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Biomedical subjects

K S Andersen

Publications and source records attributed to K S Andersen.

At least 19 recordsLinked to original sources
PubMed1991

[Deep accidental hypothermia with asystole. A successful treatment with heart-lung machine after prolonged cardiopulmonary resuscitation].

Extracorporeal circulation can be utilized successfully to rewarm accidental hypothermia victims. This paper describes a 51 year-old man who had been immersed in cold sea water for about 45 minutes. At the time of rescue his ECG was isoelectric. The core temperature was 27 degrees C. Cardiopulmonary resuscitation was performed for 190 minutes before extracorporeal circulation was established. Without active surface rewarming the temperature had dropped to 24 degrees C. Biventricular heart failure became evident during rewarming. Sternotomy and pericardiotomy were carried out to exclude cardiac tamponade, which was not found. After two hours of reperfusion the patient could be weaned from bypass supported by high-dose vasopressor infusion. He was extubated the following day. He was discharged after 12 days without any signs of permanent damage to organs.

Accidents↗
PubMed1990

Accidental hypothermia with cardiac arrest: complete recovery after prolonged resuscitation and rewarming by extracorporeal circulation.

A 51-year-old male remained immersed in sea water (6 degrees C) for 40 min. Brought ashore, the ECG showed asystole. Advanced life support was immediately commenced. On arrival in hospital his rectal temperature was 27 degrees C, but continued to fall to 24 degrees C. The ECG remained isoelectric. Cardiopulmonary resuscitation was continued until extracorporeal circulation was established 190 min after rescue. Upon rewarming ventricular fibrillation occurred which was converted to sinus rhythm with a bolus of lignocaine followed by D.C. conversion at 31.5 degrees C. When rewarming was complete after 60 min, signs of severe heart failure became evident. Sternotomy and pericardiotomy were performed to exclude cardiac tamponade. After 60 min of re-perfusion the patient was be weaned from bypass supported by a high-dose vasopressor infusion and nitroglycerine. He was discharged after 13 days with no evidence of any permanent organ damage. Given the advantage of providing circulatory support, extracorporeal circulation may be useful when rewarming hypothermic victims with cardiac arrest.

Extracorporeal Circulation↗
PubMed1986

Is reduced cardiac performance the only mechanism for myocardial infarct size reduction during beta adrenergic blockade?

Equal reductions in heart rate (44 beats X min-1) were obtained in cats by treatment with either the beta blocking agent timolol or alinidine, an agent claimed to cause bradycardia without interfering with beta adrenoceptor function. Infarct size was measured by staining with triphenyltetrazolium-chloride after 5 h of coronary occlusion and related to the area of hypoperfused myocardium as measured by autoradiography. Regional myocardial blood flow was measured by 15 micron radiolabelled microspheres. Compared with the control cats, in whom 87.4 (SEM 2.2)% of hypoperfused myocardium developed into necrosis, timolol reduced infarct size to 65.8 (SEM 2.6)% (p less than 0.001) and alinidine to 76.2 (SEM 3.1)% (p less than 0.01) of the hypoperfused area. Timolol reduced infarct size more than did alinidine (p less than 0.01). Necrosis was more extensive in the endocardium than in the epicardium in all groups. In the subendocardium timolol and alinidine reduced infarct size to the same extent, whereas timolol reduced infarct size more than alinidine in the subepicardium. Although heart rate proved to be the dominant haemodynamic predictor of infarct size, this study indicates that mechanisms other than reduced oxygen demand associated with bradycardia and cardiodepression are operating in the ischaemic myocardium during beta adrenergic blockade.

Animals↗
PubMed1986

Does infarct size influence loss of embolised 15-micrometer microspheres from ischaemic myocardium?

The relationship between myocardial infarct size and loss of 15-micron microspheres from ischaemic tissue was investigated in anaesthetized cats. Radioactive microspheres were injected in the left atrium before and 5 h after left anterior descending coronary artery occlusion. Left ventricular hypoperfused zone (HZ) averaged 36.6% and infarct size (IS) 31.6%. Thus, 86% of HZ evolved into necrosis. Preocclusion blood flow was lower in ischaemic (1.62 ml/min per g) compared with non-ischaemic myocardium (2.09, p = 0.002), indicating 22% microsphere loss. In ischaemic subendocardium, oedema (3.7%) could account for the apparent loss. In ischaemic subepicardium, oedema was less pronounced and 18% physical sphere loss occurred. Subepicardial loss increased in proportion to IS and IS/HZ ratio (r2 = 0.71; p less than 0.005). Non-entrapment of 15-micron spheres in coronary circulation averaged 0.6%, and preocclusion spheres appeared in coronary sinus blood throughout the ischaemic period. In systemic circulation, non-entrapment during injection of preocclusion spheres was 7.8%, but only 1.8% 5 h later. Release of postocclusion spheres took place during KCl injection. Thus, myocardial ischaemia is associated with alterations in microvascular function allowing release of entrapped 15-micron spheres. Also, the magnitude of microsphere loss per gram tissue is related to infarct size.

Animals↗
PubMed1985

Measurement of local blood flow in acute myocardial infarction: loss of 15-micron microspheres during the first hour.

Distribution of radiolabelled microspheres is widely utilized for determination of regional blood flow in experimental myocardial infarction studies. The purpose of this investigation was evaluation of the microsphere method during 1 h of regional ischaemia. Special attention was focused upon loss of preocclusion microspheres from ischaemic myocardium; mechanisms for loss and blood flow distribution in non-ischaemic left ventricle. Microspheres (15 micron) were injected into the left atrium in nine pentobarbital anaesthetized cats prior to coronary artery occlusion and again after 1 h of occlusion. Preocclusion blood flow estimates were lower in ischaemic compared with non-ischaemic myocardium (1.36 vs. 1.62 cm3 X min-1 X g-1, P = 0.002), corresponding to 16% apparent loss. In endocardial ischaemic tissue, development of oedema could account for the loss. In epicardial ischaemic tissue, oedema was not present and loss was therefore due to migration of microspheres. Epicardial loss increased in proportion to restoration of left ventricular contractility. There was no evidence for significant microsphere loss through lymphatic pathways. In non-ischaemic left ventricular tissue, myocardial blood flow was evenly distributed from apex to base, and also between endocardial and epicardial layers. This study quantitates an important limitation to measurements of local blood flow in ischaemic myocardium by radiolabelled microspheres.

Animals↗
PubMed1985

Myocardial blood flow conditions at re-perfusion following acute ischaemia.

The purpose of this study was to investigate the effect of re-perfusion upon distribution of radioactive microspheres in ischaemic myocardium. Ten anaesthetized cats were given 15-micron microspheres prior to left anterior coronary artery occlusion, at 1 h of occlusion, and after 1 h of subsequent re-perfusion. Pre-occlusion blood flow estimates were lower in tissue which had been ischaemic compared with nonischaemic regions in the same heart (1.44 versus 1.87 ml X min-1 X g-1, p less than 0.001), corresponding to 23% apparent loss. Loss also occurred in ischaemic right ventricular tissue (32%). In left ventricular ischaemic endocardium, apparent loss was due to development of oedema. Oedema was also significant in epicardial ischaemic tissue. Correction for oedema eliminated two-fifths of the loss, while three-fifths was due to physical loss. Oedema increased linearly with the level of re-perfusion. During re-perfusion, myocardial blood flow in previously ischaemic tissue was inhomogeneously distributed and, on average, 28% lower than in non-ischaemic myocardium. The 15-micron spheres appeared to pass through capillaries in the ischaemic subepicardium, but this process was not enhanced by reperfusion.

Animals↗
PubMed1983

Stability of 8-, 15-, and 26-micron microspheres entrapped in feline myocardium.

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.

Animals↗
PubMed1982

Effects of timolol on blood flow distribution in the feline myocardium with acute regional ischaemia during controlled haemodynamic conditions.

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.

Animals↗
PubMed1981

Pulmonary circulation and loss of microspheres from the lung following acute pulmonary venous occlusion.

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.

Animals↗