Objective-To determine the effects of stress in cats with feline idiopathic cystitis (FIC) by evaluating bladder permeability, sympathetic nervous system function, and urine cortisol:creatinine (C:Cr) ratios during periods of stress and after environmental enrichment. Design-Prospective study. Animals-13 cats with FIC and 12 healthy cats. Procedure-Cats subjected to an acute-onset moderate stressor for 8 days received IV injections of fluorescein. Serum fluorescein concentrations were determined and compared with those of controls to evaluate bladder permeability, and urine C:Cr ratios were compared to evaluate function of the hypothalamic-pituitary-adrenal (HPA) axis. Plasma catecholamine concentrations were analyzed in a subset of cats. After 8 days of moderate stress, cats were moved to an enriched environment, and tests were repeated after 21 days. Results-Serum fluorescein concentrations were significantly higher in cats with FIC at all time points. In the cats in which plasma catecholamine concentrations were determined, concentrations of dihydroxyphenylalanine, norepinephrine, and dihyroxyphenylglycol were significantly higher in cats with FIC at all time points, whereas no differences in urine C:Cr ratio between groups were observed. Conclusion and Clinical Relevance-Cats with FIC appeared to have altered bladder permeability, most notably during the period of initial stress. The increase in plasma dihydroxyphenylalanine concentration suggests that there may be stress-induced increase in the activity of tyrosine hydroxylase, which catalyzes the rate-limiting step in catecholamine synthesis. In contrast, no effects of stress on C:Cr ratios were observed, which suggests there was dissociation between the sympathetic nervous system and HPA-axis responses to stress.

We examined the electromyographic activity of the costal portion of the diaphragm and the transverse abdominal and external oblique muscles in 6 chronically instrumented awake adult horses during eupneic breathing during 2 levels of hypercapnia (fractional concentration of inspired CO2; FICO2 = 0.4 and 0.6), and during 2 levels of hypocapnic hypoxia (FIO2 = 0.15 and 0.12). Using the inert gas technique, we also measured the end-expiratory lung volumes of the 6 horses during eupnea, 6% CO2 challenge, and 12% O2 breathing. During eupneic breathing, phasic electrical activity of these 3 muscles was always present and was preceded by the onset of mechanical flow. At progressive levels of hypercapnia, the magnitude of inspiratory and expiratory electrical activity increased, and for the expiratory muscles, this recruitment coincided with significant (P < 0.05) increases in peak expiratory gastric pressure. However, during hypocapnic hypoxia, differential recruitment patterns of the respiratory muscles were found. The electrical activity of the diaphragm increased in magnitude and occurred sooner relative to the onset of mechanical flow. The magnitude and onset of abdominal expiratory activity failed to increase significantly during these episodes of hyperpnea and this pattern of activity coincided with decrements in peak expiratory gastric pressure. Despite alterations in muscle recruitment patterns during these hyperpneic episodes, end-expiratory lung volume remained unchanged. Thus, we conclude that adult horses respond similarly to awake dogs during peripheral and central chemoreceptor stimulation.

To determine whether abnormal airway pressures have a role in development of dorsal displacement of the soft palate (DDSP), measurements of tracheal and pharyngeal pressures were correlated with nasopharyngeal morphology in exercising horses. Exercising videoendoscopy and measurement of tracheal and pharyngeal pressures were used in 14 clinically normal horses and 19 horses with intermittent DDSP. The pressure signals were superimposed on the videoendoscope image, and both images were saved simultaneously on a videocassette for slow motion analysis to determine the instant displacement occurred in the respiratory cycle. Horses were submitted to an escalating 8-minute high-speed test with a maximal speed of 14 m/s. Compared with clinically normal horses, horses with intermittent DDSP did not have excessively negative inspiratory pressures during exercise. Eight horses displaced the soft palate during inspiration, 4 horses displaced it during expiration, and 7 displaced it by swallowing. Some horses displaced the soft palate at the beginning of the exercise trial, before reaching maximal speed, some horses displaced it at the peak speed, and some horses displaced it when slowing down. Epiglottic size in horses with DDSP was within normal limits, ruling out epiglottic hypoplasia as a cause of DDSP during exercise. Airway pressures were significantly (P < 0.002) altered after DDSP. Pharyngeal and tracheal inspiratory pressures were less negative, whereas pharyngeal expiratory pressure became less positive and tracheal expiratory pressure became more positive after displacement, suggesting a decrease in airflow and an increase in expiratory resistance in the upper airway.

Objective: To determine whether standard manual frequency filters in the ON and OFF settings affected P-QRS-T voltages, discover whether recorded P-QRS-T voltages vary between commercial electrocardiographs, assess effects of frequency filters on base-line artifact, and evaluate ECG frequency content by high-fidelity recordings subjected to digital filters with variable frequencies. Design: Sequential 10-lead ECG were recorded in 30 cats, using 3 commercial electrocardiographs to assess effects of manual frequency filters on the P-QRS-T wave forms. Three clinically normal cats were evaluated for ECG frequency content. Animals: Thirty cats (13 with hypertrophic cardiomyopathy; 4 with restrictive cardiomyopathy; 3 hyperthyroid; 1 with ventricular septal defect; 1 with aortic stenosis; and 8 with no detectible cardiovascular disease). Three additional clinically normal cats were studied for effects of frequency filters on the ECG frequency content. Procedure: Ten-lead ECG were recorded on each cat by use of 3 commercial electrocardiographs sequentially. For each machine, a recording was made with manual filters ON, immediately followed by a recording with manual filters OFF. High-fidelity lead-II ECG recordings were made with filters set with their rolloff frequency at 0.1 Hz and 3.0 kHz; output voltage (0.2 mV/V) was fed to an analog-to-digital converter, then to attendant software, which sampled the signal at 6 kHz with a 12-bit sampler, and were digitally filtered at various corner frequencies. Results: Voltages recorded by all 3 electrocardiographs were greatest when filters were OFF (most prominent on R- and S-wave voltages). In all recorded leads, it-wave voltage was significantly greater when filters were OFF than ON. Comparison of voltages indicated significant (P < 0.05) differences between R-wave voltages recorded in all leads with manual filters ON, but not with filters OFF. With filters ON, each electrocardiograph produced a smaller percentage of recordings with moderate to severe baseline artifact than with filters OFF. R-Wave amplitudes of high-fidelity lead-II ECG were significantly decreased with digital filters set at corner frequencies < 150 Hz. Conclusion: Significant (P < 0.05) voltage attenuation was recorded by each of the 3 commercial electrocardiographs when frequency filters were ON, compared with OFF. Comparison of waveform voltages among electrocardiographs with filters ON indicated significant variation in R-wave amplitudes in all leads. With manual filters ON, each electrocardiograph recorded a smaller percentage of recordings with baseline artifact than with filters OFF. Substantial frequency components greater than or equal to 150 Hz are present in the feline ECG waveform. Thus, filters with frequencies < 150 Hz markedly attenuate the feline R wave. Clinical Relevance: Attenuation of feline ECG signals occurs with use of commercial electrocardiographs and varies greatly between manufacturers. This is attributable largely to internal manual frequency filters. These consequences may be important when applying standard feline reference values or when equivocal voltage measurements are recorded.

The effects of 3 occlusive dressing materials and a standard, nonadherent dressing material on healing of full-thickness skin defects were evaluated in dogs. Two wounds measuring 2 X 2 cm were created bilaterally (4 wounds/dog) on the dorsolateral aspect of the trunk of 12 Beagles. Wound treatments were evenly distributed between 4 sites, using a Latin square design. Treatments evaluated were: equine amnion (group A), biosynthetic hydrogel dressing (group B), transparent polyethylene sheeting (group T), and a semi-occlusive rayon/polyethylene, nonadherent dressing (group C). Rates of contraction and epithelialization of group-A wounds were significantly greater than those of wounds of groups C, B, and T. On days 14, 21, and 28, mean percentage of wound contraction and mean percentage of total wound healed in group A exceeded those wounds in groups C, B, and T. On day 28, wounds in group A were significantly smaller than wounds in groups B and T, but were not significantly smaller than wounds in group C. All wounds in group A achieved 100% healing during the 28-day study period. Mean time for complete healing of group-A wounds was 21 days. The percentages of wounds completely healed by day 28 for groups B, C, and T were 25, 67, and 25%, respectively. Results indicate that use of equine amnion as an occlusive biological dressing on full-thickness wounds in dogs increases rate of healing.

Effects of endotoxemia on left ventricular contractility and systemic hemodynamics were determined in pentobarbital-anesthetized swine. A multielectrode conductance (volume) catheter and a high-fidelity pressure transducer catheter were passed retrograde into the left ventricle to continuously measure pressure and volume. End-systolic pressure-volume relationships were determined during transient (8 to 10 s) caudal vena caval balloon occlusion. Lactated Ringer's solution was administered at a rate sufficient to maintain left ventricular end-diastolic pressure > 6 mm of Hg. Following baseline measurements, Escherichia coli endotoxin (O55-B5) was infused IV at 2.5 micrograms/kg of body weight/h for 3 hours. Left ventricular end-systolic elastance (Ees), the slope of the end-systolic pressure-volume relationship; end-systolic elastance normalized for left ventricular end-diastolic volume (Ees norm); the rate of increase of left ventricular pressure (dP/dtmax); and preload recruitable stroke work (PRSW, stroke work-to-end-diastolic volume relationship) did not change in endotoxemic swine, compared with baseline measurements or with values from control (physiologic saline solution-treated) swine. Left ventricular pressures and volumes had marked pig-to-pig variability in the control and endotoxin-treated groups. Determination of Ees, Ees norm, and PRSW was further confounded by development of frequent premature ventricular contractions during caudal vena caval balloon occlusion. Endotoxin significantly (P < 0.05) decreased left ventricular end-diastolic pressure, compared with that in control swine, and significantly (P < 0.01) decreased left ventricular end-diastolic volume, compared with baseline. Endotoxin decreased cardiac index and arterial blood pressure, whereas heart rate, central venous pressure, and mean pulmonary arterial pressure increased. Endotoxin did not decrease myocardial contractility, as measured by Ees, Ees norm, dP/dtmax, or PRSW in anesthetized swine.

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.

Although it is known that the QT interval is dependent on the preceding RR interval, QT interval does not vary during respiratory sinus arrhythmia, despite a wide variation in heart rate. To assess the rate of change of the QT interval following an abrupt increase or decrease in heart rate, QT intervals were measured from ECG of healthy, anesthetized, thoracotomized dogs in which a junctional rhythm had been induced by destroying the sinoatrial node. Atria were paced at 800- or 600-millisecond cycle durations until a steady state was reached, and then the cycle duration was changed suddenly to a new cycle duration (600 or 800 milliseconds, respectively). The time and number of heart beats required until the QT interval achieved a value of 63% (1 time constant) of the new steady state were calculated. Time constants for change in QT interval vs the number of beats following the change were 2.8 (SD = 1.3 s) seconds when heart rate was accelerated and 4.7 (SD = 2.1 s) seconds when heart rate was slowed. Differences were not statistically significant. The time constants for change in QT interval duration vs duration after the sudden change in heart rate were 1.7 (SD = 0.8 s) seconds when heart rate was accelerated and 3.7 (SD = 1.7 s) seconds when heart rate was slowed. These time constants differed significantly (P < 0.01). Response of QT interval, therefore, depended on the number of heart beats following sudden change in heart rate, but not time, except as time determined the number of heart beats. The QT interval did not change until 3 to 5 beats after the heart rate was suddenly changed. This number of beats would be more than that which would occur in 1 respiratory cycle in dogs; therefore, QT interval memory would prohibit changes in QT intervals that occur during respiratory sinus arrhythmia.

The usefulness of tidal breathing flow-volume loops (TBFVL) to evaluate pulmonary function was investigated in 6 Standardbreds during treadmill exercise. Tidal breathing flow-volume loops are a graphic representation of airflow rate vs tidal volume for each individual breath. These TBFVL were obtained from horses exercising it speeds corresponding to 75 and 100% of maximum heart rate. Measurements were recorded in each horse before and after ovalbumininduced allergic lung disease. Moderate obstructive lung disease, characterized by a significant increase in pulmonary resistance, was observed while the horses were at rest. We found that in horses with airway obstruction exercising at 75 or 100% of maximum heart rate, the quantitative indices describing TBFVL shape and size were not markedly different from those in clinically normal horses exercising at similar speeds.

Plasma concentration of immunoreactive atrial natriuretic peptide (ir-ANP) was investigated in 83 Cavalier King Charles Spaniels with variable severity of mitral regurgitation caused by chronic valvular disease (CVD). Severity of mitral incompetence was assessed by echocardiography. Significant differences in plasma concentrations of ir-ANP were not found between clinically normal dogs (New York Heart Association functional class O), dogs with only cardiac murmur (class I), and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation (class II). Dogs with severe left atrial and ventricular dilatation and clinical signs of congestion (classes III and IV) were found to have significantly (P < 0.001) increased plasma concentration of ir-ANP. Overall, moderate degree of association was found between plasma concentration of ir-ANP and left atrial and left ventricular diameters (Pearson's r = 0.65, 0.60, respectively, P < 0.001), as well as heart rate (r = 0.47, P < 0.01). However, left atrial enlargement as found to have the predominant effect on plasma ir-ANP concentration. It is concluded that the plasma concentration of ir-ANP did not become markedly increased before decompensation of chronic mitral regurgitation associated with severe enlargement of the left atrium and ventricle in Cavalier King Charles Spaniels.