EFFECTS ON TISSUE FUNCTIONS 947 



contain SH groups, a conclusion previously reached by Turpaev (1955). 

 Nistratova and Turpaev (1959) titrated the SH groups in a frog ventricle 

 homogenate and found that the presence of acetylcholine alters the shape 

 of the titration curve, but not the total number of SH groups titrated — 

 part of the SH groups becomes less reactive in the presence of acetylcholine. 

 Inasmuch as cholinesterase is inhibited to some extent by mercurials (Ta- 

 ble 7-13). it is possible that this can account for the vagal sensitization, a 

 secondary blocking of the receptors for acetylcholine reversing this effect. 

 There is no evidence for specific interference with the action of .the cate- 

 cholamines on the heart, but epinephrine potentiates the profibrillatory 

 action of the mercurials (Jackson, 1026 a). Yet Salant and Brodman (1929 

 c) claimed that the cat heart is most sensitive to Hg++ when the sympa- 

 thetics are blocked by ergotamine, and that high concentrations of epineph- 

 rine actually protect the heart against the mercurials. In any event, it is 

 likely that the over-all effects of the mercurials on the heart, especially in 

 the whole animal, must to some extent involve the sympathetic and para- 

 sympathetic innervation. Mercurials can release catecholamines from ad- 

 renal medulla granules (D'lorio, 1957) but it is not known if such a release 

 can occur in the heart or other tissue. 



(E) Consideration of some mechanisms of cardiac action. There is little 

 justification for discussing mechanisms by which the mercurials affect the 

 heart because essentially no basic work to elucidate the cellular actions has 

 been done. The interesting observations of Salant and Nagler (1930, 1931) 

 on the relation of the response to Hg++ of the frog heart and the level of 

 Ca++ in the medium may provide some clue. If the Ca++ is reduced to around 

 one half normal, the heart is depressed much more readily by Hg++, but if 

 the Ca++ is reduced further (this in itself suppressing contractions), Hg++ 

 may then actually stimulate the amplitude. High Ca++ somewhat antago- 

 nizes the action of Hg++. Increasing the K+ slows the rate and then Hg++ 

 accelerates the heart and seems to have less effect on the contraction. The 

 authors suggested that the alterations in response to Hg++ might be due 

 to permeability changes brought about by Ca"^+, but we now know that 

 Ca++ has other, perhaps more important, effects on the heart. It would 

 be interesting to know how mercurials affect the positive inotropic action 

 of Ca++. It would also be worthwhile to determine if mercurials inhibit the 

 various ATPases of the heart. Padykula and Herman (1955) showed histo- 

 chemically that p-MB strongly inhibits cardiac ATPase, but it is not known 

 if this occurs in vivo. 



For the purpose of this volume it would be of some importance if the 

 cardiac effects could be correlated with any of the well-known enzymic or 

 metabolic inhibitions exerted by the mercurials, but this cannot be done 

 because there are no investigations of metabolic changes during mercurial 

 action. Even the results reported on respiratory inhibition, for example by 



