320 /. /. Christian 



symptoms so frequently observed (Hamilton, 1937; Green and Larson, 

 1938 ; Green, et al., 1939) were the result of hypoglycemic shock as a result of 

 pituitary-adrenocortical exhaustion. The subject remains at that point to- 

 day, except that Frank (1953) has succeeded in showing that hypoglycemic 

 shock, which is uncorrected by epinephrine but is corrected by glucose in- 

 jection, occurs in Microtus. Frank (1953) also succeeded in producing mass 

 mortality from hypoglycemic shock by crowding voles in enclosures. How- 

 ever, he believes that in addition to increased density alone, which sets the 

 conditions for a mass mortality, a trigger, such as competition for food must 

 also be present. This seems a reasonable suggestion which perhaps can be 

 modijfied to be included in density-dependent factors. On the basis of 

 Frank's and other experimental data it appears that competition for any 

 factor is also a matter of relative population density and inseparable from 

 it. In this case it seems that the voles were reducing the environmental 

 capacity at high densities and were therefore themselves setting up the 

 conditions for increasing competition among themselves above the level 

 that was already present. 



It has been mentioned that mass mortality in sika deer was probably a 

 result of electrolyte imbalances brought about by prolonged adrenocortical 

 hyperactivity. There were indications of a prominent role of the zona 

 glomerulosa, presumably with increased secretion of aldosterone, to explain 

 the evidence of potassium deficiency (Christian et al., 1960; Christian, 

 1963). 



Frank (1953) was able to eliminate infectious disease and climatic 

 factors as causative agents in precipitating the mortality in these animals, 

 as were Adams, Bell, and Moore (Christian, 1959b) in Microtus montanus. 

 Rausch (1950) also indicated that neither parasitism nor infectious disease 

 could account for the sudden decline in the lemming population he was 

 studying. In a study of mortality in an experimentally induced epidemic 

 in Norway rats, Davis and Jensen (1952) found that mortality rate was not 

 significantly changed and probably would be so only under special circimi- 

 stances. A precipitous population decline due to mass mortality from hypo- 

 glycemic shock is probably only one of several mechanisms which may 

 operate to reduce population density drastically and it may be a rather 

 special occurrence. Our knowledge of the physiologic mechanisms involved 

 in invoking "shock disease" in natural or experimental populations is little 

 better understood now than previously. It was originally postulated that 

 adrenocortical exhaustion was the cause, but it is just as likely, if not more 

 so, that readily mobilizable sources of glycogen and glucose become totally 

 exhausted with continued overstimulation of the adrenal medulla and cor- 

 tex. There may be exhaustion of other parts of the responsive system, such 

 as the pituitary, hypothalamus, or of the adrenal medulla. None of these 



