Mercuric chloride and, to a lower extent, nickel sulfate, stimulated DNA synthesis of both thymocytes and peripheral blood lymphocytes. The metal allergens stimulated both celltypes at a lower degree than lectinic mitogens (PHA, Con A and PWM) did. In peripheral blood lymphocytes the stimulation degree was higher than in thymocytes after addition of metal allergens as well as lectinic mitogens. The presence of serum seemed to have a protective and potentiating role regarding the effect of mercuric chloride and lectinic mitogens, the effect of nickel sulfate being mainly unchanged. With increasing age of the individuals, an increase in the stimulation degree with mercuric chloride and lectinic mitogens was indicated, while nickel sulfate gave a decrease.

No abstract

Twenty cases of failing transcervical thymectomy are reported. They were selected for transsternal re-exploration from a series of 95 patients who had previously undergone transcervical thymectomy because of myasthenia gravis (MG). A specific method for pre-operative detection of remnants of the non-tumorous thymic gland is lacking, but the applied clinical selection criteria were so far reliable: generalized, disabling, fluctuating MG despite cholinesterase inhibitor and/or immunosuppressive treatment, and no or inconsistent improvement after transcervical thymectomy. At transsternal re-exploration the commonest findings were intact lower thymic lobes with persistent venous drainage into the brachiocephalic vein. Presence of thymic tissue was histologically confirmed in all the excised specimens (weight range 10-60, mean 23 g), and the examination showed thymic hyperplasia in 18 cases, fatty involution of the gland in two, and a lympho-epithelial thymoma in one case. The re-operation was followed by objectively registrable improvement in all but one of the 20 patients during observation periods of 8-75 (mean 21) months. There was statistically significant reduction in disability scores (means 8.2-4.9) and in need for anticholinesterase medication (to 67% of pretreatment dose). Immunosuppression became unnecessary in 6 of 11 patients and could be reduced in 4 patients. The incidence of failure in transcervical thymectomy was alarmingly high (27%), and more re-operations are anticipated. Since the transcervical approach involves a high risk of incomplete thymectomy, its use should be abandoned. However, in most of the patients with re-operation, subsequent progress has been sufficiently promising for advocacy of sternotomy whenever the clinical criteria of failure are fulfilled.

Early patency (two weeks) of 331 aortocoronary vein grafts was 89%. Late patency (one year) of 122 restudied grafts was 80%. A cumulative one year patency of 72% was calculated. Patency was similar for SV grafts, sutured distal to stenosis and segmental obstruction. Early patency was significantly decreased when the peroperative graft blood flow was 20 ml/min or less or the diameter of the recipient coronary artery was smaller than 1.5 mm. Cumulative one year patency was lower in symptomatic patients (54%) than in those who underwent consecutive reevaluation (80%). There was a trend towards improved patency rates for graft anastomosed to the left anterior descending coronary artery and grafts without pre-existing pathological changes. Patient parameters, such as at operation, sex, smoking habits, hypertension, lipid abnormalities, diabetes, previous myocardial infarction or depressed left ventricular function, had no bearing on patency. Graft failure occurring, despite refined surgical technique, is usually due to pathological changes of the vein graft per se or the recipient coronary artery and its vascular bed.

In the clinical setting great efforts have been made with contradictory results to operate upon acutely myocardial ischaemic patients. The reasons for the absence of clear-cut results are not well understood nor are they scientifically explored. To resolve this problem further, we attempted to design an experimental in vivo model to mimic acute myocardial ischaemia followed by extracorporeal circulation (ECC) and reperfusion. One of the main targets of our protocol was monitoring of myocardial energy metabolism by microdialysis (MCD) during the periods of coronary occlusion (60 min), hypothermic (30 degrees C) ECC and cardioplegia (45 min), followed by reperfusion with (30 min) and without (60 min) ECC. In eight anaesthetized, open-chest pigs, myocardial lactate, pyruvate, adenosine, taurine, inosine, hypoxanthine and guanosine were sampled with MCD in both ischaemic and non-ischaemic areas. Myocardial area at risk and infarct size were quantified with the modified topographical evaluation methods. The principal finding with this experimental setup was a biphasic release pattern of lactate, adenosine, taurine, inosine, hypoxanthine and guanosine from ischaemic myocardium. Lactate levels were equally high in reperfused ischaemic and non-ischaemic myocardial tissue. Pyruvate demonstrated consistently higher values in non-ischaemic myocardium throughout the experiment. A pattern was discernible, lactate being a marker of compromised cell energy metabolism, and taurine being a marker of disturbed cell integrity. Of special interest was the increased level of pyruvate in microdialysates of non-ischaemic myocardium as compared with its ischaemic counterpart. In conclusion, we found disturbances in energy metabolism and cell integrity not only in ischaemic but also in non-ischaemic tissue during reperfusion implying that non-ischaemic myocardium demonstrated an unexpected accumulation of lactate and pyruvate. These new findings could at least partly be explicatory to the increased risk of heart surgery in connection with acute myocardial infarction.