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Objective: To assess selenium (Se) status of cats in 4 regions of the world and to compare results for Se status with reported incidence of hyperthyroidism in cats in those regions., Animals: 50 cats (30 from 2 regions with an allegedly high incidence of hyperthyroidism and 20 from 2 regions in which the disease is less commonly reported)., Procedure: Hematologic samples (heparinized whole blood, plasma, and RBC fractions) were obtained from 43 healthy euthyroid cats and 7 hyperthyroid cats. Plasma concentration of Se and activity of glutathione peroxidase (GPX) in whole blood and plasma were determined., Results: Plasma concentration of Se and GPX activity in whole blood or plasma did not differ significantly among cats from the 4 regions. However, cats had a plasma concentration of Se that was approximately 5 times the concentration reported in rats and humans. The GPX activity in whole blood or plasma in cats generally was higher than values reported in rats or humans., Conclusions and Clinical Relevance: Cats have higher Se concentrations in plasma, compared with values for other species. However, Se status alone does not appear to affect the incidence of hyperthyroidism in cats. High Se concentrations may have implications for health of cats if such concentrations are influenced by the amount of that micronutrient included in diets.

Shock is defined as a secondary condition constituting a complication to a primary disease of which more than 100 are recorded in the literature. Shock is characterized by prolonged circulatory inadequacy leading to insufficient tissue perfusion and cell death. According to etiology shock is classified into three main groups: hypovolemic, vasogenic and cardiogenic shock. Taking hypovolemic shock as a model the pathgenesis of shock is presented. Hypovolemia acts on the baroreceptors giving rise to a sympatho-adrenal response resulting in increased vasoconstriction, which again leads to viscerocutaneous ischemia. This phase is known as the ischemic anoxic or centralized shock phase. Without treatment this phase develops into the second socalled stagnant anoxic or paralytic shock phase. "Irreversible shock" is discussed. The pathogenesis of vasogenic and cardiogenic shock is mentioned and compared with hypovolemic shock. It is emphasized that the sympatho-adrenal response is the central and common feature in every shock development. Special reference is made to septic shock with its outstanding circulatory conditions (arteriovenous shunting). Lacticacidemia and metabolic acidosis are described as the most important metabolic alterations in shock. With reference to pathenesis the main clinical symptoms of shock are presented: increased heart rate, initially pale later hyperemic, congested and terminally cyanotic mucosae, increased capillary filling time, cold skin and low body temperature. All these signs are related to the sympatho-adrenal response. It is pointed out that the patient in shock is depressed. Inevitably the primary disease will modify the shock symptoms. Hyperemia with edema, hemorrhages and thrombosis in organs and tissues are morphological manifestations of shock. Later microscopically detectable degenerative and necrotic alterations develop, and there are signs of intravascular coagulation (hyaline thrombi and spheres). Due to the rather nonspecific macroscopic alterations a post mortem shock diagnosis necessitates for completion histology and/or a clinical shock diagnosis. Some of the most important shock-provoking primary diseases dealt with in veterinary practice are mentioned along with their possible shock pathogenesis. Referring to the shock pathogenesis the therapy is discussed. The first and indispensable therapeutical measure in treating shock per se is increasing the circulating blood volume, Balanced electrolyte solutions are preferred. Examples of composition, doses (up to 80--200 ml/kg body weight) and infusion rate (initially 15--30 ml/kg body weight during the first 10--20 min., then quantum satis) are given.

42 horses were examined. The physical signs with relation to circulatory insufficiency and the abdominal disease were registered following a two-phased examination procedure. Great prognostic value was found in the degree of circulatory insufficiency judged by pulse rate and character, filling of the jugular vein, skin temperature, colour of mucous membranes, capillary refill time, sweating, depression, skin turgor and degree of enophthalmus. In making a causal diagnosis the abdomen was examined for shape, tenderness, peristaltic sounds, gastric dilation by siphoning, abnormal rectal findings and macroscopic changes in peritoneal fluid. Greatest diagnostic difficulties were encountered in cases of intestinal atonia, acute enteritis and torsion of the colon. In selected (severe) cases laboratory tests were obtained. Blood samples were examined for packed cell volume, hemoglobin, red and white blood cell counts, differential white blood cell count, blood gases and acid-base status, lactate, serum total protein and albumin, plasma sodium, potassium, chloride, calcium, magnesium, inorganic phosphorus, glucose, creatinine, BUN, total bilirubin, ASAT, CK, BASP and GGT. Peritoneal fluid was examined for red blood and white cell counts, total protein, specific gravity, pH and lactate, and enzymes as in blood. Laboratory results generally confirmed the clinical signs of shock, and packed cell volume and blood lactate were regarded to be of greatest prognostic interest. Although the performed laboratory information, macroscopic evaluation was thought to reveal sufficient information in most cases. It was concluded that supervening shock is of decisive importance in severe forms of colic, and that a careful and repeated evaluation of the circulatory insufficiency often provides one with a tentative prognosis although the final diagnosis is not obtained. In spite of therapy fatal outcome was found in all seriously shocked horses.

Some hemodynamic and hematologic effects of acute experimental lactic acidemia in 3 healthy cows are presented. Lactic acidemia was induced by intravenous infusion of a 10% solution of racemic lactic acid. The prominent features of the acidification of the blood were increases in carotid artery blood pressure and responses to intravenously injected norepinephrine, slight bradycardia and slight hyperventilation. Intravascular hemolysis with hemoglobinuria was a constant finding. Otherwise, no adverse effects of the acidemia were noted. These changes were paralleled by a progressive fall in arterial blood pH, base excess and PCO2 and increasing venous blood L (+)-lactate concentrations A reasonable explanation for the hemodynamic effects of the acidemia is peripheral vasoconstriction elicited by either stimulation of the sympathetic nervous system or increased sensitivity of vasoconstrictive receptors. The results are discussed with special reference to primary lactic acidosis encountered in grain engorgement in ruminants and to the secondary lactic acidosis of shock. These conditions are characterized by hemoconcentration and hypovolemia. Therefore, the results of this study of healthy normovolemic cows may not be valid in the severely dehydrated, hemoconcentrated and acidemic cow as hypotension is reported in the literature in connection with ruminal acidosis in sheep.

Two cases of male pseudohermaphroditism in the dog are described, including clinical, macroscopic, microscopic, karyotypic and therapeutic features. The external appearance of both dogs was that of an otherwise normal bilateral cryptorchid. Both dogs developed signs of male feminizing syndrome at 7 and 5 years of age respectively. This prompted exploratory laparotomy, disclosing an uterus, testes at the ovarian sites and Sertoli cell tumours. It is emphasized to include malformations of the genital apparatus in the differential diagnosis of canine urological and endocrine disease.

One-day-old chickens were fed ochratoxin A-contaminated diets at 2 levels: 0.3 and 1 mg ochratoxin A per kg feed, for 341 days. The only observable lesion to develop was a kidney damage comparable with the naturally occurring avian nephropathy. The changes in renal function were characterized by impairment of glomerular and tubular function, indicated by a decreased inulin clearance, TmPAH and decreased urine concentrating capacity. The changes of renal structure included degeneration of the tubular epithelium accompanied by regeneration. At slaughter, the kidneys, liver and muscular tissue of the birds contained residues of ochratoxin A (up to 50 mug per kg). As all the birds would have passed the meat inspection because no macroscopical lesions were present, this represents a possible health problem.

Experimental closed loop small intestinal volvulus was studied in the anesthetized horse. Volvulus was simulated by ligation of the mesenterial veins to a segment of small intestine. Physical signs and hemodynamic, hematologic, clinical chemical, bacteriologic and peritoneal fluid values were examined. Compared to conscious horses anesthesia highly delayed and modified the clinical signs of shock (changes in mucosal colour, dehydration, decreased skin temperature, elevated pulse rate, low blood pressures) and of small intestinal volvulus (altered peristalsis, gastric dilation). Plasma glucose response to shock was also modified by unconsciousness. However, a dose response relationship was indicated between the extent of small intestinal damage and clinical symptoms. The same was applicable to changes in blood pressures, blood acid-base balance, lactate, potassium, chloride, glucose, inorganic phosphorus, creatinine, creatine kinase, red blood cell and total white blood cell counts and serum total protein. The relationship was also indicated in the following peritoneal fluid values: volume, lactate, pH, total white cell counts, alkaline phosphatase and bacteriology. Changes related to shock (insufficient tissue perfusion) were low blood pressures and metabolic acidosis due to anaerobic glycolysis with accumulation of lactic acid. Also low plasma glucose and elevated plasma potassium, creatinine, inorganic phosphorus and creatine kinase were regarded as consequences of shock.