Vasotop 1.25 mg tablets: beige oblong flavoured tablets half scored on both sides. Each tablet contains 1.25 mg ramipril.
Vasotop 2.5 mg tablets: yellow oblong flavoured tablets half scored on both sides. Each tablet contains 2.5 mg ramipril and 0.5 mg yellow ferric oxide (E 172).
Vasotop 5 mg tablets: light pink oblong flavoured tablets half scored on both sides. Each tablet contains 5 mg ramipril and 0.25 mg red ferric oxide (E 172).
Administration of ramipril in patients with congestive heart failure improves cardiovascular function, the related clinical signs and the prognosis. Ramipril has also been shown to reduce the mortality rate among patients with persistent or transient heart failure following an acute myocardial infarction (man, dog).
The therapeutic dose in the dog is 0.125 mg ramipril per kg bw per day. Depending on the severity of pulmonary congestion the dose may be increased after 2 weeks to 0.25 mg ramipril per kg bw per day. Treatment is once daily by mouth.
The table provides a suggested tablet regime only. To ensure accurate dosing, each individual should be carefully weighed before calculating the standard or double dose to be administered.
The product may also be used in combination with the diuretic furosemide and/or the cardiac glycosides digoxin or methyl-digoxin. Not to be used in clinical cases of vascular stenosis (e.g. aortic stenosis) or obstructive hypertrophic cardiomyopathy.
Substances that deplete blood volume, such as diuretics, or which vasodilate, such as angiotensin converting enzyme (ACE) inhibitors, may contribute to lowering systemic blood pressure. This may result in pre-renal uraemia (azotaemia). Renal function should be monitored both before and seven days after commencement of treatment with ACE inhibitors. This also applies when the dosage of an ACE inhibitor or of a concurrently administered diuretic is increased. It is advisable to periodically monitor renal function throughout treatment.
No studies have been carried to assess the use of the drug in pregnancy or lactation in bitches. ACE inhibitors have been found to be teratogenic in the second and third trimesters in other species. An angiotensin converting enzyme is known to be critical to the development of the neonatal kidney, this product should not be used in pregnancy or lactation.
At the start of treatment with ACE inhibitors or after a dosage increase, reduced blood pressure can occur in rare cases, which may manifest itself by fatigue, lethargy or ataxia. In such cases treatment should be discontinued until the patients condition has returned to normal and then resumed with 50% of the original dose. As high doses of diuretics can also lead to a fall in blood pressure, the concurrent administration of diuretics in the early phase of treatment with ACE inhibitors should be avoided in these patients.
If signs of hypotension occur, treatment with Vasotop should be suspended until fluid and electrolyte status is corrected. Treatment with Vasotop should then be continued at 50% of the original dose. In patients at risk of hypotension, it is advisable to introduce Vasotop gradually over one week (starting with half the therapeutic dose).
Diurectics and a low sodium diet both potentiate the effect of ACE inhibitors by activating the renin-angiotensin-aldosterone system. High doses of diuretics and a low-sodium diet should therefore be avoided during treatment with ACE inhibitors to prevent hypotension (with clinical signs such as apathy, ataxia, rarely syncope or acute renal failure). In patients treated concurrently with Vasotop and frusemide, the dose of diuretic can be reduced to achieve the same diuretic effect as with frusemide alone.
Do not administer potassium-sparing diuretics.
The concomitant administration of ACE inhibitors with non-steroidal anti-inflammatory drugs (NSAIDS) leads to poor autoregulation of the glomerular blood pressure and can therefore trigger acute renal failure. Pregnant women should take special care to avoid accidental exposure, because ACE inhibitors have been found to affect the unborn child during pregnancy in humans. Wash hands after use. In case of accidental ingestion by children seek medical advice immediately and show the label to the doctor.
For animal treatment only. Keep out of reach and sight of children. Do not store above 30°C. Store in a dry place. Keep container in outer carton.
After each opening, replace the cap tightly. Do not remove the desiccant capsule. Use before the expiry date printed on the pack. Dispose of used packaging in the household refuse. Unused product should be returned to the veterinary surgeon.
Ramipril is rapidly and completely absorbed in the gastrointestinal tract after oral administration. Ramipril is a pro-drug and is metabolised in the liver to its active metabolite, ramiprilat. This conversion may be reduced in dogs with impaired liver function. Ramiprilat inhibits angiotensin-converting enzyme (ACE). This enzyme catalyses the conversion of angiotensin I to angiotensin II in blood plasma and in vascular endothelial tissues and degrades bradykinin. As angiotensin II acts as a strong vasoconstrictor and bradykinin as a vasodilator, the net effect of ramipril administration is systemic vasodilation. Angiotensin II also causes the release of aldosterone secretion. This in turn leads to an increase in the serum potassium concentration.
Inhibition of tissue ACE in the heart results in locally reduced levels of angiotensin II and in potentiation of Bradykinin effects. Angiotensin II induces cell proliferation in smooth muscle, while bradykinin leads to increase in local prostacyclin (PGI2) and nitric oxide (NO), both inhibiting smooth muscle proliferation. The effects of local ACE inhibition act synergistically in reducing myotropic factors and result in distinct reduction of cardiac and vascular smooth muscle cell proliferation. In this way ramipril prevents or reduces, with lasting effect, myogenous hypertrophy in patients with congestive heart failure (CHF) and results in reduction of peripheral vascular resistance.
The plasma ACE activity was measured as the principal criterion of the pharmacodynamic effect.
After oral administration of Ramipril a significant inhibition of this activity occurs quickly and gradually increases again during the dosage interval, reaching of 50% of the initial value by 24 hours post administration.