Objective—To determine the effect of fetal bovine serum (FBS) and heat-inactivated FBS (HI-FBS) on lipopolysaccharide (LPS)- and zymosan-induced procoagulant activity of equine and canine mononuclear cells.
Sample Population—Mononuclear cells from 18 horses and 3 dogs.
Procedures—Cells were incubated with various concentrations of FBS, HI-FBS, LPS, zymosan, polymyxin B, and anti–LPS-binding protein monoclonal antibody or combinations of these constituents. A 1stage recalcification assay was used to determine procoagulant activity.
Results—Addition of FBS to media significantly increased procoagulant activity; equine and canine cells were stimulated by 1% and 10% FBS, respectively. Coincubation of cells with FBS and polymyxin B did not reduce this effect, suggesting that the response was not attributable to LPS contamination. Addition of HI-FBS to media did not stimulate procoagulant activity of equine or canine cells, and the sensitivity of the equine cells to LPS was significantly increased by HI-FBS. This increased LPS sensitivity was reduced 40% with monoclonal antibody directed against human recombinant LPSbinding protein. Increasing concentrations of HIFBS significantly increased LPS- and zymosaninduced procoagulant activity of canine cells.
Conclusion and Clinical Relevance—Procoagulant activity production in equine and canine mononuclear cells was significantly increased by addition of FBS, whereas heat inactivation of FBS eliminated this effect. Heat inactivation did not eliminate the function of serum proteins involved in enhancement of LPSand zymosan-induced procoagulant activity. Results suggest that HI-FBS can be used as a source of serum proteins that increase the sensitivity of mononuclear cells to bacterial and yeast cell wall components.
Case Description—A 16-year-old 6.8-kg (15-lb) castrated male domestic shorthair cat was evaluated because of a 3 × 6-cm mass in the right medial lobe of the liver.
Clinical Findings—The cat had a history of frequent vomiting and anorexia along with 10% weight loss over the past year.
Treatment and Outcome—Transcatheter arterial embolization was selected because surgery (standard first-line treatment) was declined and only 1 vessel feeding the tumor was apparent on contrast-enhanced CT. A 4F sheath was placed in the left carotid artery, and a 3.3F guide catheter was advanced into the celiac artery. A 0.014-inch guidewire and 1.7F microcatheter were inserted into the hepatic artery through the guiding catheter and advanced into the feeding vessel. A mixture of polyvinyl alcohol particles and contrast agent was injected for embolization. A hypoechoic area in the tumor was identified on ultrasonography on posttreatment day 6, and necrotic and degenerated cells in the area were identified cytologically. By posttreatment day 71, vomiting had resolved and CT revealed decreased tumor size, but altered attenuation suggested a more solid mass on day 205. No feeding vessel for embolization was found on contrast-enhanced CT, so ultrasonic emulsification to remove the tumor was performed on day 231. No recurrence was seen on contrast-enhanced CT on day 420 or day 721.
Clinical Relevance—Findings suggested that transcatheter arterial embolization may be suitable for treating hepatic tumors in cats, but alternative approaches are needed in cats, compared with dogs, owing to anatomic differences.
Objective—To evaluate effects of a high dose of methylprednisolone sodium succinate (MPSS) on function of polymorphonuclear neutrophilic leukocytes (PMNs) in dogs.
Animals—7 healthy male Beagles (body weight, 10.5 to 15 kg; age, 2 to 4 years).
Procedures—All dogs were treated by IV administration of a high dose of MPSS (30 mg/kg). Additional doses of MPSS (15 mg/kg) were administered IV at 2 and 6 hours and then at 6-hour intervals until 48 hours after the initial dose. Blood samples were collected before and 1, 2, 4, 7, and 14 days after completion of the MPSS administrations and used for evaluation of PMN functions. Isolated PMNs were used for assessment of functions, such as adhesion, migration, phagocytosis, and oxidative burst.
Results—On days 1, 2, and 4 after completion of MPSS administration, there was a decrease in PMN expression of adhesion markers such as CD11b and CD18. There was a decrease in the phagocytotic ability of PMNs on days 1, 2, and 7 after completion of MPSS administration, with a reduction in the oxidative burst of PMNs detected on day 7. No significant changes were identified for migration. All functional changes returned to their pretreatment values by 14 days after completion of MPSS treatment.
Conclusions and Clinical Relevance—Treatment with a high dose of MPSS suppressed PMN functions in dogs. Analysis of these results suggested that treatment with a high dose of MPSS can suppress some of the major functions of PMNs for at least 7 days.