In normal animals (dogs, cats and rabbits) which were killed by exsanguination, the beginning of rigor in practically all cases was separated from respiratory death by two well characterized periods: (1) a period of pulsation during which each ventricle still exhibited some spontaneous contractions, and (2) a period of relaxation during which the ventricles, while showing neither spontaneous contractions nor rigor, are more relaxed than in normal diastole, and during which the ventricles gradually lose their irritability. (The cardiac rigor or tonic contraction which was observed by recent investigators to set in immediately after death is an artificial phenomenon produced by filling the heart with saline and connecting it with a manometer.)
In the right ventricle both periods are longer than in the left ventricle, i. e., rigor sets in later. Moreover the development of rigor from onset to maximum is also longer in the right ventricle than in the left, although here the difference is less striking.
The stopping of spontaneous beating, the disappearance of irritability, and the development of rigor, manifest in both ventricles a topographical progress from the base toward the apex, i. e., the stoppage of beating, the disappearance of irritability and the setting in of rigor occur first at the uppermost part of the ventricle and last at the lowest point of the ventricle. It often occurred that rigor was already present in the basal part of a ventricle while the apex was still beating. It is probable also that the loss of vital activity and irritability and the development of rigor progress topographically from the endocardial to the epicardial surfaces.
Prolonged etherization retards the onset, but hastens the development of rigor; atropinization hastens both onset and development.
Repeated prolonged stoppages of the heart caused by antemortem (and postmortem) stimulations of the pneumogastric nerves hasten the onset as well as the development of rigor of the heart. All three periods are affected by the inhibitory influence of the stimulation, the period of relaxation, however, seems to be the one which is shortened most. The most probable interpretation of this phenomenon is the assumption that it is caused by an asphyxiation of the cardiac tissues. The stimulations of the pneumogastric nerves seem to hasten also the onset of the general rigor—probably this, too, is the result of some premature asphyxiation of the skeletal muscles.
33 – Glp-2 Increases Electrogenic Anion Secretion and Inhibits Circular Muscle Spontaneous Contractions Via Vip Release in Mouse Proximal Colon
