913 vide a national service. He had an additional suggestion that would cost little and should be taken up. Doctors willing to help with contraception were now identifiable (the "C" list); why not an "A" list of those sympathetic to abortion? Another way to improve access would be to establish centres giving a comprehensive service on contraception, abortion, and sterilisation. Meanwhile, why is the Department of Health so slow to introduce outpatient abortion? And how is it that extra money is being paid to gynaecologists for sterilisation but not for abortion? The answer to these questions means the only, or the was touched on: doctors most vociferous, group who seek to impose their morals upon the community of women; and, politically, abortion is at present dangerous ground.
are byBno
WHAT THE BLADDER DOESN’T DO IT is obvious that the mammalian bladder stores urine until a convenient time for micturition, and thus soiling and sores and ascending infection are avoided. Less obvious is its failure to allow any important reabsorption of the components of urine. Frog bladder is different ; it can reabsorb both sodium and water from its relatively dilute contents, and does so under hormonal control, so that it is by no means a mere temporary receptacle but rather a postscript to the nephron. The same is true of the turtle’s bladder.’ On the other hand, mammalian kidneys can produce a concentrated urine, the desert rat’s reaching an osmolarity 16-20 times that of plasma, and mammalian bladder walls face the problem of restricting both osmotic uptake of water by the contents from capillaries only a few microns away in the bladder wall, and loss to these capillaries of the concentrated solutes in the bladder’s contents. This barrier function is quite lacking in other viscera such as parts of the gut, which consequently serve as rather indifferent replacements for the bladder, and undo much of the excretory work the kidneys have performed, by allowing concentrated solutes to leak back into the circulation. The barrier is the transitional epithelium, the urothelium,3 and it differs radically from gut epithelium such as lines the small intestine. It is normally extremely slow-growing, some cells having a lifespan probably exceeding 200 days,4 while human ileal enterocytes have a lifespan of only about 3 days.5 But urothelium has a remarkable capacity for rapid regeneration after damage, and in dogs can cover a seromuscular graft within three weeks. The association between this large reserve capacity for growth in the bladder wall and a tendency to neoplastic change is presumably not fortuitous ; the enterocyte, normally multiplying at a maximal rate, is much less prone to neoplasia. The luminal surface of the urothelium carries a unique thick (12 nm) membrane.6 It consists of plaques united to each other by thinner regions. When the bladder is full, the surface is even. But on emptying it buckles at the thin regions, and portions of the previous surface 1.
Lefevre,
M.
E., Gennaro, J. F., Brodsky, W. A. Am. J. Physiol. 1970, 219,
716.
Dicker, S. E. Mechanisms of Urine Concentration and Dilution in Mammals. London, 1970. 3 Melicow, M. M. J. Urol. 1945, 54, 186. 4. Cooper, E. H. Ann. R. Coll. Surg. Eng. 1972, 51, 1. 5 Lipkin, M., Sherlock, P., Bell, B. Gastroenterology, 1963, 45, 721. 6. Hicks, R. M. Biol. Rev. 1975, 50, 215. 2.
become the walls of large fusiform vacuoles within the underlying cells. Since the vacuoles are elongated, they include much less urine than if they were spherical, and thus much less of any carcinogen present in the urine. The vacuoles account for the foamy appearance of cytoplasm in the superficial cells of urothelium from the contracted bladder. On refilling, their walls can become luminal membrane once more, and in effect stretching of the membrane is avoided by supplying extra membrane. The ultrastructure of the membrane shows a precise geometric pattern whose significance is being explored.6 Its chemical composition includes much cerebroside, in which it resembles only myelin among known membranes. Functionally it seems to provide most of the permeability barrier against water and ions in the bladder wall. Certainly damage to it by chemical agents or during experimental carcinogenesis results in an increased per-
meability.7 Some years ago a discussion on bladder permeability concluded: "The concept of the bladder as an inert container of urine no longer holds water."8 The bladder under discussion had had a cystostomy for some 28 months and could scarcely be termed normal. The relative impermeability of the normal bladder wall is clearly established,9 10 as is the relative permeability of the damaged bladder." How the healthy bladder succeeds in barring water and solutes is now becoming clearer. THE HOSPITAL DOCTORS’ BALLOT ONE of the causes of the dispute between the Governand the junior hospital doctors is that both sides have said one thing and then moved away from that decision. Once upon a time, the Government persuaded the junior doctors’ negotiators that no-one would be worse off under the proposed new contracts; and then the 6-a-week incomes policy appeared and, for many, the contracts somehow became less attractive. Had Mrs Castle gone back on her word? How could there be "new contracts" (of the kind agreed), "no detriment", and "no extra money". Early in the year, the junior doctors’ representatives accepted Mrs Castle’s proposals for closed contracts; second (or first) thoughts then began to emergel2; and the road has been down hill all the way since then. "No extra money" say the Government: "no detriment" demand the junior doctors. Mrs Castle twists and turns: 13 the housemen strike. A ballot of junior hospital doctors was devised in Edinburgh last weekend; and it is no bad guess that the foremost question in it may be whether or not Mrs Castle’s latest formula for compromise carries any conviction. Can "no detriment" be made compatible with "no extra money"? The answer is "possibly", so the junior doctors should return, as calmly as they can, to normal work and, since their representatives have proved more or less unrepresentative, await the outcome of the ballot. ment
7.
Hicks, R. M., Ketterer, B., Warren, R. C. Phil. Trans. R. Soc. B, 1974, 268,
23. 8. Kerr, W. K., Barkin, M., D’Aloisio, J., Menczyk, Z. J. Urol. 1963, 89, 812. 9. Englund, S. E. Acta radiol. 1956, suppl. 135, p. 9. 10. Rapoport, O., Nicholson, T. F., Yendt, E. R. Am. J. Physiol. 1960, 198, 191. 11. Hicks, R. M. J. Cell Biol. 1966, 28, 21. 12. See Lancet, Sept. 13, 1975, p. 489.
13. ibid. Oct. 25, 1975, p. 805.
are byBno
WHAT THE BLADDER DOESN’T DO IT is obvious that the mammalian bladder stores urine until a convenient time for micturition, and thus soiling and sores and ascending infection are avoided. Less obvious is its failure to allow any important reabsorption of the components of urine. Frog bladder is different ; it can reabsorb both sodium and water from its relatively dilute contents, and does so under hormonal control, so that it is by no means a mere temporary receptacle but rather a postscript to the nephron. The same is true of the turtle’s bladder.’ On the other hand, mammalian kidneys can produce a concentrated urine, the desert rat’s reaching an osmolarity 16-20 times that of plasma, and mammalian bladder walls face the problem of restricting both osmotic uptake of water by the contents from capillaries only a few microns away in the bladder wall, and loss to these capillaries of the concentrated solutes in the bladder’s contents. This barrier function is quite lacking in other viscera such as parts of the gut, which consequently serve as rather indifferent replacements for the bladder, and undo much of the excretory work the kidneys have performed, by allowing concentrated solutes to leak back into the circulation. The barrier is the transitional epithelium, the urothelium,3 and it differs radically from gut epithelium such as lines the small intestine. It is normally extremely slow-growing, some cells having a lifespan probably exceeding 200 days,4 while human ileal enterocytes have a lifespan of only about 3 days.5 But urothelium has a remarkable capacity for rapid regeneration after damage, and in dogs can cover a seromuscular graft within three weeks. The association between this large reserve capacity for growth in the bladder wall and a tendency to neoplastic change is presumably not fortuitous ; the enterocyte, normally multiplying at a maximal rate, is much less prone to neoplasia. The luminal surface of the urothelium carries a unique thick (12 nm) membrane.6 It consists of plaques united to each other by thinner regions. When the bladder is full, the surface is even. But on emptying it buckles at the thin regions, and portions of the previous surface 1.
Lefevre,
M.
E., Gennaro, J. F., Brodsky, W. A. Am. J. Physiol. 1970, 219,
716.
Dicker, S. E. Mechanisms of Urine Concentration and Dilution in Mammals. London, 1970. 3 Melicow, M. M. J. Urol. 1945, 54, 186. 4. Cooper, E. H. Ann. R. Coll. Surg. Eng. 1972, 51, 1. 5 Lipkin, M., Sherlock, P., Bell, B. Gastroenterology, 1963, 45, 721. 6. Hicks, R. M. Biol. Rev. 1975, 50, 215. 2.
become the walls of large fusiform vacuoles within the underlying cells. Since the vacuoles are elongated, they include much less urine than if they were spherical, and thus much less of any carcinogen present in the urine. The vacuoles account for the foamy appearance of cytoplasm in the superficial cells of urothelium from the contracted bladder. On refilling, their walls can become luminal membrane once more, and in effect stretching of the membrane is avoided by supplying extra membrane. The ultrastructure of the membrane shows a precise geometric pattern whose significance is being explored.6 Its chemical composition includes much cerebroside, in which it resembles only myelin among known membranes. Functionally it seems to provide most of the permeability barrier against water and ions in the bladder wall. Certainly damage to it by chemical agents or during experimental carcinogenesis results in an increased per-
meability.7 Some years ago a discussion on bladder permeability concluded: "The concept of the bladder as an inert container of urine no longer holds water."8 The bladder under discussion had had a cystostomy for some 28 months and could scarcely be termed normal. The relative impermeability of the normal bladder wall is clearly established,9 10 as is the relative permeability of the damaged bladder." How the healthy bladder succeeds in barring water and solutes is now becoming clearer. THE HOSPITAL DOCTORS’ BALLOT ONE of the causes of the dispute between the Governand the junior hospital doctors is that both sides have said one thing and then moved away from that decision. Once upon a time, the Government persuaded the junior doctors’ negotiators that no-one would be worse off under the proposed new contracts; and then the 6-a-week incomes policy appeared and, for many, the contracts somehow became less attractive. Had Mrs Castle gone back on her word? How could there be "new contracts" (of the kind agreed), "no detriment", and "no extra money". Early in the year, the junior doctors’ representatives accepted Mrs Castle’s proposals for closed contracts; second (or first) thoughts then began to emergel2; and the road has been down hill all the way since then. "No extra money" say the Government: "no detriment" demand the junior doctors. Mrs Castle twists and turns: 13 the housemen strike. A ballot of junior hospital doctors was devised in Edinburgh last weekend; and it is no bad guess that the foremost question in it may be whether or not Mrs Castle’s latest formula for compromise carries any conviction. Can "no detriment" be made compatible with "no extra money"? The answer is "possibly", so the junior doctors should return, as calmly as they can, to normal work and, since their representatives have proved more or less unrepresentative, await the outcome of the ballot. ment
7.
Hicks, R. M., Ketterer, B., Warren, R. C. Phil. Trans. R. Soc. B, 1974, 268,
23. 8. Kerr, W. K., Barkin, M., D’Aloisio, J., Menczyk, Z. J. Urol. 1963, 89, 812. 9. Englund, S. E. Acta radiol. 1956, suppl. 135, p. 9. 10. Rapoport, O., Nicholson, T. F., Yendt, E. R. Am. J. Physiol. 1960, 198, 191. 11. Hicks, R. M. J. Cell Biol. 1966, 28, 21. 12. See Lancet, Sept. 13, 1975, p. 489.
13. ibid. Oct. 25, 1975, p. 805.
