==================================BSR07================================== 7. I am looking for any information I can get on the complement system in dogs. 1 UI - 87086144 AU - Muraji T ; Okamoto E ; Hoque S ; Toyosaka A TI - Plasma exchange therapy for endotoxin shock in puppies. AB - The efficacy of plasma exchange (PE) therapy for endotoxin (ET) shock has not been evaluated. The following experimental study was designed to evaluate the feasibility of PE in infants and children and determine the efficacy as a therapeutic modality for ET shock. A compact circuit for PE designed for this experiment consists of two pumps and a membrane plasma separator for a venovenous extracorporeal circulation with the limited prime volume of 100 mL. The capacity of this device for PE was tested. When a membrane separator of 0.3 m2 in surface area was used, a plasma flux of 5 to 13 mL/min was satisfactorily obtained with the blood flow rate of 25 to 40 mL/min, which was taken through centrally placed catheters of 18 gauge or larger. Transmembrane pressure was maintained in a safe range (0 to 50 mm Hg) in the first 90 minutes, during which time a PE of 100 mL/kg was completed with a sieving coefficient greater than 0.8. In 14 puppies (1.8 to 3.5 kg), a shock state was produced by infusion of ET (Escherichia coli, 055:B5). Eight puppies were resuscitated simply with lactated Ringer's solution and bicarbonate. Six puppies were treated with PE using 100 mL/kg of fresh-frozen plasma prepared from adult dogs. A significant decrease in the mean blood pressure, platelet and leukocyte counts, total protein, and CH50 was documented in all animals after ET administration. Seven of eight control animals died within 24 hours of post-ET infusion. All of the six PE-treated animals survived for 48 hours or longer.(ABSTRACT TRUNCATED AT 250 WORDS) MH - Animal ; Blood Pressure ; Complement/ANALYSIS ; Dogs ; Hematocrit ; Leukocyte Count ; *Plasma Exchange ; Platelet Count ; Proteins/ANALYSIS ; Shock, Septic/BLOOD/PHYSIOPATHOLOGY/*THERAPY SO - J Pediatr Surg 1986 Dec;21(12):1092-5 2 UI - 87073522 AU - Johnson JP ; McLean RH ; Cork LC ; Winkelstein JA TI - Genetic analysis of an inherited deficiency of the third component of complement in Brittany spaniel dogs. AB - Genetically determined C3 deficiency in Brittany spaniel dogs shares a number of biochemical and clinical characteristics with the human disorder. In humans, the gene for C3 deficiency is a null gene that is allelic to the structural gene for C3 and is not linked to the major histocompatibility locus. The current study used allotype analysis of canine C3 in order to demonstrate that the gene for C3 deficiency in these dogs is also a null gene allelic to the structural gene for C3. In addition, preliminary pedigree analysis suggests that the gene for canine C3 deficiency is apparently not closely linked to the major histocompatibility complex of the dog. Thus, it appears that C3 deficiency in Brittany spaniel dogs not only shares biochemical and clinical features with C3 deficiency in humans, but also shares some genetic characteristics with the human disorder. MH - Alleles ; Animal ; Complement 3/*DEFICIENCY/GENETICS ; Dogs/*GENETICS ; Histocompatibility Antigens/GENETICS ; Linkage (Genetics) ; Major Histocompatibility Complex ; Pedigree ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Am J Med Genet 1986 Nov;25(3):557-62 3 UI - 86308886 AU - Macdougall DF ; Cook T ; Steward AP ; Cattell V TI - Canine chronic renal disease: prevalence and types of glomerulonephritis in the dog. AB - In a prospective survey, one hundred and eleven dogs with canine chronic renal disease, presenting to 24 veterinary practices in East Anglia and the West Midlands (geographical area 8,600 square miles) were identified. More than 20 different breeds were represented. In 76 cases, clinical details, blood and urine biochemistry, serology and kidney tissue for light and electron microscopy, and immunohistochemistry were obtained. Forty (52%) had glomerular (GN) and 36 (48%) non-glomerular (NGN) disease. Types of GN identified were (W.H.O. classification, number of cases in brackets): focal glomerulonephritis (gn) (5), diffuse mesangial proliferative gn (8), diffuse endocapillary proliferative gn (2), mesangiocapillary gn type I (8), diffuse crescentic gn (1), diffuse sclerosing gn (7), amyloid (6), unclassifiable gn (3). Eight dogs with GN and 13 with NGN had extra-renal lesions. In only one GN case (bacterial endocarditis) was the etiology clear. Proteinuria, but not age, breed, sex, serum creatinine or hematuria, discriminated between GN and NGN groups. This prospective survey identifies GN, with morphological types as found in humans, as a common cause of canine chronic renal disease. MH - Amyloidosis/PATHOLOGY/VETERINARY ; Animal ; Autoantibodies/ANALYSIS ; Capillaries/ULTRASTRUCTURE ; Comparative Study ; Complement 3/ANALYSIS ; Dog Diseases/*PATHOLOGY ; Dogs ; Glomerulonephritis/PATHOLOGY/*VETERINARY ; Kidney Failure, Chronic/PATHOLOGY/VETERINARY ; Kidney Tubular Necrosis, Acute/PATHOLOGY/VETERINARY ; Microscopy, Electron ; Pyelonephritis/ PATHOLOGY/VETERINARY ; Support, Non-U.S. Gov't SO - Kidney Int 1986 Jun;29(6):1144-51 4 UI - 86305700 AU - Matsumura K ; Kazuta Y ; Endo R ; Tanaka K ; Inoue T TI - Detection of circulating immune complexes in the sera of dogs infected with Dirofilaria immitis, by Clq-binding enzyme-linked immunosorbent assay. AB - The presence of circulating immune complexes (CIC) in the sera of dogs infected with Dirofilaria immitis was detected by using a Clq-binding enzyme-linked immunosorbent assay. Specificity of this assay with different concentrations of heat-aggravated canine IgG (ACG) was observed, i.e., the ELISA readings, expressed as microgram equivalents ACG/ml, increased with increasing amounts of ACG. The intra-assay variability was below 10%. The CIC levels of infected and uninfected dogs were 177.0 +/- 104.7 micrograms/ml and 22.8 +/- 45.8 micrograms/ml (mean +/- SD), respectively. The highest level was observed in 12 dogs with amicrofilaraemic infection. Age distribution of CIC levels in the 23 infected dogs also showed a significant positive correlation. These findings suggested that the CIC are present in the sera of dogs with dirofilariasis and may relate to canine glomerulonephritis. MH - Age Factors ; Animal ; Antigen-Antibody Complex/*ANALYSIS ; Antigens, Helminth/*IMMUNOLOGY ; Complement Activating Enzymes ; Dirofilaria immitis/*IMMUNOLOGY ; Dirofilariasis/*IMMUNOLOGY ; Dogs ; Enzyme-Linked Immunosorbent Assay ; Filarioidea/*IMMUNOLOGY ; Human ; IgG SO - J Helminthol 1986 Sep;60(3):239-43 5 UI - 86268759 AU - Day MJ ; Penhale WJ TI - Immunodiagnosis of autoimmune skin disease in the dog, cat and horse. AB - Skin biopsies from 47 dogs, 6 cats and 5 horses with suspected autoimmune skin disease were submitted for immunofluorescence from 1978 to 1985. These cases were predominantly Western Australian in origin, although a number were also referred from Queensland and Victoria. In 5 dogs, 2 cats and 2 horses immunoglobulin binding to intercellular cement substance and/or basement membrane was demonstrated by direct immunofluorescence. Antinuclear antibody was also demonstrated in several of these cases. Immunofluorescence was used in combination with histopathological examination to confirm the clinical diagnosis of autoimmune disease in 19/47 dogs, 4/6 cats and 2/5 horses. There was no age, breed or sex predisposition amongst the 19 positive dogs, however there was a higher incidence of antinuclear antibody (54%) than the normal canine population (10%) and other autoantibodies (rheumatoid factor) were sometimes present. Abnormalities in serum protein electrophoresis and serum complement C4 levels were also recorded in this group. MH - Animal ; Antinuclear Factors/ANALYSIS ; Autoimmune Diseases/DIAGNOSIS/ *VETERINARY ; Blood Protein Electrophoresis ; Cat Diseases/*DIAGNOSIS ; Cats ; Complement 4/ANALYSIS ; Coombs' Test ; Dog Diseases/*DIAGNOSIS ; Dogs ; Female ; Fluorescent Antibody Technic ; Horse Diseases/*DIAGNOSIS ; Horses ; Male ; Rheumatoid Factor/ANALYSIS ; Skin/IMMUNOLOGY ; Skin Diseases/DIAGNOSIS/*VETERINARY SO - Aust Vet J 1986 Mar;63(3):65-8 6 UI - 86262199 AU - Wakefield TW ; Lindblad B ; Whitehouse WM Jr ; Hantler CB ; Stanley JC TI - Attenuation of hemodynamic and hematologic effects of heparin-protamine sulfate interaction after aortic reconstruction in a canine model. AB - This investigation documented the effect of protamine sulfate pretreatment on the adverse hemodynamic and hematologic sequela of rapid intravenous protamine administration in heparinized dogs having undergone prior implantation of aortic prostheses. Fourteen dogs underwent infrarenal aortic replacement with 6 mm inner diameter by 7 cm knitted Dacron double-velour grafts. Carotid arterial, central venous, and pulmonary arterial catheters were placed for continuous hemodynamic monitoring. All dogs were adequately anticoagulated with heparin (150 IU/kg) and reversed with protamine (1.5 mg/kg/10 sec) after graft insertion. Pretreatment regimens studied included normal saline (n4), protamine 0.75 mg/kg (n5), and protamine 2.25 mg/kg in three divided doses of 0.75 mg/kg each (n5). All pretreatment agents were administered 3 minutes before heparinization. Blood pressure (BP), heart rate (HR), pulmonary artery pressure (PAP) and cardiac output (CO) were measured. Hematologic assessments included platelet count (PC), leukocyte count, thrombin clotting time, and total hemolytic complement. Significant salutory effects were associated with protamine pretreatment regarding BP, HR, PAP, CO, and PC. It is concluded that adverse hemodynamic effects of protamine reversal are blocked and certain hematologic effects are reduced with protamine pretreatment before heparinization and its reversal in this canine experimental model. MH - Animal ; Aorta, Abdominal/SURGERY ; Blood Pressure/DRUG EFFECTS ; Cardiac Output/DRUG EFFECTS ; Complement ; Disease Models, Animal ; Dogs ; Drug Interactions ; Female ; Heart Rate/DRUG EFFECTS ; Hemodynamics/*DRUG EFFECTS ; Heparin/*ADMINISTRATION & DOSAGE/ADVERSE EFFECTS ; Heparin Antagonists/*PHARMACODYNAMICS ; Injections, Intravenous ; Leukocyte Count/ DRUG EFFECTS ; Male ; Platelet Count/DRUG EFFECTS ; Premedication ; Protamines/ADMINISTRATION & DOSAGE/ADVERSE EFFECTS/*PHARMACODYNAMICS SO - Surgery 1986 Jul;100(1):45-51 7 UI - 86220672 AU - Hamilton RG ; Wagner E ; April M ; Winkelstein JA ; Sobotka AK ; Bleeker E ; Adkinson NF Jr TI - Dirofilaria immitis: diethylcarbamazine-induced anaphylactoid reactions in infected dogs. AB - The immunopathogenesis of the anaphylactoid Mazzotti reactions has been studied by comparing physiologic and immunologic aspects of diethylcarbamazine-induced shock in Dirofilaria immitis infected dogs with antigen induced anaphylaxis in infected and uninfected controls. Filarial antigen, specific host IgG antibody, and C1 and C3 complement levels were quantitatively measured over time in relation to the levels of histamine and prostaglandin D2 in the blood and changes in mean blood pressure. D. immitis antigen injected into uninfected dogs having no detectable IgG antibody to D. immitis or Toxocara canis produced a rapid drop in blood pressure that paralleled a drop in C1 and C3 levels and an increase in prostaglandin D2. Antigen injected into infected dogs with IgG antibody produced a similar drop in blood pressure and complement and increase in prostaglandin D2 which differed from the uninfected group only in the slower clearance of antigen from the blood. Diethylcarbamazine alone produced no measurable changes in blood pressure or complement in uninfected hosts. Diethylcarbamazine, however, administered into skin test positive infected dogs, produced a temporally slower but quantitatively similar loss in blood pressure, drop in complement, and increase in prostaglandin D2 and histamine to that induced by antigen injection. Complement activation and immune complex formation are initiated by antigen release, and subsequent vasoactive mediator release leads to shock with prostaglandin D2 being quantitatively higher in blood than is histamine. MH - Airway Resistance ; Anaphylaxis/*CHEMICALLY INDUCED ; Animal ; Antigens, Helminth/ANALYSIS ; Blood Pressure/DRUG EFFECTS ; Complement Activation ; Complement 1/ANALYSIS ; Complement 3/ANALYSIS ; Diethylcarbamazine/ *TOXICITY ; Dirofilaria immitis/IMMUNOLOGY ; Dirofilariasis/*IMMUNOLOGY/ PHYSIOPATHOLOGY ; Dogs ; Histamine/BLOOD ; IgG/ANALYSIS ; Prostaglandins D/BLOOD ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Exp Parasitol 1986 Jun;61(3):405-20 8 UI - 86213387 AU - Brigham KL ; Meyrick B TI - Endotoxin and lung injury. AB - Two things are certain: endotoxin has dramatic effects on the structure and function of the lungs in intact animals and also on isolated lung cells, and both the in vivo and in vitro effects of endotoxin are complex. In whole animals, endotoxin causes obvious and subtle effects on functions of both airways and the pulmonary circulation. These effects include diffuse lung inflammation and injury of pulmonary vascular endothelium. Endotoxin can also directly injure endothelial cells in vitro. In vivo, lung injury caused by endotoxin is at least partly dependent on the presence of granulocytes, and some evidence also suggests that both lymphocytes and macrophages may participate in the response either directly or by directing cell traffic. At least in the sheep preparation, platelets do not seem to play a major role in the lungs' response to endotoxemia. Although endotoxin can activate complement and activated complement infused into whole animals affects the lungs, it seems unlikely that complement activation alone is sufficient to explain the severe and prolonged lung injury caused by endotoxin. Cyclooxygenase metabolites of arachidonic acid appear to mediate both changes in lung mechanics and pulmonary vasoconstriction after endotoxemia. Lipoxygenase products may play a role in these responses as well as the inflammatory response and increases in vascular permeability, although evidence for these latter speculations is not firm. Lung cell injury caused by endotoxin probably is mediated at least in part by generation of free radicals. Inflammatory cells, especially neutrophils, are one source of these toxic oxygen species, but intracellular generation of free radicals within lung cells per se may also be stimulated by endotoxin and account for some of the lung injury. Likewise, inflammatory-cell-derived proteinases may mediate endotoxin-induced injury of lung cells and, as with chronic lung diseases, balance between proteinases and antiproteinases could be important. The fact that free radicals can inactivate antiproteinases, and antiproteinases can act as free radical scavengers, may suggest a complex relationship among the several possible mediators of toxicity. Cyclic nucleotide metabolism is affected in whole animals and isolated lung cells by endotoxin and these classic second messengers could be involved in the pathogenetic sequence, but exactly how is unclear. Chronic effects of endotoxin on the lungs may provide a pathogenetic link between acute lung injury and chronic changes in lung structure and function.(ABSTRACT TRUNCATED AT 400 WORDS) MH - Animal ; Arachidonic Acids/PHYSIOLOGY ; Blood Platelets/PHYSIOLOGY ; Capillary Permeability ; Complement/PHYSIOLOGY ; Dogs ; Endotoxins/ *ADVERSE EFFECTS ; Human ; Inflammation/PHYSIOPATHOLOGY ; Leukocytes/ CYTOLOGY ; Lung/CYTOLOGY/*DRUG EFFECTS/PATHOLOGY/PHYSIOPATHOLOGY ; Lung Diseases/PATHOLOGY/*PHYSIOPATHOLOGY ; Lymphocytes/PHYSIOLOGY ; Macrophages/PHYSIOLOGY ; Neutrophils/PHYSIOLOGY ; Nucleotides/PHYSIOLOGY ; Oxygen/PHYSIOLOGY ; Peptide Peptidohydrolases/PHYSIOLOGY ; Respiratory Distress Syndrome, Adult/PHYSIOPATHOLOGY ; Review ; Sheep ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - Am Rev Respir Dis 1986 May;133(5):913-27 9 UI - 86210480 AU - Rzepczyk CM ; Bishop CJ ; Atwell RB TI - The ability of microfilariae to evade in vitro cell-mediated cytotoxicity. AB - When microfilariae (Mf) of Dirofilaria immitis, both uterine and systemic, were incubated in an in vitro cytotoxicity assay with neutrophils and sera from dogs with occult infections, some Mf remained free of adherent cells and consequently evaded cytotoxicity. The ability to evade cytotoxicity could not be related to the age of the Mf, and host albumin was not detected on any Mf, either uterine or systemic. However, it was shown that some Mf failed to bind IgM, IgG and C3 when incubated with occult sera. It is suggested that the ability of some Mf to evade serum-dependent, neutrophil-mediated cytotoxicity in vitro was related to differences in their antigenicity. MH - Age Factors ; Animal ; Comparative Study ; Complement 3/IMMUNOLOGY ; Cytotoxicity Tests, Immunologic ; *Cytotoxicity, Immunologic ; Dirofilaria immitis/*IMMUNOLOGY/METABOLISM/ULTRASTRUCTURE ; Dirofilariasis/*IMMUNOLOGY/PARASITOLOGY ; Dogs ; Female ; Filarioidea/ *IMMUNOLOGY ; IgG/IMMUNOLOGY ; IgM/IMMUNOLOGY ; Immunoenzyme Technics ; Microfilaria/IMMUNOLOGY ; Microscopy, Electron ; Neutrophils/*IMMUNOLOGY ; Serum Albumin/METABOLISM ; Uterus/PARASITOLOGY SO - Z Parasitenkd 1986;72(2):241-9 10 UI - 86209405 AU - Prendergast MM ; Bradstock KF ; Broomhead AF ; Hughes WG ; Kabral A ; Berndt MC ; Tiver K TI - Monoclonal antibody analysis of canine hemopoietic cells. Role of Ia-like and Thy-1 antigens in bone marrow engraftment. AB - The expression of Ia-like (class II MHC) antigens on canine hemopoietic cells was investigated using a cytotoxic murine monoclonal antibody, WM-2, reactive with dog Ia-like antigens. Another monoclonal antibody, WMD-1, reactive with canine Thy-1 antigen, was used as a positive control. Depletion of Ia+ cells from dog bone marrow by complement-mediated lysis with WM-2 antibody failed to inhibit growth of granulocyte-macrophage progenitors (CFUGM) in vitro, while WMD-1 produced complete inhibition of CFUGM. Lethally irradiated dogs receiving bone marrow autografts depleted of Ia-positive cells ex vivo showed initial engraftment, followed by prolonged pancytopenia, and eventual complete recovery of marrow function in the majority of animals. In contrast, dogs receiving autografts treated with WMD-1 and complement all died of marrow failure. We interpret these results as indicating: (1) that Thy-1 antigen is present on hemopoietic stem cells essential for marrow engraftment; and (2) that the expression of Ia antigens on hemopoietic cells is heterogeneous and related to the level of stem cell maturation. While Ia appears to be present on a stem cell population at an earlier stage than CFUGM, as evidenced by the transient phase of graft failure seen in dogs receiving Ia-depleted marrow, the most primitive stem cell, responsible for long-term engraftment, is effectively Ia-negative. MH - Animal ; Antibodies, Monoclonal/DIAGNOSTIC USE ; Antigens, Immune Response/*IMMUNOLOGY ; Antigens, Surface/*IMMUNOLOGY ; Blood Platelets/ IMMUNOLOGY ; Bone Marrow/*TRANSPLANTATION ; Cell Differentiation ; Colony-Forming Units Assay ; Complement/IMMUNOLOGY ; Dogs ; Hematopoietic Stem Cells/*IMMUNOLOGY ; Neutrophils/IMMUNOLOGY ; Support, Non-U.S. Gov't ; T Lymphocytes/IMMUNOLOGY SO - Transplantation 1986 May;41(5):565-71 11 UI - 86200275 AU - Kapur MM ; Jain P ; Gidh M TI - The effect of trauma on serum C3 activation and its correlation with injury severity score in man. AB - The sera of 12 patients with mechanical trauma were studied to determine C3 levels and activation. The injury severity score (ISS) was then related to serum C3 levels and activation. It was found that in the immediate postinjury period, serum C3 activation occurred in cases where ISS was greater than or equal to 12. The mean ISS of patients with complement activation was 25.2. In comparison, in patients with nonactivation of complement, the mean ISS was 9.5 (p less than 0.05). Serum C3 levels were inversely related to ISS. The mean serum C3 level of patients with ISS greater than or equal to 12 was 73.3 mg% and mean serum C3 level with ISS less than 12 was 109.4 mg%. This difference was again statistically significant (p less than 0.05). There is indication that complement depletion occurs in the immediate postinjury period in moderate to severe injury (ISS greater than or equal to 12). This finding could explain, in part, the immunosuppressive effect of trauma and can be used as a marker to predict possible septic complications. MH - Adult ; Animal ; Child ; *Complement Activation ; Complement 3/*ANALYSIS ; Complement 5/ANALYSIS ; Dogs ; Female ; Human ; Male ; Respiratory Distress Syndrome, Adult/IMMUNOLOGY ; Time Factors ; Wounds and Injuries/ *IMMUNOLOGY SO - J Trauma 1986 May;26(5):464-6 12 UI - 86196260 AU - Cramer EB ; Milks LC ; Brontoli MJ ; Ojakian GK ; Wright SD ; Showell HJ TI - Effect of human serum and some of its components on neutrophil adherence and migration across an epithelium. AB - The effect of human serum and some of its components on the process of transepithelial migration of human neutrophils was investigated in an in vitro system. 10% autologous serum caused an increase in neutrophil adherence to and migration across canine kidney epithelial cells. This increase in neutrophil binding also occurred if the epithelium but not the neutrophils had been preincubated with serum. The binding was lost if the serum was either preabsorbed over the kidney epithelium before use or heat inactivated. Indirect immunofluorescence studies indicated that IgG, IgM, and a component of C3 bound to the epithelial surface, whereas IgA, IgE, or C5a were not detectable. The majority of epithelial cells were immunofluorescent, however epithelial cells with varying degrees of reactivity were also apparent and approximately 5% of the epithelial cells did not bind IgG, IgM, and C3. When epithelia were simultaneously tested for the presence of either IgG, IgM, or C3, and bound neutrophils the few epithelial cells which did not bind IgG or IgM also did not bind C3 or neutrophils. Studies with monoclonal antibodies against Fc and C3 receptors indicate that neutrophil adherence to the epithelial surface was mediated predominately by the receptors for C3b and C3bi. In response to a chemotactic gradient, bound neutrophils were able to detach and migrate across the epithelium. A separate heat-stable factor(s) in serum was able to increase neutrophil migration across the epithelial monolayer. This factor acted independently of the factors which caused the increase in neutrophil binding as the increase in neutrophil migration also occurred under conditions (preabsorption over the kidney epithelium or heat inactivation) that prevented the increase in neutrophil binding. The increase in neutrophil migration may be caused by the permeability-increasing properties of this factor as both serum and heat-inactivated serum lowered the transepithelial electrical resistance an average of 38 and 35%, respectively, in 40 min. Upon removal of serum or heat-inactivated serum, the resistance returned 100 and 81%, respectively, in 5 h. MH - Animal ; Blood Proteins/*PHYSIOLOGY ; Cell Adhesion ; Cell Line ; Cell Movement ; Cells, Cultured ; Chemotaxis, Leukocyte ; Complement 5/ PHYSIOLOGY ; Culture Media ; Dogs ; Electrophysiology ; Epithelium/ PHYSIOLOGY ; Fluorescent Antibody Technic ; Heat ; Human ; Immunoglobulins/PHYSIOLOGY ; Neutrophils/*PHYSIOLOGY ; Receptors, Complement/PHYSIOLOGY ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. SO - J Cell Biol 1986 May;102(5):1868-77 13 UI - 86186510 AU - Day MJ ; Penhale WJ ; Eger CE ; Shaw SE ; Kabay MJ ; Robinson WF ; Huxtable CR ; Mills JN ; Wyburn RS TI - Disseminated aspergillosis in dogs. AB - Clinical and pathological findings are reported from a series of 12 cases of disseminated aspergillosis (A. terreus) in 11 German Shepherd dogs and one Dalmatian referred to Murdoch University Veterinary Hospital (MUVH) over the period 1980 to 1984. A preliminary study of humoral and cell mediated immune components and complement levels revealed no consistent abnormality in 9 dogs tested apart from raised IgG levels. Serum IgA levels were depressed in 30% of cases. Serial data from one extensively monitored case is presented. The unusual epidemiological and pathogenetic features of the disease are discussed. MH - Animal ; Aspergillosis/IMMUNOLOGY/PATHOLOGY/*VETERINARY ; Bone and Bones/ PATHOLOGY ; Complement/ANALYSIS ; Dog Diseases/IMMUNOLOGY/*PATHOLOGY ; Dogs ; Female ; Immunity, Cellular ; Immunoglobulins/ANALYSIS ; Intradermal Tests ; Lymphocytes/IMMUNOLOGY ; Male ; Support, Non-U.S. Gov't SO - Aust Vet J 1986 Feb;63(2):55-9 14 UI - 86186116 AU - Rommes JH ; Sangster B ; Berrens L ; Borst C ; van Heijst AN TI - Biocompatibility of haemoperfusion. AB - To evaluate the influence of haemoperfusion on haemodynamics, complement system, leucocyte and thrombocyte concentration, a controlled study was performed in three groups of five dogs each. During the first 30 min of haemoperfusion with columns containing cellulose-coated activated charcoal, a significant decrease of mean aortic pressure, cardiac output and stroke volume was observed, while heart rate and total systemic resistance decreased. A comparable phenomenon, although to a much lesser extent, was observed during perfusion using columns containing polystyrene resin. Perfusion with columns containing cellulose-coated activated charcoal caused a significant decrease in total haemolytic complement, indicating activation of the complement system. A significant decrease in the leucocyte and thrombocyte concentration due to sequestration of granulocytes and thrombocytes in the columns was observed during the first 30 min of perfusion in both groups. Pulmonary leucostasis, without decrease of arterial oxygen tension, occurred during perfusion with columns containing cellulose-coated activated charcoal. Both the simultaneous occurrence and the transient character of the haemodynamic changes, complement activation and sequestration of granulocytes and thrombocytes in the perfusion column suggest a relationship between these various changes. The results stress the importance of close monitoring of the haemodynamic parameters of the intoxicated patient, particularly during the early phase of haemoperfusion. MH - Animal ; Aorta/PHYSIOLOGY ; Body Temperature ; Calcium/BLOOD ; Complement/ ANALYSIS ; Dogs ; Hematocrit ; Hemodynamics ; *Hemoperfusion ; Leukocyte Count ; Oxygen/BLOOD ; Platelet Count SO - Arch Toxicol 1986 Feb;58(3):187-95