e.ir.sA'.v OF \i:(h'i)Sis 371 



temiK'raturc I'oefficicnt is also considerably lower in dead than in living 

 tissne.'^ AVlien seeondary disintegrative changes occnr in the proto- 

 plasm, with the formation of many small molecules from the large 

 molecules of the cell, both osmotic pressure and electrical conductiv- 

 ity increase rapidly. Changes in the permeabilit}^ of cell protoplasm, 

 however, may be of considerable degree without necessarily indicating 

 serious injury of the cells (Osterhout).^"'' 



A principle of colloid chcmistrv, the alteration of colloids with time, has an 

 interestinpr bearing on liie question of ajjing and natural death of tissues. i-' It 

 is cliaracteristic of colloidal solutions (\vliicli, of course, is what cells are), tliat 

 they continuously clianfj:e in tlieir properties, the change being generally in the 

 direction of aggregation of the disperse colloidal particles, with a resulting ten- 

 dency to ])recipitatioii or coaguiatio!! : the gels tend to decrease in elasticity and 

 U> l)econie moi-e turbid, associated with which are alterations in tlieir per- 

 meability to crystalloids. A gelatin mass possesses its maximum elasticity tiiree 

 or four hours after it is first formed; and crystalloids penetrate fresh, quickly- 

 formed gels at first more rapidly than later. As Bechhold says, we can inuigine 

 (1) a relation of such facts to the greater elasticity of young tissues; (2) to a 

 ))resumably greater permeability for crystalloids and hence more rapid metab- 

 olism: (3) to the decreasing water of tlie tissue with age (94 per cent, of water 

 in the fetus of three months. 00-60 per cent, at birth, and 58 per cent, in adults) : 

 (4) to the demonstrated greater permeability of yoiuig nerve tissues for vital 

 stains, etc. ''In general we can say that the tissue colloids decrease in their 

 water attinity (Qiiellharl-eit) both in animal organisms, which become poorer in 

 water with age, and in plants, as shown by the hardening of older j^lant tissues.'' 

 The bearing of these principles on the problem of senility and degeneration of 

 elastic tissue, regeneration and many other subjects is obvious. 



CAUSES OF NECROSIS 

 Anemia. — After the cutting off of blood-supply, cells soon undergo 

 morphological changes that we recognize as indicating tlieir death, 

 and after a time they also become incapable of returning to their nor- 

 mal condition when the blood-supply is re-established, probably be- 

 cause of these structural changes. In just what way lack of nourish- 

 ment causes death has not been determined, but, as has been before 

 suggested, it seems probable that it is because catabolic processes are 

 no longer balanced by anabolic processes, and with these latter oxi- 

 dizing enzymes seem to be inseparably associated, as far as our pres- 

 ent knowledge shows us. That the loss of oxygen alone, with other 

 materials presumably supplied to the cells in adequate amount, may 

 cause necrosis, is shown by the presence of marked hepatic necrosis 

 in animals kept a week in atmospheres extremely low in oxygen (5-9 

 per cent.).^-^ The nature of the chemical changes taking place in a 

 cell when oxygen is deficient must be very different from the normal 

 changes, and hence abnormal toxic substances maj accumulate, e. g., 

 excessive amounts of organic acids. Were it not that the proteolytic 



11 Oaleotti's earlier observations with animal tissues (Zeit. f. Biol., 100.3 (45). 

 65) do not harmonize with Osterhout's results, and Galeotti's idea that there is a 

 special degree of ionization cliaracteristic of living cells is not established. 



loe Botan. Gaz., 1015 (50), 242. 



12 See H. Bechhold, "Die Kolloide in Biologie und Medizin." Dresden, 1012, p. 65 

 12a Martin, Bunting and Loevenhart, Jour. Pharmacol., Proc, 1916 (8), 112. 



