The purpose of this study was to compare the thermodilution technique for estimation of cardiac output with the indocyanine green dye dilution technique at flows between 10 and 39 L/min in halothane-anesthetized horses. The estimation of area of dye dilution cardiac output curves was made by using the fore-'n-aft (FA) triangle method. This shorthand technique was compared with logarithmic exponential extrapolation and summation (extrapolated area), using 64 cardiac output curves. Then, 256 simultaneous thermodilution measurements were compared with dye dilution measurements calculated by use of the FA technique. Forty milliliters of iced 0.9% NaCl solution containing 15 mg of indocyanine green dye was used as the indicator. This was delivered in < 1 second to the right atrium, using a power injector. A thermistor positioned in the pulmonary artery detected the thermal indicator. Blood was withdrawn from the carotid artery through a densitometer cuvette to measure the dye concentration. The FA estimations of area were higher than those determined by use of extrapolated area. A multiplicative adjustment of 0.837 was estimated. On average, thermodilution estimates of cardiac output exceeded the adjusted FA determinations. Using a weighted linear regression, we determined the following calibration adjustment: thermal dilution cardiac output/1.048 = indocyanine green dye dilution cardiac output.

The lateral distribution and temporal changes in the eye standing potential of 15 dogs with normal eyes (as determined by use of an ophthalmoscope and electroretinography) were measured by use of noninvasive methods. The standing potential was converted to an alternating potential by controlled eye movement. The light peak occurred 6 minutes after a stimulus intensity increase of 4 log units. The ratios of the highest measured voltage after the light step divided by the voltage measured immediately before the light step ranged from 1.27 to 2.07 (mean 1.74 +/- SEM, 0.064). The responses typically decayed slowly after the light peak. The potential after the light peak did not return to prelight step values during the observation period. The field potential of the standing potential decreased nonlinearly in temporal direction from the outer canthus.

Specimens of the uterine tube epithelium (ampulla) were obtained from 20 healthy, prepubertal, ovariohysterectomized gilts. A 2 to 3% proportion of atypical cilia was observed. Of 6,600 transversely sectioned cilia, 122 (1.8%) had microtubular disorganization, whereas 444 of 48,080 totally examined cilia (0.9%) were compound, 104 (0.2%) were swollen, and 44 (0.09%) were intracytoplasmic.

Conditions for psittacine beak and feather disease (PBFD) virus hemagglutination and hemagglutination-inhibition (HI) test reactions are defined. The PBFD virus was found to hemagglutinate cockatoo and some guinea pig erythrocytes. The HI test was used to assay serum antibody titer in birds with active PBFD virus infections and in others that had been exposed to diseased birds. On the basis of HI antibody titers in psittacine birds that had been exposed to PBFD virus, but remained clinically normal, we suggest that some birds exposed to the virus are able to mount an effective immune response. Birds with active PBFD virus infections had lower antibody values than did birds that had been exposed to the virus, but remained clinically normal. On the basis of these findings, the ability to develop a suitable HI antibody response may be crucial in determining the disease status of susceptible birds exposed to the PBFD virus. If HI antibodies are found to have neutralizing activity, then the fact that a high HI titer was induced in birds inoculated with purified PBFD virus might suggest that an immunization program would be effective in preventing PBFD virus infections.

Five groups of Hereford steers were monitored for 293 days. One group of 3 was not given selenium supplementation; the other 4 groups of 3 steers each were given 2, 4, 6, or 8 reticulorumen selenium pellets. Health, body weight, and blood selenium concentration were monitored during the study. At the finish, steers were slaughtered, and various tissues from the carcasses were analyzed for selenium content. Initial blood selenium concentration did not differ significantly among groups. However, significant (alpha = 0.01) difference among means was detected during the early period of rapid increase in blood selenium concentration in steers of supplemented groups. Means of maximal blood selenium concentration also differed among groups; however, even the highest value, 0.253 microgram/g, was lower than the 3 microgram/ml reported in chronic clinical cases of toxicosis in the literature. Carcass analysis indicated significant (alpha = 0.05) differences in selenium concentrations among treatment groups for almost all tissues tested. Only kidney samples (7.9 microgram/g) from steers of the 8-pellet treatment group exceeded published normal values (7.6 microgram/g). Health variables for most dates were not significantly different among groups, and selenium toxicosis was not evident in any steer. Analysis did not indicate risk to human beings consuming tissues from these steers.

The effects of whole-body potassium depletion induced by food deprivation on plasma, erythrocyte, and middle gluteal muscle K concentrations was quantified in 16 healthy, adult horses before, during, and at the end of a 7-day period of food deprivation during which water and sodium chloride were available ad libitum. Potassium concentrations were determined by atomic absorption spectroscopy. Plasma K concentration remained constant (3.49 +/- 0.09 mM K/L of plasma; mean +/- SEM) throughout the study. Erythrocyte potassium concentration decreased from 93.10 +/- 1.94 mM K/L of erythrocytes on day 0 to 88.63 +/- 2.39 mM K/L of erythrocytes on day 2 (decrease of 4.8%; P < 0.05) and thereafter did not change. The K concentration of the middle gluteal muscle decreased from 91.06 +/- 2.96 micromole K/g of muscle (wet weight) to 79.61 +/- 2.09 micromole K/g of muscle (decrease of 12.6%; P < 0.05) on day 4 and decreased further on day 7 to 73.62 +/- 1.85 micromole K/g of muscle (decrease of 19.2%; P < 0.05). There was no correlation between the plasma and erythrocyte K concentrations (r = -0.066), the erythrocyte and middle gluteal muscle K concentrations (r = 0.167), or the plasma and middle gluteal muscle potassium concentrations (r = -0.018). The water content of the middle gluteal muscle remained constant (73.23 +/- 0.36%) throughout the study. Erythrocyte membrane potential did not change (-99.26 +/- 0.87 mV) during the study, whereas the magnitude of the membrane potential of the middle gluteal muscle decreased from -105.84 t 1.67 mV on day 0 to -100.93 +/- 2.10 mV on day 7 (P < 0.05).

A study was conducted to determine the immune (increased antibody) and protective (reduced colony-forming units) responses induced in mice by a: (i) single vaccinal inoculation, using various concentrations of Brucella cell surface protein (BCSP) or lipopolysaccharide (LPS); (ii) primary inoculation, using various concentrations of BCSP, followed by a secondary inoculation, using a standard concentration of BCSP; and (iii) primary inoculation, using 1 concentration of BCSP or LPS, followed by a secondary inoculation, using various concentrations of BCSP or LPS. Four weeks after the primary inoculation, mice were challenge exposed with approximately 1 X 10(4) colony-forming units of Brucella abortus strain 2308 and all mice were euthanatized at 6 weeks. Reduced splenic weights and reduced colony-forming units in the spleens of vaccinated mice, compared with nonvaccinated mice, were the criteria of protection. Increase in serum IgM and IgG was defined as immunity. Both BCSP and LPS induced protective and immune responses that were proportional to the dose given up to an optimal limit. However, concentrations higher than optimal decreased the protective and immune responses. This was true for mice given either 1 or 2 vaccinal inoculations. Enhanced secondary protective responses were seen only when suboptimal doses were used in the primary inoculation. Excessive or optimal doses in the secondary inoculations prevented or obscured the protectiveness and immunity by primary inoculations. The protective effects appeared to be additive when suboptimal doses were used in the primary and secondary inoculations. Inoculation of subimmunogenic doses induced a relative reduction in the antibody concentration after challenge exposure, compared with nonvaccinated mice. The overall results indicated that the protective responses induced by BCSP were probably attributable to LPS. The results also indicated a linear increase in protection and immune response corresponding to increasing doses up to an optimal dose, and this stoichiometric optimum may be achieved by the use of 1 or more vaccinal inoculations. However, once this optimum was obtained, additional amounts of BCSP or LPS cause perturbation of both the protective and serologic responses.

Concentrations of amino acids in the plasma of 13 neonatal foals with septicemia were compared with the concentrations of amino acids in the plasma of 13 age-matched neonatal foals without septicemia. Analysis of the results revealed significantly lower concentrations of arginine, citrulline, isoleucine, proline, threonine, and valine in the plasma of foals with septicemia. The ratio of the plasma concentrations of the branched chain amino acids (isoleucine, leucine, and valine) to the aromatic amino acids (phenylalanine and tyrosine), was also significantly lower in the foals with septicemia. In addition, the concentrations of alanine, glycine, and phenylalanine were significantly higher in the plasma of foals with septicemia. Therefore, neonatal foals with septicemia had significant differences in the concentrations of several amino acids in their plasma, compared with concentrations from healthy foals. These differences were compatible with protein calorie inadequacy and may be related to an alteration in the intake, production, use, or clearance of amino acids from the plasma pool in sepsis.

Hexosamine concentration, DNA concentration, and [35S]sulfate incorporation for articular cartilage obtained from various sites in the metacarpophalangeal and carpal joints of horses were measured. The same measurements were made on the repair tissue filling full-thickness articular defects in the intermediate carpal bone and on cartilage surrounding partial-thickness defects 6 weeks after the defects were created arthroscopically. Cellularity (measured as DNA concentration), proteoglycan content (measured as hexosamine concentration), and proteoglycan synthesis (measured as [35S]sulfate incorporation) varied according to the site sampled. Cartilage from the transverse ridge of the head of the third metacarpal bone and the radial facet of the third carpal bone had the lowest hexosamine concentration, whereas rate of proteoglycan synthesis was lowest in cartilage from the transverse ridge of the head of the third metacarpal bone and the distal articular surface of the radial carpal bone. Repair tissue filling a full-thickness cartilage defect at 6 weeks was highly cellular. It was low in proteoglycan content, but was actively synthesizing these macromolecules. In contrast, the cartilage surrounding a partial-thickness defect was unchanged 6 weeks after the original defect was made.

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+ dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P < 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow. The rapid administration of large-volume ISS appears superior to small-volume HSS for initial resuscitation of acutely endotoxemic, anesthetized calves. At this time, we do not advocate rapid infusion of ISS to septicemic calves because exacerbation of pulmonary hypertension may potentially depress respiratory function, and rapid increase in preload may hemodynamically compromise calves with depressed cardiac contractility.