[Surgical technical procedures in gastroenterologic and endocrine surgery].
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Biomedical subjects
Publications and source records attributed to K S Andersen.
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The stability of 8-, 15-, and 26-micron radioactive microspheres entrapped in ischemic and nonischemic myocardium and possible mechanisms for microsphere loss were investigated. Anesthetized cats were given microspheres prior to left anterior descending coronary artery occlusion (or sham operation) and 8 h later. Eight-micron microspheres, compared with 15-micron spheres, underestimated preocclusion myocardial blood flow in ischemic and nonischemic tissue by 30%. With 26-micron spheres, endocardial-to-epicardial blood flow ratio was 1.28. In nonischemic tissue, no loss of 15- and 26-micron microspheres occurred during 8 h. In ischemic myocardium, however, 15% apparent loss of 15- and 26-micron preocclusion spheres took place. In endocardial ischemic tissue, edema could account for 50% of the 15-micron microsphere loss and almost completely for loss of 26-micron spheres. In epicardial ischemic tissue, microsphere loss was not influenced by edema. We found no hemodynamic variable that could predict the magnitude of microsphere loss. Only weak evidence for migration of 15- and 26-micron microspheres through lymphatic pathways was found. Most likely the spheres migrated through venous pathways to embolize in the lungs. We conclude that 15-micron microspheres provide the most reliable tissue blood flow estimates in normal myocardium, but even for these spheres significant loss occurs during 8 h of ischemia.
The beta-adrenergic blocking agent timolol was given to cats with acute coronary artery ligation under controlled haemodynamic conditions. Regional myocardial tissue flow was measured by the distribution of labelled microspheres. Timolol reduced cardiac contractility and left ventricular end-diastolic pressure rose, whereas heart rate and ventricular systolic pressure were kept constant by atrial pacing and aortic clamping. The systolic period increased following timolol administration under these conditions. Myocardial blood flow remained unchanged in central ischaemic and border areas, whereas flow increased both endocardially and epicardially in normally perfused area following timolol administration. Without pacing there was a significant flow reduction in the epicardium of the normally perfused area, compared with the situation where heart rate was constant. Under controlled haemodynamic conditions, therefore, timolol appears to improve coronary perfusion in normal myocardium, whereas blood flow to ischaemic myocardium remains essentially unchanged.
The pulmonary vein from right upper lobe was ligated in 15 rats while 15 others served as controls. Prior to occlusion, 15 mum microspheres were injected into the superior caval vein. Another population of 15 mum microspheres was similarly given 1 min, 10 min or 30 min after ligation. All rats were killed 5 min after the second microsphere injection. The weight of the ligated lobe was 63% higher than that of the controls. This was probably due to acute vascular congestion since no significant oedema developed. Increased weight caused a reduction in the number of preocclusion microspheres per gram of tissue in the ligated lobe. In addition a gradual loss of preocclusion microspheres took place following pulmonary venous ligation. After 35 min of ligation, 30% of the preocclusion spheres had disappeared from the ligated lobe. Postocclusion flow through the pulmonary artery into right upper lobe was estimated by microspheres from the second injection, and averaged 5% of normal flow. Following acute venous occlusion, a rapid dilatation of the bronchopulmonary communicating system probably takes place. By reversal of the flow in this system, blood and microspheres can be drained into the bronchial venous circulation. In spite of methodological problems caused by acute congestion and loss of microspheres after pulmonary venous occlusion, we consider the microsphere method to be useful for further studies of collateral lung circulation.
The beta-adrenergic blocking agent timolol was given to cats with acute coronary artery ligation. Regional myocardial tissue flow was measured by the distribution of 15 micrometers labelled microspheres. Timolol reduced heart rate, cardiac contractility and left ventricular systolic pressure, but end-diastolic pressure rose. Ischaemic tissue blood flow remained unchanged following timolol, thus improving the marked imbalance between oxygen demands and delivery. In normal areas of the myocardial tissue flow was reduced, indicating the beta 2-adrenergic blocking effect of timolol. This was also the case for the border area between ischaemic and non-ischaemic tissue, but significantly less flow reduction was found on the endocardial side than on the epicardial side in the border area. Except for this latter observation, timolol does not appear to improve coronary perfusion. The present study, therefore, indicates that beneficial effects of timolol on ischaemic myocardium are mainly related to a reduction of myocardial oxygen demand.
The fate of 15 micrometers microspheres in ischaemic myocardial tissue was investigated. The spheres were delivered to the left atrium before acute coronary artery ligation. 10 h later the myocardium was examined for its contents of preocclusion spheres, as well as spheres delivered immediately before sacrifice. The ischaemic tissue contained 11 to 60% less preocclusion spheres, compared with nonischaemic tissue in the same hearts. On average, 26% of preocclusion spheres were lost during the 10 h period. Negligible amounts of the lost spheres could be retrieved from cardiac lymph nodes in the mediastinum. Most likely, the spheres migrated through venous pathways; a substantial number of preocclusion spheres were present in the lungs after 10 h, the bulk of which had originated from other organs than the infarct. These results quantify an important limitation to the use of microsphere distribution as a method for tissue blood flow measurements in infarcted myocardium when the period of coronary artery occlusion exceeds a few hours.
cis-Diamminodichloroplatinum(II) (cis-PDD) and diaquoethylenediamineplatinum(II) induce histidine revertants in Salmonella typhimurium strains TA98 (frame-shift mutation) and TA100 (base-pair substitution mutation). A linear dose--response relationship is found with cis-PDD acting on TA98 and TA100. Salmonella typhimurium strains TA1535, TA1537 and TA1538 are not sensitive to the mutagenic action of cis-PDD. All 5 strains are sensitive to the toxic effect of cis-PDD. Platinum(II) complexes induce mutations (frame-shift or base-pair substitution) only in strains carrying the R-factor plasmid.
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On the basis of 21 cases of congenital pseudarthrosis of the tibia, which were radiologically typed and later personally examined, it was found that all cases of the dysplastic type also showed evidence of neurofibromatosis. No evidence of neurofibromatosis was found among the cystic and the clubfoot type of pseudarthroses.
Forty-six patients with congenital pseudarthrosis of the leg were followed for twelve years or more. Forty of these patients were examined, interviewed, or both from 1974 to 1975. Congenital pseudarthrosis is a condition most often combined with neurofibromatosis. In neurofibromatosis the prognosis of the pseudarthrosis is dependent on the roentgenographic type. Of the procedures used, insertion of intramedullary rods and grafting gave the highest rate of union. Atrophy, shortening, valgus deformity, and limited range of motion complicated the functional results.
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