47 Increased serum-lipids, hypertension, cigarette smoking, and diabetes are predisposing factors for myocardial infarction. 10 The African has all these risk factors save increased serum-lipid. The rarity of myocardial infarction in the African could be because the mean serum-lipid levels are lower than in other races. Walker" found that in the 30-39 agegroup a serum-cholesterol above 220 mg/dl. was present in 55% of Whites, 45% of Indians, 25% of urban Africans, and 10% of rural Africans in South Africa. The studies in Africa suggest that hypertension alone is not an important predisposing factor in the etiology of myocardial infarction. However, it may be an important correlate with other factors that predispose to myocardial infarction.

obesity,

Department of Medicine, University of Natal and King Edward VIII Hospital, Durban, South Africa

Evaggelismos Hospital, Athens, Greece

Y. K. SEEDAT N. PILLAY HELEN

MARCOYANNOPOULOU-FOJAS

STROKE IN AFRICA

Sin—1 was interested to read Anah’s suggestion 12 that hypokalxmia may predispose to hypertensive stroke in Nigeria. Whilst studying stroke patients in the Savannah region of northern Nigeria at the Ahmadu Bello University Hospital in Kaduna, I often had difficulty in deciding if strokes were the result of high blood-pressure: most patients had not had their blood-pressure taken previously, and blood-pressure readings after a stroke are a poor guide to previous hypertension. Moreover, signs of end-organ damage cannot be relied upon to provide further clues of previously raised blood-pressure, for in this region cardiomyopathy is common, urinary schistosomiasis confounds the clinical assessment of hypertensive renal damage, and the fundal signs of hypertension are said to be rare.

Anah comments that strokes

are

often

seen

in younger peo-

ple in Nigeria. I too was impressed by the number of strokes occurring in young people, many having no signs of hypertension. Some had developed cerebral haemorrhage after snakebite, a cause of stroke in the tropics which has received little attention in the literature. But there are many young people with colourless cerebrospinal fluid in whom no obvious cause for the stroke can be found. Others have encountered similar patients elsewhere in Nigeria,13 in other parts of Africa, 14 and in other tropical areas.’s5 What is the cause of these strokes? Gowers 16 described hemiplegia after acute infectious diseases, such as typhoid, malaria, diphtheria, scarlet fever, and measles. Others" have suggested that typhus, trichinosis, and S. mansoni may present as stroke, although well-documented cases are hard to find. Arteritis secondary to pyogenic and tuberculous meningitis may rarely present as a stroke, and syphilitic arteritis is well documented. Infections of the ears, face, and paranasal sinuses may result in cerebral-vein thrombosis; venous thrombosis may explain the hemiplegia often seen during or shortly after childbirth. The pathogenic importance of non-infective conditions such as sickle cell disease and trait has not yet been fully ascertained. Most stroke studies in Africa have been retrospective and have not given full consideration to the possible role of 10. Kannel, W. B. Ann. intern. Med. 1961, 55, 33. 11. Walker, A. R. P. S. Afr. med. J. 1973, 47, 85. 12 Anah, C. O. Lancet, 1976, i, 1185. 13. Osuntokun, B. O., Odeku, E. L., Adeloye, R. B. A. West

Afr. med J. 1969, 19, 160. 14. Cosnett, J E. S. Afr. med J. 1969, 43, 501. 15. Abraham, J in Tropical Neurology (edited by J. D. Spillane), p. 86. London, 1973. R. in A Manual of Diseases of the Nervous System. London, 1888. 17 Fisher, C. M., Mohr, J. P., Adams, R. D. in Harrison’s Principles of Internal Medicine (edited by M. M. Wintrobe and others); p. 1745. New York, 1974.

16

Gowers, W.

common

local disease. More detailed

required

to

improve

our

understanding

prospective of this

studies are condi-

common

tinn

Department of Medicine, General Hospital,

Nottingham NG1

6HA

GRAHAM MULLEY

CEREBROVASCULAR RESPONSE TO HYPERCAPNIA

SIR,-Our laboratory has lately published some findings which may indicate the mechanism of the failure of the cerebrovascular response to hypoxia and hypercapnia in liver dis1 ease which was the subject of your editorial.’ We have been using baboons (Papio ursinus) with a surgically ligated common bileduct as a model for obstructive jaundice. Two weeks after this procedure the animals develop an obstructive jaundice with a depressed cerebrovascular response to hypercapnia.2 This is similar to the findings of Stanley et al. who found no crerbrovascular response to hypercapnia in the goat treated with carbon tetrachloride.34 We have investigated this attenuation over a wide range of Paco2 values and find that its magnitude increases with increments in Paco2. By contrast, the cerebral vasoconstrictor response to hypocapnia was exaggerated in obstructive jaundice.2 In further studies we have shown that some constituent in the plasma of our jaundiced animals potentiates the vasoconstrictor actions of noradrenaline. This potentiation occurred in vitro,’ and in vivo within the cerebral6 and renal’ circulations. These results suggest that vascular sympathetic stimulation may also be potentiated in jaundice. Thus the failure of hypercapnic cerebral vasodilatation may be explained by a potentiated cerebrovascular pressor response to sympathetic stimulation. This would appear to be the case in our experiments as x-adrenoreceptor blockade shifted the CO2 reactivity back towards normal.2 It is more difficult to explain the finding of a larger decrease in C02 responsiveness at higher Paco2 levels. This implies a larger sympathetic constrictor tone with increasing C02 in the jaundiced animals. It has been suggested that the sympathetic nerves modulate the cerebrovascular CO2 response and that the dilation is partly due to a reduction in sympathetic tone.8 Our results may be explained if, in the normal animals, hypercapnia produces cerebral dilatation partly via a decreased cerebral sympathetic constrictor tone. In the jaundiced animals this component of the CO2 dilatation may have been abolished by the adrenergic vascular hypersensitivity to noradrenaline described previously.5-’ Conversely, the potentiation of hypocapnia constriction in jaundice would suggest that this constriction is normally partly mediated by an increase in cerebral sympathetic tone. This evidence would further underline the point you made, that even mild hypoxaemia or hypercapnia should be corrected in jaundice. However, our evidence would suggest that hypocapnia should also be corrected in obstructive jaundice in order to avoid a potential cerebral hypocapnic vasoconstriction. It may be that there are fundamental differences between our experimental model and the model of Stanley et al. Thus it would be interesting to see our work repeated in the goat treated with carbon tetrachloride and in the cirrhotic patient. Physiology Department, Medical School, University of the Witwatersand,

Johannesburg 2001, South Africa

T. A. MCCALDEN C. ROSENDORFF B. H. EIDELMAN

1. Lancet, 1976, i, 731. 2. McCalden, T. A., Eidelman, B. H., Bloom, D. Stroke, 1976, 7, 190. 3. Stanley, N. N., Salisbury, B. G., McHenry, L. C., Cherniack, N. S. Clin. Sci. mol. Med. 1975, 49, 157. 4. Stanley, N. N., Cherniack, N. S. ibid. 1976, 50, 15. 5. McCalden, T. A., Bloom, D., Rosendorff, C. Experientia, 1975, 31, 1173. 6. Bloom, D., McCalden, T. A., Eidelman, B. H. Gut, 1975, 16, 732. 7. Bloom, D., Bomzon, L., Rosendorff, C., Kew, M. C. Clin. exp. Pharmac. Physiol. 1976, 3, 69. 8. James, I. M., Millar, R. A., Purves, M. J. Circulation Res. 1969, 25, 77.