Case report: an alternative approach to stenting the obstructed ureter.
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Biomedical subjects
Publications and source records attributed to R W Thomson.
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In a randomized controlled clinical trial single dose antibiotic prophylaxis (gentamicin 80 mg IV) was evaluated in 36 patients with indwelling urethral catheters undergoing transurethral prostatic resection. Prophylaxis resulted in a significant reduction in postoperative bacteriuria (P less than 0.01), pyrexia (P less than 0.001), bacteraemia (P less than 0.01) and septicaemia (P less than 0.05). During the same period there was one case of postoperative bacteriuria but no systemic infection in 25 consecutive patients undergoing elective prostatectomy with no local risk factors and in the absence of prophylaxis. A policy of selective antibiotic prophylaxis is justified and in high risk patients with in-dwelling catheters single dose prophylaxis is highly effective.
As a preliminary to establishing a frozen valve bank for replacement surgery, the possible effects of the proposed freezing and thawing procedure on tissue structure were assessed in 16 human pulmonary valves removed from cadavers at necropsy and nine dog valves obtained fresh. The valves were frozen and stored in liquid nitrogen for intervals ranging from 23 to 380 days. Blocks of tissue cut from the central area of one leaflet, and including some adjacent arterial wall and ventricular myocardium, were obtained both before freezing and after thawing and examined by a large specimen resin embedding technique for light and electron microscopy, with histochemical staining for matrix material. Control and thawed tissue from all valves appeared similar, indicating good preservation irrespective of storage time. Fine structural alterations in the cellular elements correlated with the total interval of autolysis (from death to freezing) rather than the cause of death or other variables and were not uniform in any of the specimens.
Eighty isolated rat heart preparations were used to study relationships among creatine kinase (CK) release, the loss of vascular competence (no-reflow), and the distribution of morphological changes across the left ventricular wall which occur during 60 min global ischaemia or anoxia and following subsequent oxygenated reperfusion. Hearts were either fixed with glutaraldehyde for light and electron microscopy or were injected with 1% fluorescein to define the distribution of perfusable vessels. The extent of no-reflow in half of the hearts was reduced experimentally by maintaining the diastolic volume of the left ventricular lumen during ischaemia and anoxia with a water-filled balloon. The amount of CK released during 20 min of reoxygenation or reperfusion was inversely proportional to the extent of the no-reflow area observed just prior to reoxygeneration, and also reflected the transmural extent and the severity of myocardial cell damage. Extensive contraction band necrosis was only observed in reperfused regions of anoxic hearts. In isovolumic hearts reoxygenation caused no-reflow to develop in the ventricular myocardium, and this appeared to be associated with hypercontraction. Thus the no-reflow phenomenon has a profound effect on the transmural distribution of myocardial cell damage and enzyme release which follows post ischaemic reperfusion and post anoxic reoxygenation.
To investigate the pathogenesis of the reperfusion defect which develops in ischaemic myocardium, intravascular casts were prepared by injection of methyl methacrylate into the coronary arteries of isolated heparinised rat hearts. Using a scanning electron microscope, the vascular morphology following 60 min of global ischaemia at 37 degrees C was compared to that of non-ischaemic control hearts injected immediately after stopping perfusion with oxygenated Krebs-Henseleit buffer. Complete casts were obtained from control hearts and from all parts of ischaemic hearts except the subendocardial half of the left ventricular wall of ischaemic hearts where the blood vessels were not filled. At the border between the perfused subepicardial and unperfused left subendocardial regions, the resin which filled the radial penetrating arteries and their branches projected from the filled capillary plexus to an extent proportional to their diameter. Intravascular events such as erythrocyte plugging and thrombosis were excluded as causative factors by the use of a cell-free perfusate. Also, there was no morphological evidence that endothelial cell swelling or constriction of any particular population of vessels was involved. The observed pattern of vascular occlusion suggests that, during global ischaemia, blood vessels in the endocardial half of the left ventricular myocardium lose their ability to be reperfused because of extravascular compression.
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During global ischemia in isolated rat hearts, the development of contracture, due to irreversible myofilament sliding, causes reduction of left ventricle luminal volume. Also, a considerable area of the myocardium cannot be reperfused after 1 hour's global ischemia. The purpose of this study was to reduce myofilament sliding by placing a fluid-filled isovolumic balloon in the left ventricular cavity of isolated rat hearts and assess the extent of reflow, after 60 minutes' ischemia, by perfusion of a 1% fluorescein tracer solution. Light and electron microscopy was used to determine the state of the vasculature and myofibrillar apparatus. In hearts without the left ventricular balloon (control) the ischemia produced a no-reflow zone comprising 45% of the myocardial wall. In contrast, if an isovolumic balloon was in place during the ischemic period, only 6% of the wall was involved. The volume of the capillary bed in the subendocardium of the control hearts was about 60% of that in th isovolumic hearts. In the isovolumic ("isometric") mode, ischemic contracture was associated with more severe myocardial cell injury than in the corresponding control ("isotonic") mode. Our results support the concept that intramyocardial pressure generated by ischemic contracture plays a major role in the production of the no-reflow phenomenon in globally ischemic rat hearts, and indicate that it is the series elastic component of cardiac muscle which imparts the stiffness necessary to prevent reopening of coronary vessels after a severe ischemic insult.
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Experimental myocardial ischaemia was induced in 12 anaesthetized mongrel dogs by ligation of the circumflex branch of the left coronary artery. Twenty minutes after ligation 1% sodium fluorescein injected into the artery distal to the ligature evenly perfused the left ventricular wall in the vicinity of the posterior papillary muscle (PPM) but, when injected 90 minutes after ligation, the PPM and adjacent subendocardial myocardium was not perfused by this tracer. Measurements with a linear variable transducer and standard load demonstrated that after 20 minutes ischaemia, the PPM had a similar percentage compressibility to the corresponding unaffected anterior papillary muscle but, after 90 minutes, the compressibility of the PPM was significantly reduced. Scanning electron microscopy of the marginal zone between the perfused and unperfused parts of the myocardium revealed many collapsed vessels which contained small groups of tightly packed erythrocytes indicating that the loss of vascular competence was probably due to the plugging of small vessels by erythrocytes.
The Cattell 16 Personality Factor Questionnaire was administered to 20 Ss from Montana and the personality scores compared to those of a similar sample of New Zealand students. Results indicated that cross-cultural differences do exist, the present group being more dominant, less expedient, and considerably more conservative than their New Zealand counterparts.
Initial experience with side-to-side anastomosis of the brachial artery to the median cubital vein is reported in 11 patients in whom it was impossible to use or continue using the more normal sites. Eleven patients have so far been dialysed for a total of 80 fistula months. There was one early failure and no late ones. The appreciable morbidity was considered acceptable in these otherwise difficult patients.
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The urinary excretion of fibrin/fibrinogen degradation products (F.D.P.) of 81 human cadaver kidney transplants has been measured serially by the techniques of tanned red cell haemagglutination inhibition immunoassay and immunonephelometry. Acute rejection episodes in functioning transplants have been associated with increased F.D.P. excretion which in 80% of cases has preceded clinical diagnosis by periods of one to seven days. Recovery from these episodes has been associated with a rapid fall of F.D.P. excretion to undetectable levels. The level of F.D.P. excretion during a rejection episode is a guide to its ultimate outcome. Irreversibly rejected kidneys excrete high levels of F.D.P. for long periods. Viable kidney transplants with prolonged oliguric phases can be distinguished, while still oliguric, from rejected kidneys by their low F.D.P. excretion. F.D.P. cannot usually be detected in the urine of well-functioning transplants. Episodes of raised F.D.P. excretion in the absence of acute clinical rejection, however, occur occasionally and may be associated with permanent impairment of renal function.
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