746 laden fibroblast-like cells and round cells. Both explants of synovium and the adherent cells secreted a large amount of latent collagenase and neutral proteinase into the culture medium. The secretion of these enzymes and the amount of mtracellular iron decreased with passage of these cultures. Werb and Reynolds (J Exp Med 1974; 140: 1482) had shown that if synovial cells phagocytosed inert particles such as latex spherules the secretion of collagenase and neutral-proteinase rose strikingly. It seems likely that in haemophilia and, probably, in rheumatoid synovitis ingestion by synovial lining cells of the various components of red blood cells after microhaemorrhage into the synovium has the same effect-a non-immune stimulation of the proliferative lesion. Perhaps an additional stimulation of collagenase production by these cells is due to iron loading resulting from ingestion of haemoglobin, haem, or iron itself. Okazaki et al. ( Lab Clin Med 1981; 97: 396) demonstrated that soluble iron in ferric form combined with nitrilotriacetate (FeNTA) was taken up by rabbit synovial fibroblasts in monolayer culture and that uptake was associated with increased production of latent collagenase and prostaglandin E2. If desferrioxamine, a specific chelator of ferric iron, was added along with FeNTA, there was no iron uptake and no induction of collagenase and prostaglandin E2 production. Thus it seems apparent that iron-loading of synovial cells can stimulate the proliferative lesion in rheumatoid arthritis. These data should be included in speculations on the role of iron in rheumatoid disease. ’
Arthritis
Center,
Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire 03755, U.S.A.
EDWARD D.
Dartmouth Medical School and Division of Digestive Diseases, V. A. Hospital White River Junction, Vermont
HERBERT L. BONKOWSKY
HARRIS, JR
13 patients experiencing diarrhoea female. Although in some of our cases diarrhoea preceded symptoms of MI, we doubt that it precipitated or contributed to the coronary event, since it never resulted in hypovolaemia or electrolyte imbalance. Most of the patients who experienced diarrhoea had inferior wall infarction. There is an increased number of vagal afferents in the inferior wall of the left ventricle. These receptors are stimulated by ventricular stretch associated with acute MI.3,4 These receptors may play a role in the bradycardia, hypotension, and vomiting’ commonly associated with diaphragmatic infarction. A similar mechanism may account for the diarrhoea. Oleske and Ciencewicki5 have suggested that faecal incontinence on admission may be a poor prognostic sign in acute MI. Only 1 of our 18 patients with diarrhoea died; thus diarrhoea, unlike faecal incontinence, does not carry a sinister prognosis.
population was female, 7 of the were
‘
Department of Medicine, Chaim Sheba Medical Centre, Tel-Hashomer, Israel *Present address: Department of Chemical Rehovot 76 100, Israel.
SIR,-Diarrhoea and the urge to defaecate are not thought of as part of the symptom complex of acute myocardial infarction (MI). In 1976 Schreder and Hardison’ drew attention to defaecation and diarrhoea as symptoms accompanying MI. In a two year period they saw six patients who experienced these symptoms; we saw five such patients in a few months. To determine the true frequency and the clinical circumstances in which urgency to defaecate and diarrhoea are presenting symptoms of MI we have done a prospective survey. 350 consecutive admissions for myocardial infarction at the TelHashomer Medical Centre were potentially eligible for our survey. They met established criteria for the diagnosis ofML2 Patients were seen during the first 24 h after the diagnosis had been established. Many patients were seen in the emergency room immediately after arrival at the hospital, one ofus being the first doctor to attend them. Patients were interviewed and examined clinically, those with any known factor predisposing to diarrhoea being excluded. 323 patients were finally included in the survey, 258 male (80%) and 65 female (20%). 84 had had a previous MI. The site of infarction was anterior in 129, diaphragmatic in 145, and subendocardial in 49. 13 patients experienced urgency to defaecate and diarrhoea during fourteen episodes of acute MI (1 had these symptoms in two episodes). The conditions under which these symptoms appeared in the original 5 patients and in the 13 patients in the prospective study are as follows. The predominant location of the MI was the diaphragmatic wall (13 out of 18 in the group with diarrhoea vs 132 out of 310 in the non-diarrhoea group). Diarrhoea preceded classical symptoms of MI in seven episodes of MI and was simultaneous with classical symptoms m the other twelve episodes. None of the 18 patients was subsequently discovered to have any other cause for the diarrhoea. Although only 20% of the survey MT, Hardison JE Chezonisus and defaecation Symptoms of acute myocardial infarction. Ann Intern Med 1976; 84: 447. Rose GA, Blackburn H Cardiovascular survey methods. WHO Monogr 1968; 56:
1 Schreeder 2.
137-54.
Immunology, Weizmann Institute of Science,
"NEW" CARDIOPULMONARY RESUSCITATION
SIR,-Dr Scott (Feb. 27, p. 504), though stressing the definition of "new" cardiopulmonary resuscitation (CPR),6 seems to have missed two important points. To develop airway pressures of 60-110 cm water requires specially preset ventilators. Most ventilators have a safety pressure relief between 60 and 80 cm water and would thus never reach the required pressure. Resuscitation bags are preset at 30-50 cm water. The synchronisation of compressions and ventilations together with a 60% compression cycle is virtually impossible manually and
requires DIARRHOEA AND URGENCY TO DEFAECATE IN ACUTE MYOCARDIAL INFARCTION
JACOB O. CHAIM* TALMA ROSENTHAL
a
computerised pneumatic piston chest-compression
described in the original papers. "New" CPR is therefore a highly specialised technique which can only be applied under predetermined conditions and with access to automated equipment.ï The increase in carotid blood flow by 252% may, as Rogers et al. pointed out, not be the best index for successful cerebral resuscitation. The blood supply to the brain is not solely from the carotid artery; the vertebrals can provide adequate cerebral circulation.8 The carotid artery supplies external as well as internal carotid arteries. A high intrathoracic pressure may result in a high intracranial pressure and a resultant decrease in net blood flow. I am therefore not optimistic about "new" CPR for the routine resuscitation in hospital. I agree with Scott that conventional basic resuscitation (expired air resuscitation/external cardiac compression) is the method of first choice. Retraining of hospital doctors in basic life support is of great importance especially in the light of Lowenstein and colleagues’ paper9showing how poor the standard has become. device
as
of Anaesthetics, Hammersmith Hospital, Royal Postgraduate Medical School, London W12 0HS
Department
D. A. ZIDEMAN
MD, Klopfenstein HS, Abbound FM, et al. Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog. Circ Res 1978, 43: 512-19 4. Felder RB, Thames MD. Interaction between cardiac receptors and sinoaortic baroreceptors in the control of efferent cardiac sympathetic nerve activity during myocardial ischemia in dogs. Circ Res 1979, 45: 728-36 5. Oleske JM, Ciencewicki MP. Fecal incontinence with myocardial infarction. N Engl J 3. Thames
Med 1979, 300: 1281. 6. Chondra V, Rudikoff M, Weisfeldt ML. Simultaneous chest compression and ventilation of high airway pressure during cardiopulmonary resuscitation Lancet 1980; i: 175-78. 7. Rogers MC, Weisfeldt ML, Trayston RJ. Cerebral blood flow during cardiopulmonary resuscitation. Anaesth Analg 1981, 60: 73-75. 8. Rapela CE, Green HB. Autoregulation of canine cerebral blood flow. Circ Res 1964.
15: 205-11 9. Lowenstein
SR, Libb LS, Mountain RC, Hansbrough JF, Hill DM, Scoggin CH Cardiopulmonary resuscitation by medical and surgical house officers. Lancet 1981, ii. 679-81.