Atrial natriuretic peptide in the dog with mitral regurgitation.

The concentration and molecular form of the plasma atrial natriuretic peptide (ANP) in dogs with mitral regurgitation was investigated. Plasma ANP concentration in dogs with mitral regurgitation was significantly increased (29.4 +/- 1.88 pmol litre-1, n = 40) compared to that in the controls (14.5 +/- 0.62 pmol litre-1, n = 20, P less than 0.01). Molecular forms of plasma ANP were determined by the gel permeation chromatogram. A single peak corresponding to alpha-ANP was detected in the plasma from the controls. However, a peak corresponding to beta-ANP and, or, gamma-ANP was detected in the plasma of the dogs with mitral regurgitation in addition to alpha-ANP. These results suggest that the process of ANP synthesis was altered and excretion of ANP from the heart was enhanced in dogs with mitral regurgitation.     

Bilateral thyrohyoideus muscle rupture in a dog

A whippet was referred to our hospital, for further assessment and treatment, two days after receiving bite wound to the neck. Physical examination and radiographs revealed caudal displacement of the larynx. At surgery, bilateral rupture of the thyrohyoideus muscle was discovered and repaired, returning the larynx to its normal position. The dog was discharged after 10 days and has only mild residual symptoms.     

Acute hemodynamic effects of hydralazine in dogs with chronic mitral regurgitation

The hemodynamic response to hydralazine administration was evaluated in 6 conscious small dogs with chronic mitral regurgitation. All dogs underwent invasive and noninvasive hemodynamic monitoring before and after hydralazine administration. Cardiac output and pulmonary capillary wedge pressure were measured with a Swan-Ganz thermodilution catheter. Systemic arterial blood pressure (AP) was measured directly by inserting a needle into the femoral artery. Standard M-mode echocardiograms and thoracic radiographs were obtained. Other hemodynamic variables were calculated. Base-line hemodynamic variables were altered severely in all dogs. Hydralazine decreased mean arterial blood pressure from 104 +/- 18 (mean +/- SD) to 78 +/- 12 mm of Hg (P less than 0.005), total systemic resistance index from 2,946 +/- 625 to 1,261 +/- 420 dynes-s-cm-5m2 (P less than 0.005), and pulmonary capillary wedge pressure from 40 +/- 5 to 26 +/- 3 mm of Hg, (P less than 0.005). Cardiac index increased from 2.92 +/- 0.72 to 5.36 +/- 1.67 L/min/m2 of body surface area (P less than 0.005). Mixed venous oxygen tension (PvO2) increased from 28.4 +/- 4.3 to 41.2 +/- 5.2 mm of Hg (P less than 0.001). Pulmonary edema resolved, as determined on thoracic radiographs. Mixed venous oxygen tension correlated well with the cardiac index (r = 0.92; P less than 0.001). It was concluded that hydralazine administration caused a small decrease in end diastolic diameter (4.8 +/- 0.9 to 4.5 +/- 0.8 cm, P less than 0.05) and end systolic diameter (2.6 +/- 0.8 to 2.3 +/- 0.7 cm, P less than 0.05). Fractional shortening and heart rate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute aortic rupture in a dog with spirocercosis following the administration of medetomidine

Spirocercosis is an emerging disease in veterinary medicine. A strong suspicion of spirocercosis is usually evident after a thorough clinical examination and radiography of the chest has been performed. Lesions seen on radiography include an oesophageal mass, spondylitis and oesophageal air. Unfortunately, radiography is not diagnostic and additional diagnostic procedures are required to confirm the diagnosis. Endoscopy is commonly performed to diagnose the condition. The dog presented in this study had radiographic and clinical signs consistent with spirocercosis and definitive diagnosis was required. Shortly after sedation with medetomidine, the dog went into cardiac arrest and failed to respond to resuscitative measures. On post mortem, the diagnosis of spirocercosis was confirmed and the cause of death was identified as acute aortic rupture. Aortic aneurysms are not an uncommon finding and cause of acute death in dogs with spirocercosis. The acute rupture of the aorta in this case is most probably the result of cardiovascular changes associated with the administration of medetomidine. Medetomidine causes an acute rise in systemic vascular resistance with hypertension. The increase in shear stress across the weakened aortic wall resulted in rupture. Caution with the use of medetomidine in patients with spirocercosis is advised.     

Acute gaseous peritonitis after rupture of a retroperitoneal rectal diverticulum in a dog

An 11-year-old, entire male coton de tulear was presented on emergency with acute and severe depression, acute abdominal pain and vomiting of 24 hours duration. Historical complaints included right perineal swelling, dyschezia and tenesmus of 18 months duration. Abdominal ultrasonography and radiography suggested a pneumoperitoneum and positive-contrast colonography showed leakage of contrast medium into the caudal abdomen and the presence of a large retroperitoneal pouch. Exploratory laparotomy allowed the visualisation of faecal leakage from the retroperitoneal space into the peritoneal cavity. Using a perineal approach, a large necrotised rectal diverticulum filled with faeces was found over the retroperitoneal structures. A standard herniorrhaphy was then performed. The dog recovered uneventfully and dyschezia did not recur at the nine month follow-up. Rectal diverticulum rupture associated with peritonitis has not been described in the veterinary literature, to the authors' knowledge, and should be considered as a rare differential diagnosis in dogs being presented with gaseous peritonitis.     

Tracheal rupture in a dog

A two-year-old male Retriever-crossbred dog was presented with progressive subcutaneous emphysema and pronounced dyspnoea following a cervical impact injury sustained ten days previously. Radiography revealed an almost complete transection of the cervical trachea and an associated pneumomediastinum and unilateral pneumothorax. The damaged tracheal segment was resected and anastomosis performed following drainage of the pneumothorax. The dog made an uneventful recovery with no evidence of stenosis detectable at the site of the repair six months post-operatively.     

Pulmonary function in dogs with mitral valve regurgitation

Mitral valve regurgitation was created in 2 groups of dogs. Groups were selected on absence (group 1) or presence (group 2) of clinical signs of congestive left ventricular failure. Group-2 dogs, in which mean left atrial pressures were greater than 30 mm of Hg, had increases in heart rate, pulmonary arterial mean pressure, left atrial diameter, and left ventricular diastolic diameter. These changes were associated with decreased arterial O2 tension, decreased static and dynamic compliance, reduced lung volumes, and increased pulmonary resistance. Group-1 dogs, in which mean left atrial pressure was less than 30 mm of Hg, had moderate changes in hemodynamics, but no changes in pulmonary function, except during exercise when arterial O2 tension decreased.     

Platelet aggregation in dogs with mitral valve regurgitation

OBJECTIVE: To compare platelet aggregation in healthy dogs and dogs with mitral valve regurgitation (MVR) to determine whether regurgitation had an effect on platelet function. ANIMALS: 32 dogs with MVR and 43 healthy dogs. PROCEDURE: Platelet aggregation was measured with an aggregometer, using adenosine 5'-diphosphate as the aggregating agent, and the maximum aggregation and the enhancement of platelet sensitivity (EPS) values were calculated. RESULTS: Platelet count and maximum aggregation were not significantly different between healthy dogs and dogs with MVR. However, EPS values in dogs with MVR were significantly higher than values in healthy dogs. Platelet count and maximum aggregation were not significantly different between dogs classified as New York Heart Association functional class I or II and dogs classified as functional class III or IV; however, EPS values were significantly higher in dogs classified as functional class III or IV. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that platelet aggregation is decreased in dogs with MVR and that the EPS value may be more sensitive to differences in disease severity than in measurement of maximum aggregation.     

Pharmacokinetics of nicorandil in dogs with mild mitral regurgitation

The aim of this study was to examine the pharmacokinetics of nicorandil, a hybrid of an adenosine triphosphate-sensitive potassium channel opener and a nitrate, and to estimate its clinical doses in dogs with mild mitral valve regurgitation (MR). Nicorandil (0.1, 0.3, and 1.0 mg/kg) was administered orally to normal dogs and those with experimentally-induced MR, and its plasma concentrations were analyzed using high-performance liquid chromatography. Plasma concentrations increased dose-dependently after the administration of nicorandil, and were not different between normal dogs and those with MR. Similar to the effective plasma values obtained in cardiac disease in humans, the findings of this pharmacokinetic study may indicate that a dose of 0.3-1.0 mg/kg has the same effectiveness in dogs with cardiac dysfunction.     

Plasma digoxin concentration in dogs with mitral regurgitation.

Fifteen and eight mature beagles, without (normal group) and with experimental mitral regurgitation (MR group), respectively, were given 0.02 mg/kg/day digoxin powder for 10 days orally. The optimum time for sample collection after administration of digoxin was observed to be 8-18 hr and 10-22 hr in the normal and MR groups, respectively. In both groups, a stable concentration was reached after 3-5 days of treatment. No differences in plasma level were observed between sexes. The optimum concentration of digoxin was attained at an earlier stage than has been previously reported for both dogs and humans.     

Surgical correction of ventricular septal defect with aortic regurgitation in a dog

An 8-month-old entire Miniature Dachshund, weighing 4.2 kg, was presented for examination following delvelopment of a cough. Ventricular septal defect had been diagnosed tentatively in its infancy on the basis of a cardiac murmur detected by auscultation and echocardiography. Echocardiography using a B mode right parasternal long-axis view showed a defect at the atrioventricular junction and a thickened cusp of the aortic valve prolapsing into the defect. Colour-flow Doppler showed shunt blood flow across the defect at the level of the atrioventricular junction, from left to right. The sinus of Valsalva was dilated, with turbulent blood flow. Aortic regurgitation was also observed. Cardiac catheterisation studies confirmed the diagnosis of a supracristal ventricular septal defect with aortic regurgitation. Despite medication with digoxin, enalapril and aminophylin, started from the first admission, left ventricular internal dimensions gradually increased, and fractional shortening of the left ventricle gradually decreased. Surgery, with the aid of extracorporeal circulation, to close the ventricular septal defect, was performed 1 year after the initial examination. The aortic valve was left untreated. Postoperatively, the systolic murmur disappeared. Shunt flow from the left to the right ventricle was no longer observed on echocardiography, however there was still a small amount of aortic regurgitation during diastole visualised with colour-flow Doppler echocardiography. The prolapse of the cusp of the aortic valve on B-mode echocardiography was no longer observed and thickening of the cusp had not progressed. Left ventricular function measurement using M mode echocardiography showed a reduced left ventricular volume overload with reduced left ventricular internal dimensions and increased fractional shortening. The cough was relieved and no follow-up medication was scheduled. Early surgical closure of the ventricular septal defect improved the patient's condition and controlled prolapse and thickening of the aortic valve.     

Aortic regurgitation in the dog.

In a review of aortic regurgitation in 12 dogs, breed or sex predilection was not found. Clinical signs included decreased exercise tolerance and diastolic murmur. Associated anomalies included ventricular septal defect and aortic stenosis. It was concluded that when aortic regurgitation develops secondary to a ventricular septal defect, the prognosis should be grave.     

Increased pulmonary transit times in asymptomatic dogs with mitral regurgitation

Pulmonary transit time (PTT) normalized to heart rate (nPTT) is a measure of the pulmonary blood volume (PBV) to stroke volume ratio (PBV/SV). It is an index of cardiac performance. To determine the effect of compensated mitral regurgitation (CMR) and decompensated mitral regurgitation (DMR) caused by valvular endocardiosis on the index nPTT, we measured nPTT by first-pass radionuclide angiocardiography and ECG in 13 normal dogs, 18 dogs with CMR, and 13 dogs with DMR. PTT was measured as time between onset of appearance of activity at the pulmonary trunk and the left atrium. In the normal dogs, the relationship between PTT and mean R-R interval (mRR) was PTT = 4.08 x mRR + 0.15 (R2 = 0.71). Normal nPTT was 4.4 +/- 0.6 (SD) (range. 3.6-5.3). in CMR, 6.3 +/- 1.6 (SD) (range, 4.0-9.7). and in DMR, 11.9 +/- 3.4 (SD) (range, 8.0-18.8). The differences among all groups were significant. Heart rates were 110 +/- 22 bpm in normal dogs, 111 +/- 20 in dogs with CMR, and 144 +/- 18 in dogs with DMR (P < .001 for difference between DMR group and normal and CMR groups). Increased nPTT in CMR indicates preclinical heart pump dysfunction. Heart rate-normalized pulmonary transit times may be a useful index of heart function in mitral regurgitation.     

Gall bladder torsion and rupture in a dog

A 6-year-old desexed female German Shepherd dog was referred to the Murdoch University Veterinary Hospital for assessment and management of acute onset vomiting, diarrhoea, polydipsia and lethargy of 2 days duration. Surgical, microbiological and histological findings were consistent with necrotising cholecystitis secondary to gall bladder torsion, resulting in gall bladder rupture and secondary non-septic bile peritonitis. A chronic peritoneopleural perforation resulting from an abdominal cavity foreign body and congenital peritoneopericardial hernia were also present. The dog made a full recovery following cholecystectomy, foreign body removal, repair of the peritoneopleural perforation and peritoneopericardial herniorrhaphy. This is the first recorded case of gall bladder torsion in the dog.     

Acute paraplegia associated with vasculitis in a dog with leishmaniasis

A 14-month-old female crossbreed dog with leishmaniasis, receiving allopurinol, was presented with acute paraplegia. A diagnosis of renal failure with pelvic limb lower motor neuron signs was made and the dog was euthanased. Histopathological examination demonstrated leukocytoclastic vasculitis in multiple organs. Malacia and haemorrhage affecting the spinal cord was associated with multiple foci of vasculitis within the nervous tissue. Rupture and thrombosis of inflamed vessels caused haemorrhage in the spinal cord and subsequent paralysis.     

Acute hepatopathy associated with mitotane administration in a dog

An adult dog with a persistent elevation in alkaline phosphatase enzyme activity was started on mitotane for suspected hyperadrenocorticism. One month later, the dog was presented for intermittent anorexia and acute icterus. The dog's liver enzyme activities and total bilirubin were markedly elevated, prothrombin time was prolonged, and blood urea nitrogen and glucose were low. Histopathology revealed marked, centrilobular, hepatocellular loss. After discontinuation of the mitotane, the dog recovered with supportive care and was normal 3 months later, which was consistent with mitotane-associated hepatic failure.