Thirteen small breed dogs with heart murmurs due to mitral regurgitation of varying severity received medetomidine as a sedative drug for teeth cleaning procedures. The dose was 30 micrograms/kg as an intramuscular injection. The drug caused a considerable reduction of the body temperatures and the heart rates over the 6 hrs of monitoring. The respiratory rates increased over the first 30 min and later decreased below control values. Systolic arterial blood pressures did not change significantly. Arterial oxygen tensions were significantly lower at 30 min after drug administration, but the arteriovenous oxygen differences and the carbon dioxide tensions changed very little. On electrocardiograms, sinus bradycardia, marked sinus arrhythmia with sinus pauses, AV-blocks 1st. and rarely 2nd. degree, supraventricular premature contractions (4 dogs) and paroxysmal tachycardia (1 dog) were observed. Echocardiograms showed an insignificant reduction of the shortening fraction and an increase of the left ventricular enlargement ratio as well as the left atrial to aortic root ratio at 30 min after drug administration. All measured parameters had returned to normal values (pre-drug levels) at 24 hrs after sedation. One dog had delayed cardiovascular complications at 3 hrs after drug administration, (period of prolonged asystole), necessitating the use of the antidote MPV 1248, which successfully reversed the abnormality. Two dogs collapsed briefly, at 4 and 5 hrs respectively, after excitement and struggling against physical restraint. In conclusion, medetomidine will have a safe clinical use for sedation of dogs with murmurs from compensated mitral regurgitation as soon as the antidote MPV 1248 (atipamezole) is licensed for clinical use. This will allow the reversion of the cardiopulmonary effects before the time of expected complications.