The magnitude of the increase in serum acute-phase proteins in dogs with parvoviral enteritis could be a useful indicator of the prognosis of the disease. In acute-phase proteins, C-reactive protein is a potent predictor of mortality in dogs with parvoviral enteritis.

Background Heart failure (HF) is associated with changes in inflammatory and oxidative stress biomarkers. This study aimed to evaluate the changes of a panel of inflammatory and oxidative stress biomarkers in dogs with different stages of HF and its relation with the severity of the disease and echocardiographic changes. A total of 29 dogs with HF as a result of myxomatous mitral valve degeneration or dilated cardiomyopathy were included and classified as stage-A (healthy), B (asymptomatic dogs), C (symptomatic dogs) and D (dogs with end-stage HF) according to the ACVIM staging system. In these dogs an ecnhocardiographic examination was performed and cytokines, and inflammatory and oxidative stress markers were evaluated in serum. Results KC-like was significantly increased in dogs of stage-C (P < 0.01) and -D (P < 0.05) compared with stage-A and -B. Stage-D dogs showed significantly higher serum CRP and Hp (P < 0.05) but lower serum antioxidant capacity (PON1, TEAC, CUPRAC, and thiol) compared to stage-A and -B (P < 0.05). After the treatment, serum levels of CRP, Hp and KC-like decreased and serum antioxidant levels increased compared to their pre-treatment values. Left ventricular dimension and LA/Ao ratio correlated positively with CRP, MCP-1, and KC-like but negatively with PON1, GM-CSF, IL-7 and antioxidant biomarkers (P < 0.01). Conclusion Our results showed that dogs with advanced HF show increases in positive acute-phase proteins and selected inflammatory cytokines such as KC-like, and decreases in antioxidant biomarkers, indicating that inflammation and oxidative stress act as collaborative partners in the pathogenesis of HF. Some of these biomarkers of inflammation and oxidative stress could have the potential to be biomarkers to monitor the severity of the disease and the effect of treatment.

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This study aimed to assess the influence of lobectomy and pneumonectomy on cardiac rhythm and on the dimensions and function of the right-side of the heart. Twelve dogs undergoing lobectomy and eight dogs undergoing pneumonectomy were evaluated preoperatively and one month postoperatively with electrocardiography and Doppler echocardiography at rest. Pulmonary artery systolic pressure (PASP) was estimated by the tricuspid regurgitation jet (TRJ) via the pulse wave Doppler velocity method. Systemic inflammatory response syndrome criteria (SIRS) were also evaluated based on the clinical and hematological findings in response to lobectomy and pneumonectomy. Following lobectomy and pneumonectomy, we predominantly detected atrial fibrillation and varying degrees of atrioventricular block (AVB). Dogs that died within seven days of the lobectomy (n = 2) or pneumonectomy (n = 1) had complete AVB. Preoperative right atrial, right ventricular, and pulmonary artery dimensions increased gradually during the 30 days (p<0.05) following pneumonectomy, but did not undergo significant changes during that same period after lobectomy. Mean PASP was 56.0 ± 4.5 mmHg in dogs having significant TRJ after pneumonectomy. Pneumonectomy, but not lobectomy, could lead to increases (p<0.01) in the SIRS score within the first day post-surgery. In brief, it is important to conduct pre- and postoperative cardiac evaluation of dogs undergoing lung resections because cardiac problems are a common postoperative complication after such surgeries. In particular, complete AVB should be considered a life-threatening complication after pneumonectomy and lobectomy. In addition, pneumonectomy appears to increase the likelihood of pulmonary hypertension development in dogs.

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Major increases of C-reactive protein concentrations in dogs with parvoviral enteritis are a marker of disease severity. In addition, higher values for anti-oxidants in severe cases compared with mild and moderate cases suggest a possible compensatory anti-oxidant mechanism.

Sepsis/endotoxemia causes platelet dysfunctions, abnormalities in coagulation and hemostatic mechanisms leading to organ dysfunctions and mortality. Choline prevents organ injury and improves survival during endotoxemia. The main objective of the present study was to determine the effects of choline or cytidine-5'-diphosphocholine (CDP-choline) on endotoxin-induced activation of coagulation and development of disseminated intravascular coagulation (DIC). Dogs were treated intravenously (i.v.) with saline, choline (20 mg/kg), or CDP-choline (70 mg/kg) three times with 4-h intervals starting 5 min before i.v. injection of endotoxin (1 mg/kg). Platelet counts and functions, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, coagulation factors, D-dimer and antithrombin (AT) were measured before and at 0.5-96 h after endotoxin. Circulating platelet, fibrinogen, coagulation factors and AT were decreased, whereas PT and aPTT were prolonged and serum D-dimer levels were elevated after endotoxin. Endotoxin-induced reductions in platelet counts and functions, fibrinogen, coagulation factors and AT were attenuated or blocked by choline or CDP-choline. Choline or CDP-choline blocked endotoxin-induced prolongation in PT and aPTT and enhancement in D-dimer. Elevated DIC scores were attenuated by choline and blocked by CDP-choline. Choline administration increased serum choline concentrations and caused bradycardia. Choline also increased choline and acetylcholine contents of circulating mononuclear cells and inhibited radioligand binding to their cholinergic receptors. These data show that choline administration, as choline chloride or CDP-choline, restores the abnormalities in the primary, secondary, and tertiary hemostasis and prevents the development of DIC during experimental endotoxemia in dogs probably by increasing both neuronal and non-neuronal cholinergic activity.