This study reports the effects of a one-time dosage of candesartan cilexetil (TCV-116), an angiotensin II receptor antagonist, on hemodynamics in experimental model dogs with mitral insufficiency. The 21 experimental dogs were administered 5 mg/kg or 10 mg/kg of TCV-116 or a placebo in the duodenum under generai anesthesia, and hemodynamic changes were observed for 12 hours . The systemic vascular resistance and arterial blood pressure began decreasing markedly just after administration of the medicine, and the effects lasted throughout the period of testing in the two different dosage experiments. Transient degradation of the heart rate, degradation of the average pulmonary arterial pressure, and transient degradation of the right ventricle pressure at contraction phase were also seen in the two dosage experiments. Cardiac output and stroke volume increased significantly in the 5 mg/kg dosage experiment. On the other hand, the cardiac output did not increase although the stroke volume slightly increased temporarily in the 10 mg/kg dosage experiment. In other words, this medicine was effective, because of its lasting vasodilatory effect, in reducing pressure overload in the cardiovascular system and in increasing cardiac output in experimental model dogs with mitrai insufficiency. The results suggested that this medicine could be useful for treating chronic cardiac failure and mitral insufficiency in dogs as well as a conventional medicine, such as an angiotensin converting enzyme (ACE) inhibitor.

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A three-year old male domestic cat was referred with paresis in pelvic limbs. In the physical examination, conscious proprioception in the left pelvic limb was diminished, and paralysis of the tail was observed. There were tumors in the anterior chamber of the eyes. These tumors were diagnosed as lymphoma by histopathology on specimens of needle aspiration. The patient cat was FeLV negative, FIPV negative, and FIV positive. Polypharmacal chemotherapy was performed on the cat. The ocular tumors disappeared after 6 days of treatment and the neurologic deficits disappeared after 20 days of treatment. Over 1 year has passed since the first presentation, and the cat remains completely normal.

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A two-year-old male cat with acute neurological symptoms of unknown cause, such as paralysis of the four limbs, was examined by magnetic resonance imaging (MRI), and treated with medicine successfully. The MRI scan showed abnormal findings including high density on T2-weighted and flare images in areas ranging from the right midbrain to the left brainstem and from the left cerebrum to the cerebellum. These findings indicated the presence of extensive cerebral edema. Taking into consideration the cat's medical history and the acuteness of its clinical signs, other possible diseases were excluded, and a tentative diagnosis of feline ischemic encephalopathy was made. Treatment with glycerin and a corticosteroid improved the clinical problems, and the cat appeared normal by day 8. There was no recurrence until the cat was killed in a car accident one year later.

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Effects of long-term treatment of β-blocker for chronic heart failure in dogs with mitral regurgitation (MR) remain unclear. The effects of long-term β-blocker therapy was evaluated in a 11-year old male Maltese dog with severe MR. The dog showed paroxysmal coughing on the first admission and his clinical status was graded as New York Heart Association (NYHA) functional class III. The dog did not demonstrate a sufficient improvement in spite of medical therapy using digitalis, diuretic and nitrate. Thus, oral administration of β-blocker metoprolol was started with a dose of 0.5 mg/kg daily and the dose was increased gradually every two week until 2.5 mg/kg daily. During ten months after the initiation, the clinical status was improved to NYHA class I or class II. Metoprolol decreased the elevated heart rate and accelerated left ventricular fractional shortening to normal ranges, and also improved impaired diastolic function. Morphologically, metoprolol did not attenuate left ventricular cavity dilatation but rather increased left ventricular wall thickness, which resulted in to a greater extent of volume-overload induced eccentric hypertrophy. The dog, however, died due to pulmonary edema 13 months after the initiation. Marked fibrotic lesions of the myocardium were not observed by histologic examination. From this case, it is suggested that β-blocker therapy has beneficial effects on the progression of heart failure in dogs with MR.

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We report here the successful treatment of portosystemic shunt in a six-month-old papillon dog. The shunt was first ligated partially, and eight months later it was ligated completely. During the eight months, the animal was treated with lactulose, metronidzol, ursodexycholate, and glutathione. Just before the second litigation, X-rays showed the liver to have grown by about 10%, but biochemical values such as NH₃ and totai bile acid (TBA) were still abnormal. Serum biochemical abnormalities improved after the complete litigation. These findings suggested that there is not necessarily a correlation between hepatic growth and blood values such as alamine aminotransferase, NH₃, and TBA, which are usually considered to be indices of liver function.

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A four-month-old female Siberian Husky weighing 13 kg was referred to the Animal Clinical Research Foundation Hospital with a suspicion of congenital heart problem. The suspicion was based on the presence of heart murmur identified during a physical checkup prior to vaccination at the referring hospital. The dog was diagnosed by echocardiography and cardiac catheterization as having membranous ventricular septal defect (VSD) and subaortic stenosis. But the condition of the dog was not so serious, and surgical treatment was judged to be unnecessary. Instead, periodical checkups were done until the dog died at the age of ten years. During this time no medication was given. No significant change in the heart condition was noted morphologically or functionally on echocardiographs or radiographs until the dog received a checkup at the age of nine years, when the shunt flow caused by the VSD was no longer seen on echocardiograms. Necropsy showed that a cyst developed partially from the fibrous ridge at the left ventricular outflow tract blocking the VSD, and resulting in the disappearance of the shunt flow of the VSD.

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