- Email: [email protected]
STUDENT ACHIEVEMENT
495
SIR,-Your note (Aug. 16, p. 387) on Dr. Dermot McCracken’s paper is superficial and unfair. The tables are provided to verify the statements other research-workers can use them that and so made, for reference and controls. Dr. McCracken could be criticised for omitting them, but not for supplying them. You wonder how reliable the data are; you should therefore confirm or deny them by repeating the study, but not make such innuendos without evidence. You say a summary of the work in a few pages would be of more general value. Dr. McCracken provides exactly this in less than three pages of his text (p. 9, p. 134, and p. 335). The correlation of various health and social factors with examination results must be of some interest to educationalists and physicians throughout the country. Of equal importance Dr. McCracken’s figures from Leeds can be used for comparisons and for controls in research studies in other universities in the U.K. We in the British Student Health Association feel we owe him a debt for undertaking such a study in such meticulous detail.
and histograms
Cripps Health Centre University Park, Nottingham.
of arterial necrosis after X-irradiaof the various obscure arterial diseases mentioned by Dr. Kincaid-Smith and by Linton et al./ and in the arteries of grafted organs devitalised by storage but not necessarily incompatible with the recipient. Finally, may I mention two recent, apparently contradictory, findings in the rat with renal hypertension 3namely, a steep rise in the haematocrit in very early, very severe, hypertension, and a marked fall in haematocrit in severe chronic hypertension with encephalopathy ? Lack of support prevents me from studying these effects further, but they seem relevant to the arterial lesion, to the anaemia, and to the underlying-and still unexplained-hypertension. I hope some of your readers will follow them up.
explain the
STUDENT ACHIEVEMENT
S. E. FINLAY. Honorary Secretary, British Student Health Association.
VASCULAR LESIONS IN MALIGNANT HYPERTENSION
SIR,-May interpretation
I suggest a slightly different, simpler, of the complex problems discussed by Dr. Kincaid-Smith (Aug. 2, p. 266) and by Dr. Linton and his colleagues ?1 Firstly, evidence which I have analysed elsewhere2 leaves me fairly satisfied that the essential lesion of malignant hypertension is simply a result of overstretching of terminal arteries to the point where medial muscle-fibres give way locally and allow blood, plasma, or ultrafiltrate to leak into or through the vessel wall, which itself becomes saturated with the colloidal residue of ultrafiltration and fibrin. Like any other sequence of causes and effects the process may be modified by circumstances, but since the injury increases permeability and provokes thrombosis it is
tionin
occurrence
some
London
Hospital, Whitechapel, E.1.
F. B. BYROM.
BLOOD GASES AND LUNG FUNCTION SIR,-In their article5 and in their recent letter (July 5, p. 59) Dr. Palmer and Dr. Diament report that the values for the single-breath carbon monoxide transfer factor (D.L.CO) and the permeability factor (kco) of the lung are much reduced in patients with chronic obstructive disease. Furthermore, they find no correlation between the degree of airway obstruction (expressed as F.E.v.i%) and the degree to which D.L.CO and kco are reduced. We wonder whether the low values for D.L.CO might have been due, at least in part, to their using the effective residual volume, as obtained by single-breath helium dilution, in the calculation of the transfer factor. Morton and Ostensoeto whom they refer, found that the mean transfer factor, calculated from the effective residual volume, was less than that calculated from the true residual volume in patients with unevenly distributed inspired gas. PHYSICAL CHARACTERISTICS AND LUNG-FUNCTION MEASUREMENTS IN 33 PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG DISEASE*
multiplying hypotheses unnecessarily to postulate additional primary defects of permeability or coagulation.1 Intimal hyperplasia, in my view, is a rather late attempt to plug a persistent leak, usually at the cost of a greatly narrowed lumen. Given in time, anticoagulants will no doubt help to keep the vessel patent, as Dr. Kincaid-Smith says, but they rob the leaking primary lesion of its first line of defence, and, in a disease where exudation and haemorrhage at various levels of the arterial tree can have such damaging or lethal consequences, is it not dangerous to give anticoagulants unless the high pressure can be brought, and kept, under control ? If the angiopathic anasmia of this disease springs from its arterial lesions, as Brain
et
al. suggest, rational treatment should be aimed
at
healing those lesions-again by lowering blood-pressure. Secondly, I have observed2 that the vulnerability of arteries to high pressure is greatly reduced by medial hypertrophy, and increased by involution of the media; and from this I have inferred that " hypertensive " lesions
might reasonably be predicted
whenever primary arterial damage weakens the arterial wall to the point where it can no longer contain even a normal blood-pressure. This may 1.
Linton, A. L., Gavras, A. H., Gleadle, R. I., Hutchison, H. E., Lawson, D. H., Lever, A. F., Macadam, R. F., McNichol, G. P., Robertson, J. S. Lancet, 1969, i, 1277. 2. Byrom, F. B. The Hypertensive Vascular Crisis. London, 1969. 3. Brain, M. C., Dacie, J. V., Housinhane, D. O. B. Br. J. Hœmat. 1962, 8, 358.
To test this hypothesis, we compared the alveolar volume and the transfer factor as obtained by single-breath helium dilution (VA.’ and D.L.’CO) with the corresponding values (VA and D.L.CO) obtained by adding the inspired volume to the residual volume separately measured by the closedcircuit helium method. The results, and some other characteristics of 33 patients with chronic obstructive lung disease (including 8 patients with bronchial asthma seen as outpatients), are summarised in the accompanying table. It can be seen that the use of the effective residual volume lowers the average D.L.CO by about 15%. This decrease, although statistically significant (t test for paired observations—1==4-51; p< 0-001), is too small to account for the 4. 5. 6.
Russell, D. S., Wilson, W. C., Tansley, K. J. Neurol. Psychiat. 1949, 12, 187. Palmer, K. N. V., Diament, M. L. Lancet, 1969, i, 1073. Morton, J. W., Ostensoe, L. G. Dis. Chest, 1965, 48, 44.
SIR,-Your note (Aug. 16, p. 387) on Dr. Dermot McCracken’s paper is superficial and unfair. The tables are provided to verify the statements other research-workers can use them that and so made, for reference and controls. Dr. McCracken could be criticised for omitting them, but not for supplying them. You wonder how reliable the data are; you should therefore confirm or deny them by repeating the study, but not make such innuendos without evidence. You say a summary of the work in a few pages would be of more general value. Dr. McCracken provides exactly this in less than three pages of his text (p. 9, p. 134, and p. 335). The correlation of various health and social factors with examination results must be of some interest to educationalists and physicians throughout the country. Of equal importance Dr. McCracken’s figures from Leeds can be used for comparisons and for controls in research studies in other universities in the U.K. We in the British Student Health Association feel we owe him a debt for undertaking such a study in such meticulous detail.
and histograms
Cripps Health Centre University Park, Nottingham.
of arterial necrosis after X-irradiaof the various obscure arterial diseases mentioned by Dr. Kincaid-Smith and by Linton et al./ and in the arteries of grafted organs devitalised by storage but not necessarily incompatible with the recipient. Finally, may I mention two recent, apparently contradictory, findings in the rat with renal hypertension 3namely, a steep rise in the haematocrit in very early, very severe, hypertension, and a marked fall in haematocrit in severe chronic hypertension with encephalopathy ? Lack of support prevents me from studying these effects further, but they seem relevant to the arterial lesion, to the anaemia, and to the underlying-and still unexplained-hypertension. I hope some of your readers will follow them up.
explain the
STUDENT ACHIEVEMENT
S. E. FINLAY. Honorary Secretary, British Student Health Association.
VASCULAR LESIONS IN MALIGNANT HYPERTENSION
SIR,-May interpretation
I suggest a slightly different, simpler, of the complex problems discussed by Dr. Kincaid-Smith (Aug. 2, p. 266) and by Dr. Linton and his colleagues ?1 Firstly, evidence which I have analysed elsewhere2 leaves me fairly satisfied that the essential lesion of malignant hypertension is simply a result of overstretching of terminal arteries to the point where medial muscle-fibres give way locally and allow blood, plasma, or ultrafiltrate to leak into or through the vessel wall, which itself becomes saturated with the colloidal residue of ultrafiltration and fibrin. Like any other sequence of causes and effects the process may be modified by circumstances, but since the injury increases permeability and provokes thrombosis it is
tionin
occurrence
some
London
Hospital, Whitechapel, E.1.
F. B. BYROM.
BLOOD GASES AND LUNG FUNCTION SIR,-In their article5 and in their recent letter (July 5, p. 59) Dr. Palmer and Dr. Diament report that the values for the single-breath carbon monoxide transfer factor (D.L.CO) and the permeability factor (kco) of the lung are much reduced in patients with chronic obstructive disease. Furthermore, they find no correlation between the degree of airway obstruction (expressed as F.E.v.i%) and the degree to which D.L.CO and kco are reduced. We wonder whether the low values for D.L.CO might have been due, at least in part, to their using the effective residual volume, as obtained by single-breath helium dilution, in the calculation of the transfer factor. Morton and Ostensoeto whom they refer, found that the mean transfer factor, calculated from the effective residual volume, was less than that calculated from the true residual volume in patients with unevenly distributed inspired gas. PHYSICAL CHARACTERISTICS AND LUNG-FUNCTION MEASUREMENTS IN 33 PATIENTS WITH CHRONIC OBSTRUCTIVE LUNG DISEASE*
multiplying hypotheses unnecessarily to postulate additional primary defects of permeability or coagulation.1 Intimal hyperplasia, in my view, is a rather late attempt to plug a persistent leak, usually at the cost of a greatly narrowed lumen. Given in time, anticoagulants will no doubt help to keep the vessel patent, as Dr. Kincaid-Smith says, but they rob the leaking primary lesion of its first line of defence, and, in a disease where exudation and haemorrhage at various levels of the arterial tree can have such damaging or lethal consequences, is it not dangerous to give anticoagulants unless the high pressure can be brought, and kept, under control ? If the angiopathic anasmia of this disease springs from its arterial lesions, as Brain
et
al. suggest, rational treatment should be aimed
at
healing those lesions-again by lowering blood-pressure. Secondly, I have observed2 that the vulnerability of arteries to high pressure is greatly reduced by medial hypertrophy, and increased by involution of the media; and from this I have inferred that " hypertensive " lesions
might reasonably be predicted
whenever primary arterial damage weakens the arterial wall to the point where it can no longer contain even a normal blood-pressure. This may 1.
Linton, A. L., Gavras, A. H., Gleadle, R. I., Hutchison, H. E., Lawson, D. H., Lever, A. F., Macadam, R. F., McNichol, G. P., Robertson, J. S. Lancet, 1969, i, 1277. 2. Byrom, F. B. The Hypertensive Vascular Crisis. London, 1969. 3. Brain, M. C., Dacie, J. V., Housinhane, D. O. B. Br. J. Hœmat. 1962, 8, 358.
To test this hypothesis, we compared the alveolar volume and the transfer factor as obtained by single-breath helium dilution (VA.’ and D.L.’CO) with the corresponding values (VA and D.L.CO) obtained by adding the inspired volume to the residual volume separately measured by the closedcircuit helium method. The results, and some other characteristics of 33 patients with chronic obstructive lung disease (including 8 patients with bronchial asthma seen as outpatients), are summarised in the accompanying table. It can be seen that the use of the effective residual volume lowers the average D.L.CO by about 15%. This decrease, although statistically significant (t test for paired observations—1==4-51; p< 0-001), is too small to account for the 4. 5. 6.
Russell, D. S., Wilson, W. C., Tansley, K. J. Neurol. Psychiat. 1949, 12, 187. Palmer, K. N. V., Diament, M. L. Lancet, 1969, i, 1073. Morton, J. W., Ostensoe, L. G. Dis. Chest, 1965, 48, 44.