Pathophysiologic mechanism of cardiac dysfunction in experimentally induced heartworm caval syndrome in dogs: an echocardiographic study

In dogs with experimentally induced heartworm infection, the onset of caval syndrome (CS) was characterized by a murmur, loudest over the tricuspid valve, and a large worm mass in the right ventricular lumen detectable during diastole by use of M-mode echocardiography. Two-dimensional echocardiography indicated that the worm mass was located in the right atrium and venae cavae and was "flowing" into the right ventricle during rapid diastolic filling. Paradoxical septal motion and vigorous right ventricular cranial wall motion also were observed. Other echocardiographic changes included decreased size of the left atrium and ventricle, aortic root, and ratio of left-to-right ventricular diastolic luminal diameter, compared with values obtained 6 months after experimentally induced heartworm infection. Right ventricular end diastolic diameter increased considerably. Most echocardiographic indices of left ventricular function (fractional shortening, velocity of circumferential fiber shortening, ejection fraction, and preejection period) were not altered appreciably, but estimates of cardiac index and stroke volume were markedly decreased. Electrocardiography revealed ventricular and supraventricular premature complexes in 7 of the 8 dogs studied, evidence of right ventricular enlargement in 6 of the 8 dogs studied, and increased mean heart rate, compared with that measured 6 months after inoculation of infective larvae, before the onset of CS. Cardiac catheterization was performed in 3 days at the onset of CS. Severe pulmonary arterial and right ventricular hypertension and decreased cardiac index (compared with values obtained before inoculation) were observed. Evidence of right ventricular inflow obstruction was not detected. Mean aortic blood pressure decreased with the onset of CS, but right ventricular end diastolic pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)     

Performance,milk fatty acid composition and behaviour of high-yielding Holstein dairy cows given a limited grazing period

The effects of a limited grazing period on the performance, behaviour and milk composition of high-yielding dairy cows were examined. A total of 56 Holstein cows yielding 44.7 ± 0.42 kg/day were allocated to one of four treatments in one of two, 4-week periods. Treatments were as follows: control (C)—cows housed and offered TMR ad libitum; early grazing (EG)—cows grazed for 6 hr after morning milking then housed; delayed grazing (DG)—cows returned to housing for 1 hr after morning milking followed by grazing for 6 hr, then housed; restricted TMR (RT)—cows grazed for 6 hr after morning milking, then housed and fed TMR at 75% of ad libitum. Intake of TMR was highest in cows receiving C, intermediate in EG and DG, and lowest in RT at 26.9, 23.6, 24.7 and 20.3 kg DM/day respectively. Pasture intake was similar in cows receiving EG or DG, but was higher in RT at 2.4, 2.0 and 3.5 kg DM/day respectively. Milk yield was similar between cows receiving C, EG or DG, but lowest in RT at 45.7, 44.2, 44.9 and 41.7 kg/cow, respectively, while milk fat content of C18:3 n-3 was increased by grazing. Cows in C spent more than 55 min/day longer lying and had three additional lying bouts/day, while lying bouts were shorter than for cows receiving EG, RT or DG. It is concluded that high-yielding cows can be grazed for 6 hr/day with little impact on performance, provided TMR is available ad libitum when housed.     

Cardiovascular effects of acute pulmonary obstruction in horses with recurrent airway obstruction

BACKGROUND: Recurrent airway obstruction (RAO) is common in horses. Although pulmonary artery (PA) pressure increases during RAO, cardiac function in horses with RAO has received limited attention. HYPOTHESIS: The purpose of this study was to noninvasively determine the cardiovascular effects of acute pulmonary obstruction (APO) in horses with RAO and their reversibility. ANIMALS: Five geldings with RAO, inducible by exposure to moldy hay, were studied. METHODS: Pulmonary mechanics, echocardiography, serum troponin I concentrations, arterial blood gases, and hematocrit were obtained before and after 7 days of APO. Heart rate, PA diameter and flow characteristics, right and left ventricular luminal dimensions and wall thicknesses, global cardiac performance, and evidence of myocardial damage were evaluated. Pulmonary mechanics and echocardiography were reevaluated during remission. RRESULTS: Severe, transient APO did not induce chronic cor pulmonale in horses, because cardiac anatomy and function were normal between episodes. An acute episode of APO produced anatomical and functional cardiac changes in both the right and left heart (including increased PA diameter, abnormal septal motion, and decreased left ventricular diameter and estimated stroke volume), possibly because of the development of pulmonary hypertension, without apparent myocardial damage. The decrease in stroke volume was offset by the increase in heart rate. CONCLUSIONS AND CLINICAL IMPORTANCE: With APO of 7 days' duration, cardiovascular abnormalities and the functional airway changes that produce them are reversible when the offending allergens are removed.     

Plasma lipopolysaccharide elevations in cattle associated with early-stage infection by Fasciola hepatica

Fasciolosis is an endemic zoonotic parasitic disease with significant impacts on human health and both animal health and production. Early post-infection impacts on the host remain unclear. The objective of this study was to determine the changes, if any, to levels of endotoxin in cattle plasma in response to early-stage infection with Fasciola hepatica. Thirty-six (36) commercial bred cattle were experimentally infected with approximately 400 viable metacercariae. Plasma lipopolysaccharide (endotoxin) levels were examined on 24 occasions from 0 h before infection to 336 h after infection using the Limulus Amoebocyte Lysate chromogenic end point assay and compared with that of six (6) uninfected control animals. Peak lipopolysaccharide levels in infected animals were reached at 52 h after infection and returned to pre-infection levels at time 144 h after infection. Infected animals had significantly elevated lipopolysaccharide levels between 24 and 120 h after infection when compared to uninfected animals. The mean change in endotoxin units (EU)/mL over time after infection was statistically significant in infected animals. Elevations of lipopolysaccharide occurred in all infected animals suggesting a possible repeatable and titratable endotoxemia conducive to therapeutic agent model development.     

Use of echocardiography for the diagnosis of heartworm disease in cats: 43 cases (1985-1997)

OBJECTIVE: To determine the usefulness of echocardiography in the diagnosis of heartworm disease in cats and to compare this modality with other tests. DESIGN: Retrospective study. ANIMALS: 43 cats with heartworm infection that had echocardiographic examinations at 2 veterinary teaching hospitals between 1985 and 1997. Twenty-two of these 43 cats also underwent radiography of the thorax and heartworm antibody and heartworm antigen testing. PROCEDURE: Cats were determined to be infected with Dirofilaria immitis infection on the basis of 1 or more of the following findings: positive modified Knott or antigen test result, echocardiographic evidence of heartworm disease, or confirmation of the disease on postmortem examination. The percentage of echocardiographs in which heartworms were evident was compared with the percentage of radiographs in which pulmonary artery enlargement was evident and results of antigen or antibody tests in cats in which all tests were performed. RESULTS: Overall, heartworms were detectable by use of echocardiography in 17 of 43 cats, most often in the pulmonary arteries. In the 22 cats in which all tests were performed, antibody test results were positive in 18, antigen test results were positive in 12, and pulmonary artery enlargement was evident radiographically and heartworms were identifiable echocardiographically in 14. Heartworm infection was diagnosed exclusively by use of echocardiography in 5 cats in which the antigen test result was negative. CONCLUSIONS AND CLINICAL RELEVANCE: Although echocardiography was less sensitive than antigen testing, it was a useful adjunctive test in cats that had negative antigen test results in which there was a suspicion of heartworm disease. The pulmonary arteries should be evaluated carefully to increase the likelihood of detection of heartworms echocardiographically.     

Percutaneous balloon pericardiotomy as a treatment for recurrent pericardial effusion in 6 dogs

Percutaneous balloon pericardiotomy (PBP) has been performed in people and in a small number of dogs as a treatment for recurrent pericardial effusion with tamponade (PET). We performed this technique on 6 dogs with recurrent PET (5 with heart base tumors and 1 with no identifiable mass). Under general anesthesia and fluoroscopic guidance, a balloon-dilating catheter (diameters 14-20 mm) was introduced percutaneously at the 5th intercostal space through a sheath-introducing catheter, positioned across the parietal pericardium, and inflated 3 times. No dog experienced serious complications. The procedure was considered successful in 4 of 6 dogs. One dog is still alive without recurrence of PET 1 year after the procedure. Three dogs died of unrelated disease without recurrence of PET 5. 19, and 32 months after the procedure. The procedure was not beneficial in 1 dog that was euthanized 9 weeks later because of recurrence of pleural and abdominal effusion thought to be secondary to PET. One dog may have temporarily benefited but developed symptomatic PET 6 months after PBP. PBP appears to be a safe, economical, and potentially effective palliative treatment for recurrent PET and is a reasonable, less invasive alternative to surgery for dogs with recurrent PET, especially effusions caused by heart base tumors and possibly idiopathic pericardial effusion. Premature closure of the stoma is a potential cause for long-term failure and was thought to have been responsible for the recurrence of clinical signs in 2 dogs.     

Bluetongue virus serotypes 1 and 3 infection in Poll Dorset sheep

Objective To study the clinical signs following bluetongue virus serotypes 1 and 3 infection in Poll Dorset sheep.
Design A clinical and pathological study.
Procedure Twenty Poll Dorset sheep were inoculated with bluetongue virus serotypes 1 or 3, each inoculum having a different passage history. The sheep were examined daily and their clinical appearance and rectal temperatures recorded. Heparinised and non-heparinised blood samples were taken at intervals for virological and serological study. Gross pathological findings were recorded for several sheep at necropsy and tissue samples were collected from three sheep for virological studies.
Results All inoculated sheep developed clinical disease. The clinical signs and gross pathological changes varied considerably but were consistent with damage to the vascular endothelial system. There was a decline in the titres of infectious bluetongue virus and of antigen in tissues collected between 7 and 12 days after infection.
Conclusions The severity of disease was related to the speed of onset and duration of pyrexia and not the development or titre of viraemia. Generally, those animals with sensitive mouths, depression, coronitis, recumbency and reluctance to move were the most debilitated. Whole blood was the most reliable source of infectious virus from acutely and chronically infected and convalescent animals. However, tissue samples particularly spleen, collected from dead or killed animals suffering from either peracute or acute forms of disease were most appropriate for the rapid confirmation of a clinical diagnosis.     

Aldosterone breakthrough with benazepril in furosemide‐activated renin‐angiotensin‐aldosterone system in normal dogs

Pilot studies in our laboratory revealed that furosemide‐induced renin‐angiotensin‐aldosterone system (RAAS) activation was not attenuated by the subsequent co‐administration of benazepril. This study was designed to evaluate the effect of benazepril on angiotensin‐converting enzyme (ACE) activity and furosemide‐induced circulating RAAS activation. Our hypothesis was that benazepril suppression of ACE activity would not suppress furosemide‐induced circulating RAAS activation, indicated by urinary aldosterone concentration. Ten healthy hound dogs were used in this study. The effect of furosemide (2 mg/kg p.o., q12h; Group F; n = 5) and furosemide plus benazepril (1 mg/kg p.o., q24h; Group FB; n = 5) on circulating RAAS was determined by plasma ACE activity, 4–6 h posttreatment, and urinary aldosterone to creatinine ratio (UAldo:C) on days ?1, ?2, 1, 3, and 7. There was a significant increase in the average UAldo:C (μg/g) after the administration of furosemide (Group F baseline [average of days ?1 and ?2] UAldo:C = 0.41, SD 0.15; day 1 UAldo:C = 1.1, SD 0.56; day 3 UAldo:C = 0.85, SD 0.50; day 7 UAldo:C = 1.1, SD 0.80, P < 0.05). Benazepril suppressed ACE activity (U/L) in Group FB (Group FB baseline ACE = 16.4, SD 4.2; day 1 ACE = 3.5, SD 1.4; day 3 ACE = 1.6, SD 1.3; day 7 ACE = 1.4, SD 1.4, P < 0.05) but did not significantly reduce aldosterone excretion (Group FB baseline UAldo:C = 0.35, SD 0.16; day 1 UAldo:C = 0.79, SD 0.39; day 3 UAldo:C 0.92, SD 0.48, day 7 UAldo:C = 0.99, SD 0.48, P < 0.05). Benazepril decreased plasma ACE activity but did not prevent furosemide‐induced RAAS activation, indicating aldosterone breakthrough (escape). This is particularly noteworthy in that breakthrough is observed at the time of initiation of RAAS suppression, as opposed to developing after months of therapy.