413
sistent with the notion that recurrent aphthous ulceration is initiated by a cell-mediated response. Concordance studies on a small number of pairs of twins have provided some evidence that susceptibility to recurrent aphthous ulcers is genetically influenced. One might therefore expect the altered immune responsiveness to be linked with HLA type, but results here have been conflicting.10-12 Circulating immune complexes have been detected, by two techniques, in the blood of some patients with recurrent aphthous ulcers and Behçet’s syndrome.13 14 Serum C9 is raised in both conditions, more so in Behçet’s.15 Immunoglobulin and complement are demonstrable in aphthous lesions,8 but the relevance of these is doubtful since they are to be found in normal mucosa.’6 In Behet’s syndrome, but not in recurrent aphthous ulcers, the saliva and jejunal secretion lack secretory component. 17 The reduction in symptoms observed with disodium cromoglycate,18 an inhibitor of type-I-induced histamine release, also suggests that there is a humoral component in the pathogenesis of the disease. One attractive unifying concept of the pathogenesis of recurrent aphthous ulcers is based on the benefits in some patients of levamisole therapy.19 Discussing their clinical trial, Lehner and his colleagues fashionably suggested that in health a suppressor T-cell population inhibits B-cell synthesis of antibody against oral mucosa. Aphthous-ulcer patients, they postulated, have a weak suppressor T-cell population which is sufficiently stimulated by levamisole2O to control the ulcers. Alternatively, in the normal subject oral mucosal or skin antigens may circulate in low concentrations in the blood, inducing specific unresponsiveness in T but not B cells.21 22 This low dose tolerance could be abrogated in recurrent aphthous ulceration by oral microbial haptens binding to the mucosa to induce autoantibody formation or cytotoxic T cells. This emphasis on immunological mechanisms has been challenged. In a Glasgow survey,23 deficiencies of iron, folate, and vitamin B12 were detected in 17.7% of 130 aphthous-ulcer patients, compared with 8.5% of matched controls. Challacombe and colleagues24 found only iron deficiency (not anaemia) to be commoner in aphthous-ulcer patients than in controls. A Birmingham gastroenterological unit then reported that 8 out of 33 patients presenting with aphthous ulcers had histological changes in jejunal biopsy specimens compatible with coeliac disease. The oral ulceration in these 8 patients 9.
Miller, M. F., Garfunkel, A. A., Ram, C., Ship, I. I. Oral Surg. 1977, 43,
10. 11.
Platz, P., Ryder, L. P., Donatsky, O. Tissue Antigens, 1976, 8, 279. Dolby, A. E., Walker, D. M., Slade, M., Allan, C. J. J. dent. Res. 1977, 56,
886.
105. 12. Challacombe, S. J., Batchelor, J. R., Kennedy, L. A., Lehner, T. Archs Derm. 1977, 113, 1717. 13. Williams, B. D., Lehner, T. Br. med. J. 1977, i, 1387. 14. Levinsky, R. J., Lehner, T. Clin. exp. Immun. 1978, 32, 193. 15. Adolfini, M., Lehner, T. ibid. 1976, 25, 36. 16. Brandtzaeg, P. in Oral Mucosa in Health and Disease (edited by A. E. Dol-
by); p. 178. 1976. Abdou, N. I., Schumacher, H. R., Colman, R. W., Sagawa, A., Herbert, J., Pascual, E., Carroll, E. T., Miller, M., South, M. A., Abdou, N. J. Lab. clin.Med. 1978, 91, 409. 18. Frost, M. Lancet, 1973, ii, 389. 19. Lehner, T., Wilton, J. M. A., Ivanyi, L. ibid. 1976, ii, 926. 20. Sampson, D., Lui, A. Cancer Res. 1976, 36, 952. 21. Allison, A. C., Lancet, 1971, ii, 135. 22. Bankhurst, A. D., Torrigiani, G., Allison, A. C. ibid. 1973, i, 276. 23. Wray, D., Ferguson, M. M., Mason, D. K., Hutcheon, A. W., Dagg, J. H. Br. med. J. 1975, i, 490. 24. Challacombe, S. J., Barkman, P., Lehner, T. Br. J. oral Surg. 1977, 15, 37.
remitted completely on a gluten-free diet. 25 Subsequent work suggests that this is a sizeable overestimate of the prevalence of underlying coeliac disease in aphthous-ulcer patients.24 26 However, gluten could be toxic locally to the oral mucosa, since the oral ulcers of hæmatologically normal patients with normal jejunal biopsies became fewer and less painful on a gluten-free diet.27 Further studies of the development of the oral lesions-particularly immunological characterisation of the early infiltrate-might reveal basic differences or essential similarities between uncomplicated aphthæ in recurrent aphthous ulceration and Behçet’s syndrome and those clinically indistinguishable ulcers which in a small minority of patients are the presenting symptom of an underlying generalised deficiency disorder. But at present there is much in favour of Touraine’s28 view that recurrent aphthous ulcers and Beh4;et’s syndrome represent opposite ends of an "aphthosis" spectrum.
PASSIVE SMOKING AND ANGINA
growing awareness of the discomfort caused ordinary people (i.e., non-smokers) by those who smoke in their presence. Many normal people complain of stinging of the eyes or discomfort in the nose or throat in the presence of smokers, and 37% of non-smokers stated that they minded if people smoked in their homes. THERE is
to
Discomfort can be worse for sufferers from asthma or bronchitis. Until lately there has been scant evidence on the effect of passive smoking on patients with heart disease. Aronow has already shown that after smoking a cigarette1 or travelling in heavy Los Angeles traffic2 the patient with angina needs less exercise time to bring on pain. His latest study shows that even exposure to the reduce the cigarette smoke of others will significantly duration of exercise leading to angina.3 10 patients with angina (8 of them ex-smokers and 2 light smokers who had not smoked for sixteen hours) were exposed to 3 smokers in a small room who consumed five cigarettes each over two hours. The room was either well ventilated or not ventilated. In both situations the resting heart-rate, blood-pressure, and carboxyhaemoglobin levels were increased but more so when the patients were in the non-ventilated room. The duration of exercise until angina developed was decreased by 22% after passive smoking in the well ventilated room and by 38% in the non-ventilated room. It was concluded that passive smoking aggravates angina. Whether this was due to carbon monoxide, to nicotine, or to other compounds of tobacco smoke (which include nitrites of oxygen and hydrogen cyanide) was not known. The possibility of the psychological effect of exercise in a stuffy smoky room was also considered. Carbon monoxide seems to be the chief suspect. Exposure to low levels of inhaled carbon monoxide was found to decrease exercise tolerance in patients with angina
17.
25.
Ferguson, R., Basu,
M.
K., Asquith, P., Cooke, W. T. Br. med. J. 1976, i,
11. 26. Rose, J. D. R., Smith, D. M., Allan, F. G., Sircus, W. ibid. 1978, i, 1145. 27. Walker, D. M., Dolby, A. E., Mead, J., Llewelyn, J., Rhodes, J. International Association for Dental Research British Division, annual meeting,
April, 1978. (Abstr. no. 204). Touraine, A. Bull. Soc. fr. Derm. Syph. 1940, 48, 61. Aronow, W. S., Kaplan, M. A., Jacob, D. Ann. intern. Med. 1968, 69, 529. Aronow, W. S., Harris, C. N., Isbell, M. W., et al. ibid. 1972, 77, 669. 3. Aronow, W. S. New Engl. J. Med. 1978, 299, 21.
28. 1. 2.
414
pectoris,4and also
in
patients with intermittent claudi-
cation.s The most effective advice a doctor can give his patient after a coronary attack is to stop smoking: this halves the relapse-rate. Aronow’s study indicates that patients with coronary heart-disease should also avoid places of heavy pollution with tobacco smoke, such as smoking compartments in trains, smoky pubs, and exposure to tobacco smoke at work, in office, or in factory. In Britain the Secretary of State for Health and Social Services has promised to take action to increase no-smoking areas in public places, yet he has actually done little. Sitting next to smokers in committee, which includes pipe and cigar users, may be hazardous as well as unpleasant. Being nursed in a hospital bed next to a smoker may also increase the risk for a patient with chest or heart-disease. We can hardly expect the Secretary of State to act more firmly until doctors and other health workers have tried to put their own houses and hospitals in order. It is time we accepted no-smoking as normal behaviour in all health committees. We should also see that the norm for acute hospital wards should be non-smoking. This has already been implemented with success in several
hospitals. Freedom for the non-smoker must be accompanied by freedom for the smoker who. will not or cannot stop. Hospitals should have defined areas where smoking is allowed, preferably not in day rooms or televison lounges used by other patients. The majority of patients who do not smoke should be free to be nursed and relax in places free from tobacco smoke. Aronow has shown that it is not only the comfort but also the health of patients which will, in this way, be protected.
ON KEEPING A COOL HEAD
-
THERE is something, special about keeping a cool head. Not simply keeping cool, but keeping a cool head. At first only the dearer cars had ducts to blow cool air towards one’s face when required; now they nearly all do. People sponge themselves with cold water in the heat; it is the face that gets it first. Space travellers, firemen, and others who need cooling at work have special cooling helmets designed for them, which are more helpful than devices’to cool other parts of the body.6-8 Hot rodents smear saliva over their faces, not having any sweat glands to mention, but do not expend much on their backs. Crude physiological analysis talks of a body core, in theory always at 37°C, and an insulating mantle all round it. There is no hint here of anything special about the head; cool any part of the surface, and the core will to some extent cool. Yet there is clear evidence that face and head cooling are particularly effective in the heat, and neck cooling much less so.9 The subject gains an impression of rapid benefit, and it is more than an impres-
4.
Anderson, E. W., Andelman, R. J., Strauch, J. M., et al. Ann. intern. Med. 1973, 79, 46. 5. Aronow, W. S., Stemmer, E. A., Isbell, M. W. Circulation, 1974, 49, 415. 6. Shvartz, E. J. appl. Physiol. 1970, 29, 36. 7. Nunneley, S. A., Troutman, S. A., jr., Webb, P. Aerospace Med. 1971, 42, 64.
Williams, B. A., Shitzer, A. ibid. 1974, 45, 1030. 9. Shvartz, E. J. appl. Physiol. 1976, 40, 668. 8.
sion ; experiments in double chambers,
one for the head and one for the rest, showed that temperature changes in the head chamber were followed by the onset and offset of sweating much more promptly than were changes in the other chamber. The clue to what is going on comes from unilateral temperature measurements. When temperature is measured close to the tympanic membranes and also on each side of the mouth, then a change of outside temperature applied to just one side of the face promptly alters mouth temperature and tympanic temperature, but on the same side only.lOThe mechanism is countercurrent heat exchange. Such exchange is familiar enough in the way in which cold blood returning from the skin of arms and legs can cool outgoing arterial blood, by flowing centrally in venae comitantes side by side with the arteries." The advantage in cold weather is clear: instead of hot blood arriving at the cold skin and losing a great deal of heat, it arrives precooled and loses much less. In hot weather, the blood returns mostly by another route, in the dilated subcutaneous veins, which have no close relation to arteries. So much is well known; Claude Bernard noticed the essentials in 1876.7 But what about heat exchange in the human neck? Distances are not great, but the internal jugular vein receives blood from the surface of the face, and does run closely along the common carotid artery. Of the organs perfused by the common carotid artery, one-the brain-is profoundly sensitive to the temperature of the blood perfusing it, and organises active responses by the rest of the body to changes as small as 0.01°C.13 Thus changes in the temperature of the skin, though not moving much heat into or out of the body, can rapidly change the temperature of internal-jugularvein blood a little, and therefore the temperature of common carotid blood a little; the brain responds a lot to a little change here. Possibly the reputation of tea as a cooling drink originates from some such effect. The tea is usually drunk when it is above body temperature, and so cannot fail to heat the body; but the transient effect as it goes down and warms the upgoing blood starts or amplifies sweating. The drinker, the tea once down, feels his brain cooling and himself sweating, and is pleased. Heat exchange is again the rationale underlying that curious neurovascular complex, the cavernous sinus. Carotid-artery blood runs through rather than beside the flow of venous blood. This feature, improved by breaking up the artery into numerous small divisions and thus increasing its surface area, allows the oryx to keep a cool brain in a hot desert. The venous blood is returning from the nasal cavity, where it has been cooled by evaporation of water. The arterial blood passing through its may lose so much heat that the oryx can stand a rectal temperature of 46.5°C for hours without observable ill effects.14 And even the dog, when he runs, can keep his brain as much as 1 3°C below the temperature of carotid blood, by the same arrangement. 15
10. McCaffrey, T. V., McCook, R. D., Wurster, R. D. ibid. 1975, 39, 114. 11. Bazett, H. C., Love, L., Newton, M., Eisenberg, L., Day, R., Foster, R. ibid.
1948, 1, 3. C., Leçons sur la chaleur animale, la fièvre; p.114. Paris, 1876.
12. Bernard,
sur
les effets de la chaleur
13. Benzinger, T. H. Sci. Am. 1961, 204, 134. 14. Schmidt-Nielsen, K. How Animals Work; p. 68. Cambridge, 15. Baker, M. A., Chapman, L. W. Science, 1977, 195, 781.
1972.
et sur
sistent with the notion that recurrent aphthous ulceration is initiated by a cell-mediated response. Concordance studies on a small number of pairs of twins have provided some evidence that susceptibility to recurrent aphthous ulcers is genetically influenced. One might therefore expect the altered immune responsiveness to be linked with HLA type, but results here have been conflicting.10-12 Circulating immune complexes have been detected, by two techniques, in the blood of some patients with recurrent aphthous ulcers and Behçet’s syndrome.13 14 Serum C9 is raised in both conditions, more so in Behçet’s.15 Immunoglobulin and complement are demonstrable in aphthous lesions,8 but the relevance of these is doubtful since they are to be found in normal mucosa.’6 In Behet’s syndrome, but not in recurrent aphthous ulcers, the saliva and jejunal secretion lack secretory component. 17 The reduction in symptoms observed with disodium cromoglycate,18 an inhibitor of type-I-induced histamine release, also suggests that there is a humoral component in the pathogenesis of the disease. One attractive unifying concept of the pathogenesis of recurrent aphthous ulcers is based on the benefits in some patients of levamisole therapy.19 Discussing their clinical trial, Lehner and his colleagues fashionably suggested that in health a suppressor T-cell population inhibits B-cell synthesis of antibody against oral mucosa. Aphthous-ulcer patients, they postulated, have a weak suppressor T-cell population which is sufficiently stimulated by levamisole2O to control the ulcers. Alternatively, in the normal subject oral mucosal or skin antigens may circulate in low concentrations in the blood, inducing specific unresponsiveness in T but not B cells.21 22 This low dose tolerance could be abrogated in recurrent aphthous ulceration by oral microbial haptens binding to the mucosa to induce autoantibody formation or cytotoxic T cells. This emphasis on immunological mechanisms has been challenged. In a Glasgow survey,23 deficiencies of iron, folate, and vitamin B12 were detected in 17.7% of 130 aphthous-ulcer patients, compared with 8.5% of matched controls. Challacombe and colleagues24 found only iron deficiency (not anaemia) to be commoner in aphthous-ulcer patients than in controls. A Birmingham gastroenterological unit then reported that 8 out of 33 patients presenting with aphthous ulcers had histological changes in jejunal biopsy specimens compatible with coeliac disease. The oral ulceration in these 8 patients 9.
Miller, M. F., Garfunkel, A. A., Ram, C., Ship, I. I. Oral Surg. 1977, 43,
10. 11.
Platz, P., Ryder, L. P., Donatsky, O. Tissue Antigens, 1976, 8, 279. Dolby, A. E., Walker, D. M., Slade, M., Allan, C. J. J. dent. Res. 1977, 56,
886.
105. 12. Challacombe, S. J., Batchelor, J. R., Kennedy, L. A., Lehner, T. Archs Derm. 1977, 113, 1717. 13. Williams, B. D., Lehner, T. Br. med. J. 1977, i, 1387. 14. Levinsky, R. J., Lehner, T. Clin. exp. Immun. 1978, 32, 193. 15. Adolfini, M., Lehner, T. ibid. 1976, 25, 36. 16. Brandtzaeg, P. in Oral Mucosa in Health and Disease (edited by A. E. Dol-
by); p. 178. 1976. Abdou, N. I., Schumacher, H. R., Colman, R. W., Sagawa, A., Herbert, J., Pascual, E., Carroll, E. T., Miller, M., South, M. A., Abdou, N. J. Lab. clin.Med. 1978, 91, 409. 18. Frost, M. Lancet, 1973, ii, 389. 19. Lehner, T., Wilton, J. M. A., Ivanyi, L. ibid. 1976, ii, 926. 20. Sampson, D., Lui, A. Cancer Res. 1976, 36, 952. 21. Allison, A. C., Lancet, 1971, ii, 135. 22. Bankhurst, A. D., Torrigiani, G., Allison, A. C. ibid. 1973, i, 276. 23. Wray, D., Ferguson, M. M., Mason, D. K., Hutcheon, A. W., Dagg, J. H. Br. med. J. 1975, i, 490. 24. Challacombe, S. J., Barkman, P., Lehner, T. Br. J. oral Surg. 1977, 15, 37.
remitted completely on a gluten-free diet. 25 Subsequent work suggests that this is a sizeable overestimate of the prevalence of underlying coeliac disease in aphthous-ulcer patients.24 26 However, gluten could be toxic locally to the oral mucosa, since the oral ulcers of hæmatologically normal patients with normal jejunal biopsies became fewer and less painful on a gluten-free diet.27 Further studies of the development of the oral lesions-particularly immunological characterisation of the early infiltrate-might reveal basic differences or essential similarities between uncomplicated aphthæ in recurrent aphthous ulceration and Behçet’s syndrome and those clinically indistinguishable ulcers which in a small minority of patients are the presenting symptom of an underlying generalised deficiency disorder. But at present there is much in favour of Touraine’s28 view that recurrent aphthous ulcers and Beh4;et’s syndrome represent opposite ends of an "aphthosis" spectrum.
PASSIVE SMOKING AND ANGINA
growing awareness of the discomfort caused ordinary people (i.e., non-smokers) by those who smoke in their presence. Many normal people complain of stinging of the eyes or discomfort in the nose or throat in the presence of smokers, and 37% of non-smokers stated that they minded if people smoked in their homes. THERE is
to
Discomfort can be worse for sufferers from asthma or bronchitis. Until lately there has been scant evidence on the effect of passive smoking on patients with heart disease. Aronow has already shown that after smoking a cigarette1 or travelling in heavy Los Angeles traffic2 the patient with angina needs less exercise time to bring on pain. His latest study shows that even exposure to the reduce the cigarette smoke of others will significantly duration of exercise leading to angina.3 10 patients with angina (8 of them ex-smokers and 2 light smokers who had not smoked for sixteen hours) were exposed to 3 smokers in a small room who consumed five cigarettes each over two hours. The room was either well ventilated or not ventilated. In both situations the resting heart-rate, blood-pressure, and carboxyhaemoglobin levels were increased but more so when the patients were in the non-ventilated room. The duration of exercise until angina developed was decreased by 22% after passive smoking in the well ventilated room and by 38% in the non-ventilated room. It was concluded that passive smoking aggravates angina. Whether this was due to carbon monoxide, to nicotine, or to other compounds of tobacco smoke (which include nitrites of oxygen and hydrogen cyanide) was not known. The possibility of the psychological effect of exercise in a stuffy smoky room was also considered. Carbon monoxide seems to be the chief suspect. Exposure to low levels of inhaled carbon monoxide was found to decrease exercise tolerance in patients with angina
17.
25.
Ferguson, R., Basu,
M.
K., Asquith, P., Cooke, W. T. Br. med. J. 1976, i,
11. 26. Rose, J. D. R., Smith, D. M., Allan, F. G., Sircus, W. ibid. 1978, i, 1145. 27. Walker, D. M., Dolby, A. E., Mead, J., Llewelyn, J., Rhodes, J. International Association for Dental Research British Division, annual meeting,
April, 1978. (Abstr. no. 204). Touraine, A. Bull. Soc. fr. Derm. Syph. 1940, 48, 61. Aronow, W. S., Kaplan, M. A., Jacob, D. Ann. intern. Med. 1968, 69, 529. Aronow, W. S., Harris, C. N., Isbell, M. W., et al. ibid. 1972, 77, 669. 3. Aronow, W. S. New Engl. J. Med. 1978, 299, 21.
28. 1. 2.
414
pectoris,4and also
in
patients with intermittent claudi-
cation.s The most effective advice a doctor can give his patient after a coronary attack is to stop smoking: this halves the relapse-rate. Aronow’s study indicates that patients with coronary heart-disease should also avoid places of heavy pollution with tobacco smoke, such as smoking compartments in trains, smoky pubs, and exposure to tobacco smoke at work, in office, or in factory. In Britain the Secretary of State for Health and Social Services has promised to take action to increase no-smoking areas in public places, yet he has actually done little. Sitting next to smokers in committee, which includes pipe and cigar users, may be hazardous as well as unpleasant. Being nursed in a hospital bed next to a smoker may also increase the risk for a patient with chest or heart-disease. We can hardly expect the Secretary of State to act more firmly until doctors and other health workers have tried to put their own houses and hospitals in order. It is time we accepted no-smoking as normal behaviour in all health committees. We should also see that the norm for acute hospital wards should be non-smoking. This has already been implemented with success in several
hospitals. Freedom for the non-smoker must be accompanied by freedom for the smoker who. will not or cannot stop. Hospitals should have defined areas where smoking is allowed, preferably not in day rooms or televison lounges used by other patients. The majority of patients who do not smoke should be free to be nursed and relax in places free from tobacco smoke. Aronow has shown that it is not only the comfort but also the health of patients which will, in this way, be protected.
ON KEEPING A COOL HEAD
-
THERE is something, special about keeping a cool head. Not simply keeping cool, but keeping a cool head. At first only the dearer cars had ducts to blow cool air towards one’s face when required; now they nearly all do. People sponge themselves with cold water in the heat; it is the face that gets it first. Space travellers, firemen, and others who need cooling at work have special cooling helmets designed for them, which are more helpful than devices’to cool other parts of the body.6-8 Hot rodents smear saliva over their faces, not having any sweat glands to mention, but do not expend much on their backs. Crude physiological analysis talks of a body core, in theory always at 37°C, and an insulating mantle all round it. There is no hint here of anything special about the head; cool any part of the surface, and the core will to some extent cool. Yet there is clear evidence that face and head cooling are particularly effective in the heat, and neck cooling much less so.9 The subject gains an impression of rapid benefit, and it is more than an impres-
4.
Anderson, E. W., Andelman, R. J., Strauch, J. M., et al. Ann. intern. Med. 1973, 79, 46. 5. Aronow, W. S., Stemmer, E. A., Isbell, M. W. Circulation, 1974, 49, 415. 6. Shvartz, E. J. appl. Physiol. 1970, 29, 36. 7. Nunneley, S. A., Troutman, S. A., jr., Webb, P. Aerospace Med. 1971, 42, 64.
Williams, B. A., Shitzer, A. ibid. 1974, 45, 1030. 9. Shvartz, E. J. appl. Physiol. 1976, 40, 668. 8.
sion ; experiments in double chambers,
one for the head and one for the rest, showed that temperature changes in the head chamber were followed by the onset and offset of sweating much more promptly than were changes in the other chamber. The clue to what is going on comes from unilateral temperature measurements. When temperature is measured close to the tympanic membranes and also on each side of the mouth, then a change of outside temperature applied to just one side of the face promptly alters mouth temperature and tympanic temperature, but on the same side only.lOThe mechanism is countercurrent heat exchange. Such exchange is familiar enough in the way in which cold blood returning from the skin of arms and legs can cool outgoing arterial blood, by flowing centrally in venae comitantes side by side with the arteries." The advantage in cold weather is clear: instead of hot blood arriving at the cold skin and losing a great deal of heat, it arrives precooled and loses much less. In hot weather, the blood returns mostly by another route, in the dilated subcutaneous veins, which have no close relation to arteries. So much is well known; Claude Bernard noticed the essentials in 1876.7 But what about heat exchange in the human neck? Distances are not great, but the internal jugular vein receives blood from the surface of the face, and does run closely along the common carotid artery. Of the organs perfused by the common carotid artery, one-the brain-is profoundly sensitive to the temperature of the blood perfusing it, and organises active responses by the rest of the body to changes as small as 0.01°C.13 Thus changes in the temperature of the skin, though not moving much heat into or out of the body, can rapidly change the temperature of internal-jugularvein blood a little, and therefore the temperature of common carotid blood a little; the brain responds a lot to a little change here. Possibly the reputation of tea as a cooling drink originates from some such effect. The tea is usually drunk when it is above body temperature, and so cannot fail to heat the body; but the transient effect as it goes down and warms the upgoing blood starts or amplifies sweating. The drinker, the tea once down, feels his brain cooling and himself sweating, and is pleased. Heat exchange is again the rationale underlying that curious neurovascular complex, the cavernous sinus. Carotid-artery blood runs through rather than beside the flow of venous blood. This feature, improved by breaking up the artery into numerous small divisions and thus increasing its surface area, allows the oryx to keep a cool brain in a hot desert. The venous blood is returning from the nasal cavity, where it has been cooled by evaporation of water. The arterial blood passing through its may lose so much heat that the oryx can stand a rectal temperature of 46.5°C for hours without observable ill effects.14 And even the dog, when he runs, can keep his brain as much as 1 3°C below the temperature of carotid blood, by the same arrangement. 15
10. McCaffrey, T. V., McCook, R. D., Wurster, R. D. ibid. 1975, 39, 114. 11. Bazett, H. C., Love, L., Newton, M., Eisenberg, L., Day, R., Foster, R. ibid.
1948, 1, 3. C., Leçons sur la chaleur animale, la fièvre; p.114. Paris, 1876.
12. Bernard,
sur
les effets de la chaleur
13. Benzinger, T. H. Sci. Am. 1961, 204, 134. 14. Schmidt-Nielsen, K. How Animals Work; p. 68. Cambridge, 15. Baker, M. A., Chapman, L. W. Science, 1977, 195, 781.
1972.
et sur
