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K Andersen

Publications and source records attributed to K Andersen.

At least 181 records · Page 10Linked to original sources
PubMed1983

Private violence.

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Child Abuse↗
PubMed1983

Intramyocardial temperature following various cooling procedures.

In 12 dogs on cardiopulmonary bypass, the intramyocardial temperatures in the anterior and the posterior wall of the left ventricle and in the septum were measured with microthermoelectrodes when different cooling procedures were used during 60 min of anoxic cardiac arrest. External cooling with 4 degrees C glucose (5.5%) solution dripping into the pericardial sac did not lower the temperature in the septum or in the posterior wall. Packing the heart in slushed ice after injection of the same glucose solution into the coronary tree reduced the septum and posterior wall temperature to around 30 degrees C. This cooling procedure, in combination with general moderate hypothermia, lowered the temperature to about 20 degrees C in these parts of the heart. Only when combined with general hypothermia did local cooling achieve low temperatures in all regions of the myocardium.

Animals↗
PubMed1983

Myocardial preservation during anoxic arrest. Chemical cardioplegia.

Two types of cardioplegic solution--the potassium arrest and the Bretschneider solution, both at 4 degrees C--were compared with regard to protective effect against ischemic damage during 60 min of anoxic cardiac arrest in the dog heart. Both solutions provided equally good protection, which was superior to that given by hypothermia alone.

Animals↗
PubMed1983

Myocardial preservation during anoxic arrest. Premedication with propranolol, verapamil or methylprednisolone.

Anoxic cardiac arrest was studied for one hour in five groups of dogs. Groups I-III were given methylprednisolone (30 mg/kg b.w.) before aortic cross-clamping. Normothermia was used with electrically induced ventricular fibrillation in group I, and without such fibrillation in group II, while group III was studied in local hypothermia. Propranolol (10 micrograms/kg) was given to group IV and verapamil (0.2 mg/kg) to group V before the anoxic arrest in local hypothermia. Judged from the ability of the heart to take over the circulation after anoxic arrest, local cooling preceded by propranolol or verapamil gave working performance comparable with the pre-arrest values. In the cooled, steroid-pretreated hearts the work capacity was depressed to the same degree as in locally cooled hearts without steroid premedication. Methylprednisolone prevented ischemic contracture during normothermic arrest with induced fibrillation, but not in the absence of such fibrillation. As adjuvant to local cooling, pretreatment with metabolism-reducing drugs is favorable for cardiac performance after arrest. Steroid premedication should be considered when normothermic arrest with electrically induced ventricular fibrillation is planned.

Animals↗
PubMed1982

Can left main or proximal left anterior descending coronary artery disease be assessed by non-invasive means?

One hundred consecutive patients with angina pectoris referred for coronary arteriography were studied prospectively for non-invasive assessment of left main (LMCA) or proximal left anterior descending coronary artery (proximal LAD) disease. Evaluation of echocardiographic interventricular septal motion, history and exercise test response could not identify the patients with these specific lesions. It is concluded that LMCA and proximal LAD disease still remain largely unpredictable by non-invasive means.

Adult↗
PubMed1982

Role of the Frank-Starling mechanism during maximal semisupine exercise after oral atenolol.

Reproducible left ventricular dimensions were found by M-mode echocardiography in eight healthy men in the semisupine position during two maximal bicycle exercise tests, performed with four hours interval. Left ventricular end-diastolic dimension did not increase during maximal exercise, while fractional shortening increased by a decrease in end-systolic dimension. Twelve men studied by the same procedure were given 100 mg atenolol orally just after the first test which conspicuously reduced their heart rate response to exercise. End-diastolic dimension increased significantly from rest to peak exercise after the administration of atenolol in contrast to that before beta blockade, and fractional shortening at maximal exercise increased compared with the preceding control test. We conclude that atenolol changes the left ventricular response to maximal semisupine exercise in normal man, with dilatation and a concomitant increase in systolic myocardial shortening. This suggests that atenolol during maximal exercise reveals the part played by the Frank-Starling mechanism in cardiac reserve. In addition to that mechanism, the increased ventricular emptying is probably also the result of reduced afterload after administration of atenolol.

Adult↗
PubMed1982

Myocardial preservation during anoxic arrest. Experimental model ventricular fibrillation.

An experimental model with anaesthetized healthy mongrel dogs on extracorporeal circulation is described. Anaesthesia and cardiopulmonary bypass are the same as used in clinical practice. Various methods of myocardial preservation were investigated and their protective effect was judged by cardiac performance after termination of 60 min of anoxic arrest. In this study, the first part of an experimental series, electrically-induced fibrillation during 60 min of normothermic and local hypothermic anoxic arrest was investigated. In group I, the hearts were fibrillated immediately after cross-clamping. In group II, which served as controls, the hearts were allowed to fibrillate spontaneously after aortic cross-clamping. All the hearts in group I went into an ischaemic contracture, whereas those in group II showed a 50% recovery, but with a strongly reduced cardiac performance after termination of anoxic arrest and cardiopulmonary bypass. Measurements of myocardial surface pH demonstrated a rapidly developed acidosis during the period of anoxic arrest. The most impressive finding by light microscopy was pronounced myocardial oedema. External cooling by 4 degrees C glucose 5.5% continuously flushed into the pericardial sac in combination with electrically-induced fibrillation proved to be ineffective as a protective method. None of the eight dogs in this group survived. External cooling combined with intraventricular injection of 4 degrees C glucose 5.5% seemed to protect the hearts against ischaemic damage, insofar that all six hearts in this group were able to take over the circulation after declamping. The working capacity was, however, impaired and a relatively long period of mechanical support and stimulation with inotropic drugs was necessary.

Animals↗