The K42 entry into, and leakage from diaphragm muscles of the rat in vitro have been studied at low temperatures. The two processes are not of the first order type. The study revealed the existence of a substantial fraction of muscle potassium as a bound form. The bound potassium fraction was mobilized when the temperature was raised or heparin was added. Cooling the muscle to 5°C caused a net potassium loss and sodium gain. Heparin had no effect on the water, potassium and sodium content of the muscle.
No takes yet. Share an insight, caveat, or question.
S. Hashish (1958) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: