985
required to ascertain whether the abnormality is genetically determined or whether it may be acquired as a result of certain disease states-for example, uraemia-or indeed, whether these individuals simply represent the extreme lower end of a normal distribution curve of platelet behaviour. The association of albinism with a haemorrhagic tendency characterised by an unexplained long bleedingtime has previously been recorded on several occasions.14-111 and possibly this platelet abnormality forms part of the genetically determined disorder in such cases. Weiss 18 has studied a group of 6 women with a bleeding disorder characterised by a defect of plateletfactor-3 availability, impairment of aggregation by connective tissue, and defective release of aggregating activity (presumably A.D.P.) from the platelets on incubation with kaolin. He describes this condition, which appears closely to resemble that described here, as
thrombopathia-a name previously applied to a bleeding disorder thought to be due to a defect of platelet thromboplastic function. Although we do not feel that the combination of findings which we have described should yet be held to represent a single disease entity, it seems reasonable to use the term " thrombopathia in the new sense of a defect of release of platelet A.D.P. by aggregating agents, whatever its cause. Since platelet-factor-3 availability depends quantitatively on aggregation,6 this is "
consistent with the older use of the term. This work was supported by a grant from the Medical Research Council which we gratefully acknowledge. R. M. HARDISTY Department of Hæmatology, M.D. Lond., M.R.C.P., F.C.PATH. Institute of Child Health and the Hospital for Sick Children, R. A. HUTTON Great Ormond Street, London W.C.1
F.I.M.L.T.
HYPOTENSION AFTER ANGIOGRAPHY
blood-pressure of twenty patients measured before and after aortography. The blood-pressure fell consistently and significantly, particularly in hypertensive patients, apparently owing to the contrast medium used. The mechanism of the fall is obscure. Summary
The was
INTRODUCTION
AORTOGRAPHY is not without hazards. Among the complications described are cardiac arrhythmias and anaphylaxis19 renal toxicity, 20 and spinal-cord damage. 21 Other reported side-effects are transient warmth,19 22 and back pain.23 In this department we have noticed that some patients become hypotensive after aortography. The onset is gradual, the fall in pressure is at its lowest level within 8 hours of the procedure, and may be severe enough to require transfusion with plasma expanders to restore blood-pressure to normal levels. This observation led us to’ investigate the blood-pressure after 14. 15. 16.
Horler, A. R., Witts, L. J. Q. Jl Med. 1958, 51, 173. Hermansky, F., Pudlak, P. Blood, 1959, 14, 162. Larsen, M. C., Ley, A. B., Zucker, M. B., Loseke, L.
E. Ann. intern.
17.
Med. 1962, 56, 504. Sobotkowska, K., Kossmann, S. Polskie Archwrn Med.
wewn.
Weiss, H. J. Am. J. Med. (in the press). Grainger, R. G. Br. J. Radiol. 1964, 37, 568. Davidson, A. J., Abrams, H. L., Stamey, T. A.
1966, 36,
Radiology, 1965, 85,
1043. 21. 22.
pressure and lowest pressure reached.
G= general
anaesthesia; L = local anaesthesia.
in order to establish the proportion of become hypotensive, the degree of hypotension, and any contributing factors such as age or pre-existing hypertension. Since the time from angiography to the onset of hypotension might indicate the sensitivity of the patient to injected dye, a correlation between degree of hypotension and its time of onset was also sought.
angiography, patients who
PATIENTS AND METHODS
Twenty consecutive admissions to this hospital for arteriography were studied. All patients (eighteen males and two females) had peripheral vascular disease with symptoms, most with ischaemia of the legs to a greater or lesser degree. Their ages ranged from 47 to 68 years, with a mean of 59 years. Blood-pressure was measured before, during, and after angiography by means of the Riva-Rocci method. At least four control blood-pressure readings were taken at 6-hourly intervals before angiography. Thereafter, the pressure was measured at half-hourly intervals for the first 6 hours, and then hourly for 18 hours, making a total observation period of 24 hours. The pulse-rate was recorded at the same time as the blood-pressure. In thirteen of the patients angiograms were carried out under general anaesthesia with thiopentone and suxamethonium induction, with oxygen, nitrous oxide, and halothane maintenance. The remaining seven patients had 2% lignocaine local anxsthesia only. Two patients had translumbar aortograms under general anaesthesia, and in the remaining FALL OF BLOOD-PRESSURE AFTER RESUTURE OF WOUND
703. 18. 19. 20.
Fig. 1-Systolic and diastolic blood-pressures showing mean control
D.
Killen, A., Foster, J. H. Surgery, St. Louis, 1966, 59, 969. Foster, J. H., Winfrey, E. W., Killen, D. A., Sessions, R. T. med. Ass. 1962, 182, 1009. 23. Marshall, T. R., Ling, J. T., Buchannan, J. Am.J. Roentg. 1964,
J. Am. 92, 676.
986
eighteen the Seldintechnique was employed. The con-
ger
medium was Conray 280, in divided doses of 40-80 ml. trast
the
blood-volume, cardiac output, and peripheral resist-
in the post-arteriogram phase. Acknowledgments are due to Prof. G. Slaney and Mr. F. Ashton, whose patients were studied; Prof. J. S. Robinson who coordinated anaesthetic techniques; and Dr. 0. E. Smith and Dr. F. H. Howarth, of the department of radiology, for their assistance and interest. Requests for reprints should be addressed to C. W. 0. W. ance
RESULTS
PETER N. ROBERTS
Every patient showed
a
blood-pressure after angiography below the " control " value The (fig. 1). mean systolic fall to
was
50
IAN P. YOUNG
fall in
mm.
Hg
and the mean diastolic fall was 30
Hg. (Ax2 applied to these figures gives a statistically highly significant result of 40.) Fig. mm.
B.A.
University Department of Surgery, Queen Elizabeth Hospital, Edgbaston, Birmingham 15
Oxon.
COLIN W. O. WINDSOR M.B.
Birm.,
F.R.C.S.
SLOWLY DEVELOPING PRESSOR RESPONSE TO SMALL AMOUNTS OF NORADRENALINE IN RABBITS
test
Fig. 2-Fall in blood-pressure after angio- 1 shows also that graphy related to control blood-pressure.
the blood-pressure fell significantly in patients anaesthetised either locally or generally. Two patients underwent subsequent minor wound resuturing; the general anaesthetic and its duration was the same for the arteriogram and the minor operation (see accompanying table). The fall in blood-pressure after angiography was greater than after minor surgery. An attempt to correlate blood-pressure fall with age and time to onset of fall was unsuccessful. A significant relation, however, was established with the control blood-pressure level (fig. 2). In general, the higher the initial blood-pressure the greater the fall after angiography. The pulse-rate in all patients remained steady throughout the period of hypotension and showed no significant variation from the resting pulse for each patient. .
=systolic
pressure; 0 = diastolic pressure.
DISCUSSION
Two possible causes of the hypotensions are the effects of general anaesthetic and/or the effects of the angiographic procedure. General anxsthesia is unlikely to have been responsible, since falls in blood-pressure occurred with local anxsthesia (fig. 1), and general anaesthesia for minor procedures did not produce hypotension (fig. 2). If the angiographic procedure was the cause of hypotension, either the manipulation or the The contrast medium may have been responsible. manipulations (arterial punctures and catheter introduction with slight blood-loss) cannot be credibly indicted. Unfortunately, in this series no information was available about the precise amount of ’Conray 280 ’ injected, but it does seem likely that the contrast medium caused hypotension. Also it appears that the more hypertensive a patient is, the greater is the risk of severe hypotension after angiography (fig. 2). These hypertensive patients need close observation and care during the first 8 hours after the arteriogram. The cause of hypotension, without tachycardia, in our patients, is not immediately apparent. We are measuring
The continuous intravenous infusion of small concentrations of noradrenaline into conscious rabbits at rates which are initially devoid of pressor effect can bring about a slowly developing rise of blood-pressure over the course of 1-2 weeks. This observation might provide an experimental model of the sustained hypertension often seen in cases of phæochromocytoma in man. Summary
INTRODUCTION
hypertension often seen in patients with phaeochromocytoma is usually attributed to circulating noradrenaline, because the blood-pressure falls when peripheral a-adrenergic blocking drugs are given. How1 ever, previous attempts to sustain hypertension in animals and man2 by intravenous noradrenaline infusion have failed. Maintenance of hypertension needs larger and larger amounts of noradrenaline, causing progressively THE sustained
constitutional disturbances. There is some evidence depressor material may be circulating at this time, opposing the vasoconstrictor action of noradrenaline. In short-term experiments, even low infusion-rates of noradrenaline have caused necrosis of cardiac muscle cells3 which may also be a factor preventing the maintenance of hypertension with noradrenaline. Dickinson and Lawrence reported that small, initially non-pressor infusion-rates of angiotensin could gradually raise the blood-pressure of conscious rabbits over a period of 3-7 days.4 Similar results have been observed in dog,5 ratand man.2 These results suggested that severe
that
a
noradrenaline might also exert a slowly-developing indirect pressor effect when present in minute quantities for a long period of time. METHODS
We have investigated fourteen rabbits of both sexes, weight 2’0-3’9 kg., for 1-5 months, recording mean aortic pressure by means of a servo-assisted mercury manometer which produced a permanent record of mean arterial pressure on a smoked drum, and also allowed readings of highly damped 1. Blacket, R. B., Pickering, G. W., Wilson, G. M. Clin. Sci. 1950, 9, 247. 2. Ames, R. P., Borkowski, A. J., Sicinski, A. M., Laragh, J. H. J. clin. Invest. 1965, 44, 1171. 3. Schenk, E. A., Moss, A. J. Circulation Res. 1966, 18, 605. 4. Dickinson, C. J., Lawrence, J. R. Lancet. 1963, i, 1354. 5. McCubbin, J. W., DeMoura, R. S., Page, I. H., Olmsted, F. Science, N.Y. 1965, 149, 1394. 6. Koletsky, S., Rivera-Velez, J. M., Pritchard, W. H. Circulation, 1965, 32, 11. 7. Dickinson, C. J. J. Physiol., Lond. 1964, 172, 1P.