landrace pigs, five castrated males and five females, weighing between 19 and 29 kg. Materials and methods The pigs were anaesthetized with isoflurane and prepared for the measurement of heart rate (HR), mean arterial pressure (MAP) and the electroencephalogram (EEG). The inspired isoflurane concentration (Fi ′_ISO) was then adjusted until the suppression ratio (SR) exceeded 20%, after which the corresponding end‐expired concentration (Fe ′_ISO) was maintained for 30 minutes. The effects of noxious stimuli, consisting of pinching (nasal septum, interdigital web, anus, periople) and clamping (tail, claw) on spectral edge frequency 95%, median frequency, alpha/delta ratio, beta/delta ratio, theta/delta ratio, total power, suppression ratio, MAP and HR were recorded. Fe ′_ISO was then decreased by 0.3% and maintained for 30 minutes after which noxious stimulation was re‐applied. This was repeated twice with Fe ′_ISO reductions of 0.3% being applied each time. Changes in measured variables before and after noxious stimulation were then compared at each of four levels of anaesthesia. Results Noxious stimulation caused significant MAP increases at the lowest two levels for Fe ′_ISO. There were no significant changes in the other variables examined. Conclusion Of the variables examined, mean arterial blood pressure is the most sensitive indicator of nociception in isoflurane‐anaesthetized pigs. Clinical relevance When evaluating nociception under isoflurane anaesthesia in pigs mean arterial blood pressure should be monitored when surgery is performed.     

Relation of intrinsic heart rate and autonomic nervous tone to resting heart rate in the young and the adult of various domestic animals

Intrinsic heart rate (IHR) and autonomic nervous tone (ANT) were measured using the young and the adult of horses, cows, pigs, goats and chickens in order to elucidate species differences in a decrease of resting heart rate (RHR) with growth or age. The IHR and ANT were estimated from the changes in heart rate after the administration of atropine and/or propranolol. The IHR in all species decreased progressively with an increase in body weight from young to adult, and moreover the ANT altered toward the direction of parasympathetic predominance by a decrease in sympathetic tone and/or an increase in parasympathetic tone. The decrease of the RHR with growth resulted from a decrease in the IHR primarily and from a parasympathetic predominance in the ANT secondarily. A considerable species difference existed in the alteration of the ANT.     

A vaccine strain of pseudorabies virus with deletions in the thymidine kinase and glycoprotein X genes

A pseudorabies virus (PRV) mutant with deletions in genes for glycoprotein X (gX) and thymidine kinase, designated delta GX delta TK, was constructed and evaluated as a vaccine for protecting swine against PRV-induced mortality. Doses greater than or equal to 10(3) plaque-forming units (PFU) of this strain given to mice provided protection from challenge exposure with virulent PRV. Sera tested from mice inoculated with delta GX delta TK had high titers of neutralizing antibody to PRV, but reactivity in the same sera was not significantly different from that in sera from noninoculated mice (controls) when sera from both groups were evaluated by use of an ELISA with gX antigen produced in Escherichia coli. Compared with noninoculated pigs (controls), those given delta GX delta TK (greater than or equal to 10(2) PFU) were protected completely from lethal challenge exposure, without experiencing adverse effects on weight gain and with reduction of shedding of virulent challenge virus. Serotest results indicated that, although inoculated pigs responded with strong neutralizing antibody titers, the response of delta GX delta TK-inoculated pigs to gX, as determined by ELISA before challenge exposure, was not significantly greater than the ELISA values obtained from control pigs. The ELISA values from a group of pigs inoculated with a commercially available vaccine were significantly (P less than 0.05) higher than those of control pigs. The experimental vaccine, delta GX delta TK, was avirulent for mice, swine, and sheep, but was mildly virulent for calves (mortality, 1 of 12) and more virulent for dogs (mortality, 3 of 6) and cats (mortality, 2 of 6).(ABSTRACT TRUNCATED AT 250 WORDS)     

Calves' responses to repeated social regrouping and relocation.

Because of welfare concerns and increased labor efficiency, calves are increasingly housed in groups. To reduce variability in live weight within groups, farmers frequently regroup calves according to growth rate. We assessed the consequences of repeated regrouping and relocation on the welfare of 32 male Holstein calves housed in pairs. Animals of half of the pairs (regrouped calves) were placed in a new pen with a new partner once a week for 14 wk. Animals of the other half of the pairs (control calves) stayed in the same pen with the same partner. Behavior was observed for the 3 h following four mixings and for 24 h after all relocations were finished. The functioning of the hypothalamic-pituitary-adrenal axis and of the sympathetic nervous system were assessed. Calves were weighed once a week, their health was assessed daily, and abomasa were inspected when the calves were slaughtered. Calves reacted to the first mixing by interacting with the new partner and increasing their general activity (sniffing the partner in regrouped calves vs controls: 5.5 vs 2.9, P < 0.01; percentage time stepping: 3.2 vs 1.3, P < 0.001). This effect disappeared by the ninth mixing. After all relocations were completed, regrouped calves were more active at the end of the day and less active at night (P < 0.05). Cortisol responses to exogenous ACTH were higher in regrouped calves (integrated response: 6,688 vs 5,508 ng x min/mL, P < 0.01). Basal cortisol levels, ACTH responses to corticotropin-releasing hormone, activities of catecholamine-synthesizing enzymes (tyrosine hydroxylase and phenylethanolamine N-methyl transferase), and the incidence of health problems and growth rates did not differ between the two groups. Regrouped calves had fewer abomasal ulcers. Apart from the increased sensitivity of the adrenal cortex of regrouped calves to ACTH and the modification in the daily rhythm of activity, there was no clear evidence that repeated regrouping and relocation stresses calves. Aggression between calves was rare, and calves seemed to habituate to repeated mixing.     

Evaluation of Echocardiographic Parameters During Increasing Infusion Rates of Dobutamine in Isoflurane-Anesthetized Horses

The purpose of this study was to evaluate changes in echocardiographic parameters during increasing infusion rates of dobutamine in isoflurane-anesthetized horses and to compare our results with those of previous studies. Six Standardbred female healthy horses were included in this study. All animals were anesthetized and infused with dobutamine at different rates. mean arterial pressure (MAP), heart rate (HR), and some echocardiographic measurements were recorded. Statistical analysis was applied. Under basal conditions (time 0 [T0]), HR ranged between 32 and 42 beats per minute (bpm), and MAP was between 39 and 63 mm Hg. MAP increased significantly from T0 compared with values at T2, T2, and T3 in a dose-dependent manner, while HR increased significantly only at T3 if compared to the other measuring times. Left ventricular internal diameter during diastole (LVDs) decreased significantly in a dose-dependent manner, with increasing of the infusion rate of dobutamine. Interventricular septal dimension during diastole (IVSs) increased significantly, and end-systole left ventricular volumes (LVVols) decreased significantly at T2 and T3 compared to T1. Ejection fraction (%) increased significantly between T0 and T1, T2, and T3. Cardiac output increased significantly only at the higher dosage (T3 vs. others) of dobutamine, but cardiac power output was enhanced significantly at T2 versus that at T0 and T1 and at T3 versus all the previous measurements. Arrhythmias were diagnosed in 5 of 6 (83.3%). In this study, the increase of MAP was found to be dose-dependent, according with literature. The HR and MAP values registered at T0 were comparable to previous results obtained both in anesthetized and conscious horses, while at T1, T2, and T3, HR and MAP values were similar only too those reported in anesthetized horses. IVSs increased and LVDs decreased significantly with the increment of dobutamine infusion rate. These findings suggest that dobutamine, even at low infusion rates, induces an enhancement in cardiac systolic function. The dose-dependent increase of IVSs and decrease of LVDs measurements are in line with those reported for dobutamine administered in conscious horses but with lower values. The LVVols dose-dependent reduction obtained in this study is in line with that in other reports, but both LVold and LVVols values after dobutamine infusion at different dosages are lower if compared to previous studies. The low LVol values and the wide standard deviation have influenced consequently the derived indices values (stroke volume [SV], EF, cardiac output [CO]). In the present study, SV did not significantly increase during dobutamine infusion. These results disagree with those reported by others. The increment of CO might be due mainly to the enhanced HR rather than to the weak changes of SV. Cardiac power output increased significantly from the 5 mcg/kg/min dosage in a dose-dependent manner, as reported by others.     

Effects of thoracolumbar epidural anesthesia with lidocaine on the systemic hemodynamics and hepatic blood flow in propofol anesthetized dogs

General anesthesia reduces hepatic blood flow (HBF) from circulatory depression. Total intravenous anesthesia (TIVA) is associated with decreased circulatory depression compared to inhalation anesthesia, and epidural anesthesia using local anesthetics increases blood flow by blocking the sympathetic nerves and expanding blood vessels. We investigated the effects of thoracolumbar epidural anesthesia with TIVA on HBF in dogs. Six Beagle dogs had epidural catheters placed between T13 and L1 and were anesthetized with propofol and vecuronium. Physiological saline (control) or 2% lidocaine (0.2 ml/kg, followed by 0.2 ml/kg/hr) was administered at 1–2 weeks intervals. Heart rate (HR), cardiac index (CI), mean arterial pressure (MAP), and systemic vascular resistance index (SVRI) were recorded at 10-min intervals from before epidural injections (T0) to 110 min. Indocyanine green test was used to measure HBF during the awake state and until 90 min after epidural injections. HR and CI did not differ between treatments. MAP and SVRI after lidocaine were significantly lower than those of controls, and the lowest MAP value was 65 ± 11 mmHg at T10. Compared to T0, after lidocaine treatment, HBF was significantly higher at T30, T60 and T90 (P<0.05); while, after control treatment, no significant change was evident at any time point. Despite a decrease in MAP by this technique, HBF was either maintained at pre-anesthetic levels or increased in comparison to controls, probably due to vasodilation of the hepatic artery induced by the selective blockade sympathetic ganglia.