28 General Discussion 



retarded then the whole pathology seems to be pushed far out into an- 

 other time area where it doesn't occur until the rat should theoretically 

 be dead. And, of course, we need such tests as those Prof. Verzar has 

 just described, it's extremely iinportant that we have some means of 

 measuring this potential towards long life and resistance to pathological 

 changes so that we can go back into the genetics. We need criteria for 

 animals that are going to live for very long periods. 



Scliulze: I would like to stress that it is most valuable to pay attention 

 to the connection between premorbid functional conditions in the 

 arteries and the development of morphological changes in arterio- 

 sclerosis of man, and to trace out this connection. About thirty years ago 

 Biirger proved that in the progress of ageing a steadily increasing 

 deposition of organic and inorganic catabolites takes place in the 

 so-called "bradytrophic tissues" which have no or only a slight capillary 

 supply and are nourished predominantly by diffusion. This was also 

 proved for the inner layers of the aortic wall. Combining these careful 

 analyses of the biochemical structure of the arterial walls Dr. Hevelke, a 

 colleague of mine at Prof. Burger's clinic, recently pointed out that the 

 degree of arteriosclerotic; changes in human vessels is not identical on 

 both sides of the body. There is some difference to be found between the 

 right and the left side and it seems evident that riglit-handed men have 

 a reasonably higher content of cholesterol and calciuni in the walls of 

 their vessels on the right side in comparison with the left. Additionally 

 there are marked and apparently systematic differences in the bio- 

 chemical composition of arteriosclerotic vessels between the arms and 

 the legs. In my opinion these facts are likely to demonstrate a close 

 relationship between functional wasting processes and the incidence of 

 arteriosclerotic changes. This idea should be borne in mind in further 

 research work on the pathogenesis of human arteriosclerosis. 



Comfort: I want to raise the question whether senescence of the 

 endogenous type occurs in all vertebrates. It's a problem which the 

 literature doesn't seem very explicit about. I've been trying to find out, 

 and I'd welcome any suggestions that anyone here has to offer. You may 

 remember that some years ago Bidder (Brit. med. J., 1982, 2, 583) 

 suggested that fish, which never cease to gTow throughout life, don't 

 exhibit, or wouldn't exliibit if it were possible to construct their life- 

 table, the same sort of increase in the force of mortality with increasing 

 age wliich you find in mammals. There are two distinct problems here. 

 There is the group of senescent effects due wholly to accumulation of 

 injuries, which Prof. Medawar mentioned, and there is the fact that it is 

 virtually impossible to devise direct experiments by which the force of 

 mortality in these long-lived cold-blooded animals can be studied. I 

 wish I could induce the Ciba Foundation to finance me over a period of 

 years in constructing a life-table of tortoises. We have the celebrated 

 tortoise of the Queen of Tonga, which is alleged to be very old and which 

 shows very well Prof. Medawar's other group of senescent changes, the 

 accumulated injuries. It is blind in one eye from a fire and bashed in on 

 one side from falling down a cliff, and no doubt it does get less efficient 

 as it continues to live. But does the likelihood of death also increase in 



