Background: Greyhounds are known to have a higher systemic arterial blood pressure (BP) than non-Greyhound dogs. Objectives: The purpose of this study was to determine whether the high systemic BP was because of the white-coat effect. Animals: Twenty-two healthy retired racing Greyhounds (RRG) enrolled in a blood donation program. Materials/Methods: We prospectively measured systemic BP in 3 environments: in the hospital by the investigator (Hosp), in the home by the investigator (H/I), and in the home by the owner (H/O). Five serial measurements of systolic, diastolic, and mean arterial pressures (SAP, DAP, MAP) as well as heart rate (HR) were measured by an oscillometric method on the distal forelimb and distal hind limb in all 3 environments.Results: There was a significant difference for SAP, MAP, and HR between the Hosp and both H/I and H/O (P o .001); there were no significant differences for any of the parameters between the H/I and H/O environments. HR, but not SAP, MAP, or DAP (P o .05) decreased in RRG with multiple hospital visits for blood donation before this study. The hind limb SAP was significantly higher than the forelimb SAP (P o .05).Conclusions and Clinical Importance: We conclude that the high SAP, MAP, and HR seen in the hospital setting are likely because of a white-coat effect. Furthermore, consideration should be given to defining the parameters of normal BP in RRG according to the environment in which they are obtained.

Objective To determine the pharmacodynamic effects of oral ivabradine in cats. Animals Eight healthy, adult domestic short hair cats. Methods Each cat underwent four study periods of 24 h, receiving either one dose of placebo or ivabradine (0.1 mg/kg, 0.3 mg/kg, and 0.5 mg/kg) in a single-blind randomized crossover study. Clinical tolerance was assessed hourly for the first 8 h, at 12 h, and at the end of the 24-h study period. Heart rate and blood pressure were monitored continuously for 18–24 h via radiotelemetry after each treatment. Response to stress (acoustic startle) was studied before (t = 0) and after treatment (t = 4 h). Statistical comparisons were made using a linear mixed models and 1-way and 2-way repeated measures ANOVA. Results Heart rate (min−1) decreased significantly (P < 0.05) in a dose-dependent manner with peak negative chronotropic effects observed 3 h after ivabradine (mean ±SD; placebo, 144 ± 20; ivabradine 0.1 mg/kg, 133 ±22; ivabradine 0.3 mg/kg, 112 ±20; and ivabradine 0.5 mg/kg, 104 ±11). Heart rate (min−1) was still reduced (P < 0.05) 12 h after ivabradine (0.3 mg/kg; 128 ±18 and 0.5 mg/kg; 124 ±16) compared to placebo (141 ±21). The tachycardic response to acoustic startle was significantly (P < 0.01) blunted at all 3 doses of ivabradine. Myocardial oxygen consumption estimated by the rate-pressure product was significantly reduced (P < 0.05) for all doses of ivabradine. No effect of ivabradine on systolic, diastolic, and mean blood pressure was identified and no clinically discernable side effects were observed. Conclusion These findings indicate that a single oral dose of ivabradine predictably lowers heart rate, blunts the chronotropic response to stress, and is clinically well tolerated in healthy cats. This makes ivabradine potentially interesting in the treatment of feline heart disease where ischemia is of pathophysiologic importance.

Hypothermia produced by acute cooling prominently alters sympathetic nerve outflow. Skin sympathoexcitatory responses to skin cooling are attenuated in aged compared with young subjects, suggesting that advancing age influences sympathetic nerve responsiveness to hypothermia. However, regulation of skin sympathetic nerve discharge (SND) is only one component of the complex sympathetic nerve response profile to hypothermia. Whether aging alters the responsiveness of sympathetic nerves innervating other targets during acute cooling is not known. In the present study, using multifiber recordings of splenic, renal, and adrenal sympathetic nerve activity, we tested the hypothesis that hypothermia-induced changes in visceral SND would be attenuated in middle-aged and aged compared with young Fischer 344 (F344) rats. Colonic temperature (Tc) was progressively reduced from 38 degrees C to 31 degrees C in young (3 to 6 mo), middle-aged (12 mo), and aged (24 mo) baroreceptor-innervated and sinoaortic-denervated (SAD), urethane-chloralose anesthetized, F344 rats. The following observations were made. 1) Progressive hypothermia significantly (P < 0.05) reduced splenic, renal, and adrenal SND in young baroreceptor-innervated F344 rats. 2) Reductions in splenic, renal, and adrenal SND to progressive hypothermia were less consistently observed and, when observed, were generally attenuated in baroreceptor-innervated middle-aged and aged compared with young F344 rats. 3) Differences in splenic, renal, and adrenal SND responses to reduced Tc were observed in SAD young, middle-aged, and aged F344 rats, suggesting that age-associated attenuations in SND responses to acute cooling are not the result of age-dependent modifications in arterial baroreflex regulation of SND. These findings demonstrate that advancing chronological age alters the regulation of visceral SND responses to progressive hypothermia, modifications that may contribute to the inability of aged individuals to adequately respond to acute bouts of hypothermia.

. Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system. Am J Physiol Regul Integr Comp Physiol 291: R558 -R565, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00846.2005.-Splenic nerve denervation abrogates enhanced splenic cytokine gene expression responses to acute heating, demonstrating that hyperthermia-induced activation of splenic sympathetic nerve discharge (SND) increases splenic cytokine gene expression. Hypothermia alters SND responses; however, the role of the sympathetic nervous system in mediating splenic cytokine gene expression responses to hypothermia is not known. The purpose of the present study was to determine the effect of hypothermia on the relationship between the sympathetic nervous system and splenic cytokine gene expression in anesthetized F344 rats. Gene expression analysis was performed using a microarray containing 112 genes, representing inflammatory cytokines, chemokines, cytokine/chemokine receptors and housekeeping genes. A subset of differentially expressed genes was verified by real-time RT-PCR analysis. Splenic SND was decreased significantly during cooling (core temperature decreased from 38 to 30°C) in splenicintact rats but remained unchanged in sham-cooled splenic-intact rats (core temperature maintained at 38°C). Hypothermia upregulated the transcripts of several genes, including, chemokine ligands CCL2, CXCL2, CXCL10, and CCL20, and interleukins IL-1␣, IL-1␤, and IL-6. Gene expression responses to hypothermia were similar for the majority of cytokine genes in splenic-intact and splenic-denervated rats. These results suggest that hypothermia-enhanced splenic cytokine gene expression is independent of splenic SND.hypothermia; splenic cytokine gene expression; splenic sympathetic nerve discharge EVIDENCE FROM THE DISCIPLINES of neuroscience and immunology demonstrate bidirectional communication pathways between the sympathetic nervous system and the immune system (2, 3, 13, 38). Sympathetic innervation to the spleen provides a connection between central sympathetic neural circuits and immunocompetent cells in the spleen (1,6,9,16,17). For example, chemical sympathectomy alters splenic T and B cell proliferation and natural killer cell activity (36 -40, 45) and diminishes splenic production of immunoglobulin M (31). Results of our recent studies demonstrate that in rats with intact splenic nerves, whole body hyperthermia (19) and central ANG II infusion (20) increase splenic sympathetic nerve discharge (SND) and the expression of selective splenic cytokine genes. Splenic cytokine gene expression responses to whole body hyperthermia and central ANG II infusion are significantly reduced in splenic nerve-denervated compared with splenic nerve-intact rats (19,20), suggesting that activation of splenic SND can enhance splenic cytokine gene expression.Hypothermia, a common side effect of extreme cold environments, anesthesia, and serious traumatic injuries, alters the sympathetic nervous system and immune system regula...

A 74.0-kg, 1.5-year-old, castrated male Newfoundland was presented for pharmacological cardioversion of atrial fibrillation. Three months before presentation, the dog was diagnosed with ''lone'' atrial fibrillation (ie, atrial fibrillation in the absence of detectable structural heart disease), underwent successful transthoracic electrical direct current (DC) cardioversion, and was treated with sotalol a (2.0 mg/kg PO q12h). Reversion to atrial fibrillation was confirmed 2 1 2 months later by ECG. At presentation, the dog was asymptomatic and receiving sotalol a (2.0 mg/kg PO q12h). Physical examination was normal except for an irregular heart rhythm, variable pulse quality, and pulse deficits. The biochemical profile was within reference intervals for the laboratory. Echocardiography was normal. An ECG confirmed atrial fibrillation with a ventricular response rate of 130-160 bpm. The dog was admitted to the hospital Intensive Care Unit for pharmacologic cardioversion.On the 1st day, the dog received 3 doses of lidocaine b (2 mg/kg IV q10min) with no change in rate or rhythm. Dofetilide c (6.76 mg/kg PO q12h) then was administered and the dosage subsequently increased to 6.76 mg/kg PO q8h on day 2. After 5 doses, the dog remained stable without a change in heart rate or underlying rhythm, but ventricular premature complexes (VPC) were noted including couplets and triplets. Dofetilide was discontinued on day 3 for presumed lack of efficacy and possible induction of ventricular ectopy, which resolved with discontinuation. The owner then elected pharmacologic conversion with IV amiodarone over other treatment options. On day 4, the dog was sedated with acepromazine d (0.02 mg/kg IM) and butorphanol e (0.2 mg/kg IM) for venous catheter placement. Amiodarone f was administered IV as a constant rate infusion (CRI) at 300 mg/kg/ min. Before beginning the CRI, the dog's systolic blood pressure was 115 mmHg. Two minutes after administration, injection site pain was noted and the CRI was decreased (150 mg/kg/min). After a total of 175 mg had been administered, the dog began salivating and pawing at its face. Its head and trunk became diffusely and severely erythematous, the muzzle and periorbital region became swollen, and severe weakness developed. Amiodarone was discontinued. The dog's systolic blood pressure, measured by Doppler, was 40-45 mmHg and atrial fibrillation remained with a ventricular response rate of 180-260 bpm. Because of a suspected anaphylactic reaction, IV Plasma Lyte 148 g and Hetastarch h fluids (total dose: 4 and 1 L, respectively), diphenhydramine i (1 mg/kg IV), and dexamethasone sodium phosphate j (0.8 mg/kg IV) were administered. A CRI of norepinephrine (0.3 mg/kg/min) was also begun. Over the next 2 hours, the dog's systolic blood pressure increased from 90 to 110 mmHg and the ventricular rate decreased from 120 to 150 bpm. The dog was discharged without antiarrhythmic therapy the next day and was started on digoxin and diltiazem administered orally for ventricular rate control 2 weeks later. D...