The Chronotropic Function of Propofol and the Underlying Mechanism in Rabbits

The report of bradycardia caused by propofol is increasing. In the experiment, we investigated the chronotropic function of propofol and the underlying mechanism. Rabbits of both sexes were randomly divided into 4 groups: propofol 5 mg/kg group, 10 mg/kg group, 15 mg/kg group, and sham group. Heart rate and frequency of vagal efferent discharge were recorded before the injection and 0, 0.5, 1, 2, and 10 min after the injection through intravenous mode. Then, their hearts were removed, and sinoatrial nodes were dissected. The action potentials of the sinus node pacemaker cells were recorded by the intracellular glass microelectrode technique, and the sinoatrial (SA) node was exposed to propofol 1, 3, 5, and 10 µM respectively. The action potentials were recorded after the sinoatrial nodes were exposed to each concentration of propofol for 15 min. Our results show that the heart rate significantly decreased, and the vagal efferent discharge was significantly increased at 0, 0.5, 1, and 2 min after the injection, respectively. Besides, as the dose increases, the magnitude of change shows a dose-dependent manner. Propofol exerts a negative chronotropic action on sinoatrial node pacemaker cells. The drug significantly decreased APA, VDD, RPF, and prolonged APD90 in a concentration-dependent manner. These effects may be the main mechanism of propofol-induced bradycardia in clinical study.

Anatomopathological changes in canine distemper seropositive dogs and virus detection in sinoatrial nodes

Canine distemper is a viral disease that affects several systems on dogs, among them, the cardiovascular system. The aim of this study was to identify canine distemper virus (CDV) in the sinoatrial node (SAN) of dogs serologically positive for distemper by Polymerase Chain Reaction preceded by reverse transcription (RT-PCR), and to analyze gross and microscopic changes of distemper in the heart and other tissues. SAN and tissue fragments were collected from 17 serologically positive dead animals, necropsied from October 2015 to December 2016. In the heart, right heart dilatation was observed in 13 dogs (76.47%) and left concentric hypertrophy in two dogs (11.76%). Microscopically, lymphocytic myocarditis was observed in four (23.53%) dogs and 41.18% presented viral inclusion corpuscles of CDV in the bladder epithelium. Only one (5.88%) dog presented a 319 bp target fragment for distemper virus using primers CDV 1 and CDV 2 at the sinoatrial node. In conclusion, CDV can be located in the sinoatrial node of naturally infected dogs, as demonstrated in this study by the RT-PCR technique, reinforcing the hypothesis that CDV is capable of causing inflammatory lesions in the sinoatrial node of this species. Macroscopic and microscopic cardiac changes are frequently observed in dogs with distemper, mainly cardiac dilatation and myocarditis. Viral inclusions of CDV in bladder epithelial cells are an important microscopic finding for the diagnosis of distemper.

The pacemaker cell of the sinoatrial node of the rabbit

Rabbit sinoatrial nodes were isolated and studied in an attempt to determine the cell of origin of the true pacemaker potential. Cells of the sinoatrial node of the rabbit giving rise to the characteristic true pacemaker potential were iontophoretically tagged with lanthanum. The lanthanum appeared within the cytoplasm of cells, which morpholigically are (P) cells. The lanthanum appeared as small, amorphous, electron-dense globules. It is concluded from this study that the P or pale cell is the source of the true pacemaker action potential of the sinoatrial node.