Carbon dioxide narcosi. I. Specific effects of carbon dioxide upon protoplasmic streaming and consistency in Nitella, and upon the life of the cell. II. The effect of carbon dioxide compared with that of the hydrogen ion. The threshold of tolerance in Nitella to carbon dioxide and to the hydrogen ion. III. Salt antagonism. IV. Is oxygen lack a factor in the narcotic effects of carbon dioxide? V. Water and electrolytes in Nitella during exposure to carbon dioxide solutions
Jour Cell And Comp Physiol 3-3(1-3): 75-100, 341-354
Cells were exposed, at controlled temps., to unbuffered, aqueous sols. of CO2 at known concs., and the behavior of the protoplasm observed under high power. The rate of protoplasmic streaming underwent a gradual decrease, until it quite ceased, while the consistency of the cytoplasm gradually increased. Streaming was resumed after having been brought to a complete cessation, if the CO2 was replaced promptly enough by air. Beyond certain time limits, However, this reversal of the narcotic state was impossible, and coagulation with death ensued. The rate of decrease in protoplasmic streaming followed a fairly smooth sigmoid curve; the rate of recovery was more rapid than that of narcotization, and followed a hyper-boloid curve. While the cells were in a state of narcosis in the presence of CO2, and protoplasmic streaming had ceased, the included plastids exhibited a peculiar vigorous vibrational behavior, not due entirely to Brownian motion, but presumably in part to incipient gel formation. Nitella cells tolerated HC1 or acetic acid at pH 4 for indefinite periods (10 to 30 days) or the normal life span of such detached cells (other conditions being the same) ; carbonic acid at the same pH was fatal in 2-3 hrs. The threshold of tolerance of Nitella for dissolved CO2 was at about .003 [image] (pH 4.6) ; the threshold for HC1 was at about .0001 [image] and for HAc, about .0005 [image] (pH ca. 4.0). The narcotic effects of CO2 were pre vented, up to certain concs., by the presence of dissolved neutral salts such as KNOs, and traces of other common nutrient salts. The threshold of tolerance of Nitella for CO2 was raised, in the presence of very dilute solutions of such salts, by 5- or 6-fold. The narcotic effects noticed in the presence of CO2 solutions were not due to a depletion of the O supply, but to a specific lethal property of the CO2 or HaCO3 molecule. The same neutral salt solutions as were found to exert antagonistic action against the narcotic effects of C02 sols. were effective in antagonizing the injurious effects of H-ion furnished by dilute solutions of strong acids such as HC1. Immersion of Nitella cells in a heavy, colorless, inert hydrocarbon oil resulted in the syneresis of minute droplets of water, containing dissolved electrolytes, while the cells continued to live, and the protoplasm to flow. This syneresis was hastened in the presence of CO2. The protoplasm underwent a decrease in its rate of cyclosis with apparent dehydration, as its consistency increased. Narcotization by CO2 in either aqueous or oil media invariably involved violent, jerky motions of plastids in the cytoplasm not attributable either to Brownian movement alone, or to a disturbance set up by rapid water transference between cell and environment, since syneresis was shown to occur only very slowly. The phenomenon is believed to be due in part to gelation. All movement, including Brownian, ceased as coagulation became complete on continued exposure to C02.