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One of the proposed mechanisms of ventilator-associated lung injury is cyclic recruitment of atelectasis. Collapse of dependent lung regions with every breath should lead to large oscillations in PaO2 as shunt varies throughout the respiratory cycle. We placed a fluorescence-quenching PO2 probe in the brachiocephalic artery of six anesthetized rabbits after saline lavage. Using pressure-controlled ventilation with oxygen, ventilator settings were varied in random order over three levels of positive end-expiratory pressure (PEEP), respiratory rate (RR), and plateau pressure minus PEEP (Delta). Dependence of the amplitude of PaO2 oscillations on PEEP, RR, and Delta was modeled by multiple linear regression. Before lavage, arterial PO2 oscillations varied from 3 to 22 mm Hg. After lavage, arterial PO2 oscillations varied from 5 to 439 mm Hg. Response surfaces showed markedly nonlinear dependence of amplitude on PEEP, RR, and Delta. The large PaO2 oscillations observed provide evidence for cyclic recruitment in this model of lung injury. The important effect of RR on the magnitude of PaO2 oscillations suggests that the static behavior of atelectasis cannot be accurately extrapolated to predict dynamic behavior at realistic breathing frequencies.

Macrophages are commonly cultured at a Po2of 149 Torr, but tissue macrophages in vivo live in an environment of much lower oxygen tension. Despite the many potential mechanisms for changes in oxygen tension to influence nitric oxide (NO) synthesis, there have been few reports investigating the effect of Po2on macrophage NO production. With the use of a culture chamber designed to rigorously control oxygen tension, we investigated the effects of culture Po2on macrophage NO production, inducible nitric oxide synthase (iNOS) activity, iNOS protein, and tumor necrosis factor production. NO production and iNOS activity were linearly related in the range of 39.4 to 677 Torr, but not in the range of 1.03 to 39.4 Torr. Therefore, results obtained in vitro for the high oxygen tensions commonly used in cell culture were quantitatively and qualitatively different from results obtained in cells cultured at the lower oxygen tensions that more accurately reflect the in vivo environment. The influence of oxygen tension on NO production has implications for cell culture methodology and for the relationship between microcirculatory dysfunction and inflammatory responses in rodent models of sepsis.

Objective—To document the clinical, clinicopathologic, and pathologic findings in cats with severe sepsis, identify abnormalities unique to this species, and identify criteria that could be used antemortem to diagnose the systemic inflammatory response syndrome in cats. Design—Retrospective study. Animals—29 cats confirmed to have severe sepsis at necropsy. Procedure—Pertinent history, physical examination findings, and results of hematologic and biochemical testing were extracted from medical records. Results—Clinical diagnoses included pyothorax, septic peritonitis, bacteremia secondary to gastrointestinal tract disease, pneumonia, endocarditis, pyelonephritis, osteomyelitis, pyometra, and bite wounds. Physical examination findings included lethargy, pale mucous membranes, poor pulse quality, tachypnea, hypo- or hyperthermia, signs of diffuse pain on abdominal palpation, bradycardia, and icterus. Clinicopathologic abnormalities included anemia, thrombocytopenia, band neutrophilia, hypoalbuminemia, low serum alkaline phosphatase activity, and hyperbilirubinemia. Necropsy findings included multiorgan necrosis or inflammation with intralesional bacteria. Conclusions and Clinical Relevance—Results suggest that severe sepsis in cats is characterized by lethargy, pale mucous membranes, signs of diffuse abdominal pain, tachypnea, bradycardia, weak pulses, anemia, hypoalbuminemia, hypothermia, and icterus. Recognition of this combination of clinical findings should facilitate the diagnosis of severe sepsis in cats. (J Am Vet Med Assoc 2000;217:531–535)

Objective—To determine whether dogs with naturally occurring canine parvoviral (CPV) enteritis have laboratory evidence of hypercoagulability. Design—Case-control study. Animals—9 dogs with naturally occurring CPV enteritis and 9 age-matched control dogs. Procedure—Blood was collected from all dogs within 24 hours of admission for thromboelastography (TEG) and determination of activated partial thromboplastin time (aPTT), prothrombin time (PT), antithrombin III (AT) activity, and fibrinogen concentration. Fibrin-fibrinogen degradation product (FDP) concentration, Ddimer concentration, and platelet count were obtained in dogs with CPV enteritis only. Records were reviewed for evidence of thrombosis or phlebitis. Results—All 9 dogs with CPV enteritis had evidence of hypercoagulability, determined on the basis of significantly increased TEG maximum amplitude and decreased AT activity. Fibrinogen concentration was significantly higher in dogs with CPV enteritis than in control dogs. The aPTT was moderately prolonged in dogs with CPV enteritis, and FDP concentration was < 5 mg/ml in 7 of 9 dogs. No dogs had a measurable D-dimer concentration. Platelet counts were within reference range. Four of 9 dogs had clinical evidence of venous thrombosis or phlebitis associated with catheters. One dog had multifocal splenic thrombosis identified at necropsy. Conclusions and Clinical Relevance—Dogs with CPV enteritis have a high prevalence of clinical thrombosis or phlebitis and laboratory evidence of hypercoagulability without disseminated intravascular coagulopathy. Thromboelastography may help identify hypercoagulable states in dogs. (J Am Vet Med Assoc 2000;217:1500–1504)

Supernatants from feline peritoneal exudate cells (PECs) exposed to lipopolysaccharde (LPS) produced significantly (P0.05) more tumor necrosis factor (TNF) activity than supernatants from cells exposed to media. An in vitro LPS response was obtained following incubation of whole blood with 10 micrograms ml-1 LPS for 2 h. Intravenous infusion of LPS (750 micrograms kg-1 rapidly increased plasma TNF activity to a maximum at 60 min after initiation of LPS infusion. By 180 min, TNF activity returned to baseline. Cats produce TNF in response to LPS in a manner similar to other species. Measurement of TNF activity in plasma or in LPS-stimulated whole blood are methods to further characterize the inflammatory response in feline diseases.

In response to the terrorist attacks of September 11, 2001, at the World Trade Center and Pentagon, almost 50,000 rescue workers and approximately 300 search and rescue dogs participated in rescue and recovery operations. The dogs were exposed to the same hazards as the human workers, but did not have any of the personal protective gear. This prospective double cohort observational study compared annual medical history, blood biochemical and hematologic results, and thoracic radiographic findings in 95 search and rescue dogs that responded to the terrorist attacks at the World Trade Center or the Pentagon on September 11, 2001, to a control group of 55 search and rescue dogs that were not involved in the 9/11 response. Compared to controls, the deployed search dogs demonstrated mild changes in blood work and a higher incidence of radiographic cardiac abnormalities. Species differences may explain the lack of pulmonary findings in the dogs. These dogs may provide early evidence of nonpulmonary complications of the 9/11 response. Continued surveillance of all responders is warranted.

a b s t r a c t The effect of animal-assisted activities (AAA) on the animal participants has been mini- mally investigated, and the welfare of these animals has been questioned. To enhance our understanding of these animals' welfare, we measured cortisol collected from serial saliva samples of 15 healthy adult dogs registered with an AAA organization. We collected saliva every 30 min before, during, and after a standardized 60-min session across three sett- ings: an AAA session (activity) for college students in the communal area of a residence hall, a novel session located in a novel room without interaction with a stranger, and a home session inside each handler's own home. Each session was videotaped, and specific behaviors during 5-min petting interactions were coded. Salivary cortisol levels were sig- nificantly higher in the novel setting (0.397 g/dL) compared to activity (0.257 g/dL) and home (0.213 g/dL) settings at time 30 min (P = 0.01 and P = 0.03, respectively). Dogs exhib- ited significantly more standing (59% vs 0%, P = 0.008) and ambulating (5.6% vs 0%, P = 0.001) behavior in the activity setting compared to the home at time 30 min, as well. Salivary corti- sol level was negatively correlated with panting (P = 0.02) and standing (P = 0.02) at specific time points in the novel and activity settings, respectively. During the 60-min AAA session, salivary cortisol concentration and stress-associated behavior were not statistically differ- ent compared to when dogs spent the same amount of time in the home setting, suggesting that they were not distressed when participating in the AAA sessions. The predictability of the environment may be an important consideration when evaluating the effect of AAA on