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Biomedical subjects

M Molaug

Publications and source records attributed to M Molaug.

12 recordsLinked to original sources
PubMed1990

[Death assistance and terminal care--at the hospital].

Euthanasia, i.e. active termination of life in a seriously ill patient, is not performed in Norway at present. Between active and so-called passive euthanasia there is a "grey zone", and it is discussed where the border should be drawn, how and by whom. The decision to treat or not is becoming increasingly difficult, due to technical advances in the development of life-supporting devices. There is increasing sympathy for the view that it is not the duty of the medical profession to prolong the life of patients under all circumstances. The present paper discusses such problems in relation to hospitalized patients in an acute life-threatening situation, and in patients with, known, chronic disabling, or malignant disease.

Euthanasia↗
PubMed1990

Changes in cardiac dynamics by opening an interventricular shunt in dogs.

Changes in right and left ventricular (RV, LV) dynamics caused by an interventricular shunt were examined in open-chest dogs. At a pulmonary to systemic blood flow ratio of 1.7 +/- 0.2 pulmonary flow increased by 53 +/- 13%, whereas aortic flow decreased by 9 +/- 2%. Shunt flow was continuous from the left to the right ventricle throughout the cardiac cycle, but 72 +/- 4% took place during the LV ejection phase. Peak systolic LV pressure declined by 6 +/- 3 mm Hg, LV end-diastolic segment length (SL) rose, and systolic shortening of the SL increased. Peak systolic RV pressure rose from 28 +/- 3 to 36 +/- 3 mm Hg and RV end-diastolic and end-systolic SL rose almost equally. Accordingly, RV systolic SL shortening did not rise despite the substantial augmentation in RV outflow. The transseptal end-diastolic pressure gradient did not rise, while the transseptal peak systolic gradient decreased when the shunt was opened. Similarly directed alterations were observed when the shunt was opened at different preloads and when the shunt flow was varied. Local work in the anterior wall of the right ventricle (calculated from the RV pressure SL loop) rose by 26 +/- 4%, whereas RV stroke work (product of mean systolic right ventricular pressure and pulmonary flow) rose by 57 +/- 12%; difference, P less than 0.05. LV stroke work and local work in anterior LV free wall rose in proportion when the shunt was opened.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Dynamics of the interventricular septum and ventricular free walls during regional ischaemia in open-chest dogs.

The significance of ischaemia of the left ventricular (LV) and right ventricular (RV) free walls for the dynamics of the interventricular septum (IVS) and the right ventricle was examined in open-chest dogs. Left ventricular and RV ischaemia reduced stroke volume similarly, by 11.2 +/- 1.4% and 11.2 +/- 2.4%, respectively. The dynamics of myocardial segment lengths (SL), recorded in the LV and RV free walls and the IVS, differed. During LV ischaemia, end-diastolic SL (EDSL) and systolic shortening (SS) increased in the IVS, whereas SL remained unchanged in the RV free wall. During RV ischaemia, LV EDSL, and SS decreased. Interventricular septum EDSL also decreased, but this reduction was not statistically significant. During blood volume expansion, LV and RV function curves were shifted right, and/or downwards by LV ischaemia, whereas only the RV function curve was shifted downwards and to the right by RV ischaemia. Thus, ischaemia of the LV free wall induces activation of the Frank-Starling mechanism in the interventricular septum and a deterioration of right ventricular performance.

Animals↗
PubMed1986

Angiotensin II infusion during beta-adrenergic stimulation by isoproterenol. Effects on hepatic, splenic and cardiac blood volumes and on the magnitude and distribution of cardiac output in the dog.

The cardiac and peripheral vascular adjustments to angiotensin II (0.1-0.2 microgram kg-1 min-1 i.v.) during high beta-adrenergic activity by a continuous isoproterenol infusion (0.2-0.3 microgram kg-1 min-1 i.v.) were examined in anaesthetized, atropinized dogs. Hepatic, splenic and left ventricular (LV) volume changes were estimated by an ultrasonic technique, and the blood flow distribution was measured by injecting radioactive microspheres and by electromagnetic flowmetry on the caval veins, the hepatic artery and the portal vein. During isoproterenol infusion, angiotensin II increased the systolic LV pressure by 45 +/- 3 mmHg and the stroke volume by 17 +/- 6%. Concomitantly, the hepatic and splenic blood volumes declined by 29 +/- 4 and 14 +/- 6 ml, respectively, and the LV end-diastolic segment length increased by 3 +/- 1%. The flow through the inferior caval vein increased by 39 +/- 9%, whereas the superior vena caval flow remained unchanged. The hepatic arterial flow more than doubled. Thus, at high inotropy by isoproterenol infusion, angiotensin II relocates blood from the liver and the spleen towards the heart. By activating the Frank-Starling mechanism, cardiac output is increased and conducted through the lower body, especially through the hepatic artery, because of the poor autoregulation of flow through this vessel.

Adrenergic beta-Agonists↗
PubMed1984

Compensatory cardiac mechanisms evoked by acute occlusion of the right coronary artery in dogs.

The cardiac response to intermittent occlusion of the right coronary artery was examined in anesthetized open-chest dogs at different levels of blood volume. The reduction in stroke volume averaged 15 +/- 2% and was related to the extent of the ischemic area (r = 0.72), which comprised 45-70% of the free wall of the right ventricle. Ultrasonic recordings of segment lengths showed end-diastolic distention and activation of the Frank-Starling mechanism in the uninjured parts of the free wall. The transseptal end-diastolic pressure difference was abolished, suggesting movement of the interventricular septum to the left. Nevertheless, the relationship between stroke volume and left ventricular end-diastolic pressure (left ventricular function curve) as well as the relationship between stroke volume and the end-diastolic segment length of the left ventricular free wall were unaltered. Comparisons of data obtained at similar stroke volume showed activation of the Frank-Starling mechanism in the interventricular septum which may compensate for the negative effect of a change in its position.

Animals↗
PubMed1984

Cardiopulmonary blood volume during acute blood pressure elevations in dogs.

During aortic blood flow obstructions and angiotensin infusion blood may be accumulated in the heart and the lungs because of retention or redistribution of blood from compliant regions. We measured the cardiopulmonary blood volume (CPBV) when left ventricular systolic pressure was raised by about 50 mmHg by angiotensin infusion and by balloon inflation in the ascending and descending thoracic aorta, at control inotropy and during isoproterenol infusion, in 6 anesthetized, closed-chest dogs. CPBV was calculated from determinations of cardiac output (thermodilution) and the interventricular mean transit time of ascorbate (polarographic determination). Angiotensin always increased CPBV, but the rise was greater at high than at control inotropy (16.5 +/- 4.4% and 5.1 +/- 1.2%). Balloon inflation in the descending thoracic aorta increased CPBV similarly at high and control inotropy (11.1 +/- 2.4% and 16.6 +/- 4.0%) whereas CPBV was unaltered or fell during inflation in the ascending aorta at both inotropic levels. Right and left ventricular end-diastolic pressures rose only during angiotensin infusion and balloon inflation in the descending thoracic aorta. By balloon inflation, cardiac output only fell during blood flow obstruction in the ascending aorta. Thus, an increase in CPBV during these interventions is not due to retention but is caused by redistribution of blood towards the heart.

Angioplasty, Balloon↗
PubMed1983

Compensatory cardiac mechanisms evoked by septal ischemia in dogs.

To examine the cardiac responses to selective septal ischemia, the septal artery was occluded intermittently in anesthetized open-chest dogs. Myocardial segment length was recorded continuously by an ultrasonic technique in the interventricular septum and the right and left ventricular free walls. At left ventricular end-diastolic pressure of 3.0 +/- 0.6 mm Hg, occlusion of the septal artery increased left ventricular end-diastolic segment length by 3.9 +/- 0.9% and stroke volume was maintained. After blood volume expansion to a left ventricular end-diastolic pressure of 7.2 +/- 1.4 mm Hg, occlusion of the septal artery did not increase end-diastolic dimensions and stroke volume decreased significantly but by less than 10%. At all levels of blood volume expansion, occlusion of the septal artery did not alter significantly the end-systolic segment length of the free wall of the left ventricle and the dimensions of the free wall of the right ventricle. The distance between the septum and the right ventricular free wall was unchanged in end-diastole and reduced in end-systole after occlusion of the septal artery. These observations indicate paradoxical movement of the ischemic septum. The ischemic septum seems to act as a passive diaphragm pump on the right ventricle without activation of the Frank-Starling mechanism in uninjured areas. In the left ventricle, the Frank-Starling mechanism is fully exploited with unaltered end-systolic dimensions of the uninjured myocardium because of the systolic bulging of the ischemia septum.

Animals↗
PubMed1983

Dynamics of the interventricular septum and free ventricular walls during selective left ventricular volume loading in dogs.

A previous study suggests that a change in the position of the interventricular septum played an important role in regulating cardiac performance during selective right ventricular volume loading. In the present study the cardiac response to selective left ventricular volume loading induced by a shunt between the subclavian artery and the left atrium was examined in anesthetized open-chest dogs. Opening the shunt increased left and reduced right ventricular stroke volume, particularly after blood volume expansion. The end-diastolic transseptal pressure difference increased. Myocardial segment length in the septum and free walls of both ventricles and the distances between the septum and the free walls were measured by an ultrasonic technique. Comparisons at similar left ventricular stroke volume with the shunt open and closed showed that the Frank-Starling mechanisms of the free wall of the left ventricle and the septum were stimulated less with the shunt open. At similar right ventricular stroke volume the end-diastolic dimension of the right ventricular free wall was larger with the shunt open. The distance decreased across the right ventricle and increased across the left ventricle when the shunt was open. We conclude that a change in the position of the septum improves left and reduces right ventricular performance during selective left ventricular volume loading.

Animals↗
PubMed1982

Dynamics of the interventricular septum and free ventricular walls during blood volume expansion and selective right ventricular volume loading in dogs.

To examine whether the right ventricle responds differently to blood volume expansion and selective right ventricular volume loading, segment lengths in the interventricular septum and the free walls of both ventricles and right ventricular septal-to-free-wall-distance were measured by an ultrasonic technique in open-chest dogs. Blood volume expansion increased segment lengths at all recording sites in proportion to stroke volume. Selective right ventricular volume loading induced by opening a shunt between the pulmonary artery and the superior vena cava increased right ventricular stroke volume by 40-80%; end-diastolic segment length and myocardial shortening increased in the septum and free wall of the right ventricle whereas left ventricular stroke volume and segment length decreased. Comparison of data obtained before and after opening of the shunt indicated that changes in myocardial dynamics of the right ventricle and septum accounted for approximately 30% of the increase in right ventricular stroke volume. However, both end-diastolic dimension and systolic shortening of the right ventricular septal-to-free-wall distance were larger during right ventricular volume loading than during blood volume expansion. Thus, most of the increase in stroke volume during selective right ventricular volume loading is caused by a change in the configuration of the right ventricle.

Animals↗
PubMed1981

Cardiac effects of splanchnic and non-splanchnic blood volume redistribution during aortic occlusions in dogs.

Translocation of blood from the lower body dilates the left ventricle during occlusion of the descending thoracic aorta and by increased activation of the Frank-Starling mechanism, stroke volume is maintained despite raised aortic blood pressure. The contributions from the splanchnic and non-splanchnic blood volumes to the left ventricular dilation were examined by ultrasonic measurements of myocardial chord length (MCL) in atropinized open-chest dogs. End-diastolic MCL rose by 2.5 +/- 0.9% during abdominal suprarenal aortic occlusion, draining blood from the non-splanchnic region, and by 7.4 +/- 1.7% during thoracic aortic occlusion draining blood from both splanchnic and non-splanchnic regions. Systolic left ventricular pressure rose by 16 +/- 3 mmHg and 76 +/- 12 mmHg, respectively. End-diastolic MCL rose by 6.0 +/- 1.2% during combined thoracic aortic and abdominal infrahepatic vena cava occlusion draining blood solely from the splanchnic region and further by 2.5 +/- 0.8% by blood drained from the non-splanchnic region after release of the vena cava occlusion. Similar results were obtained using a shunt permitting selective drainage first from the non-splanchnic region during thoracic aortic occlusion. Blood translocation from the non-splanchnic region maintains cardiac output during abdominal aortic occlusion. During occlusion of the thoracic aorta, drainage from the splanchnic region accounts for about 70% of the increase in end-diastolic MCL.

Animals↗
PubMed1981

Myocardial function of the interventricular septum. Effects of right and left ventricular pressure loading before and after pericardiotomy in dogs.

We examined the function of the interventricular septum in six open-chest dogs by inserting piezoelectric crystals into the interventricular septum. Continuous ultrasonic recordings showed that the changes in myocardial chord length (MCL) in the septum and free walls of the right and left ventricle were similar during saline infusion and during pericardiotomy. End-diastolic MCL and myocardial shortening during ejection (MS) rose in the septum and free walls of both ventricles during saline infusion as end-diastolic MCL and MS in the septum and free walls of the ventricles, and reduced end-diastolic pressures by 1-2 mm Hg. The responses to aortic and pulmonary artery constrictions were similar before and after pericardiotomy. When aortic constriction had raised free left ventricular systolic pressure by about 60 mm Hg, end-diastolic MCL increased in the septum and free left ventricular wall, whereas end-diastolic MCL and MS of the free right ventricular wall fell. Pulmonary artery constriction increased end-diastolic MCL in the free right ventricular wall and reduced end-diastolic MCL and MS in the septum and free left ventricular wall. Thus, the myocardium, including the interventricular septum, is uniformly expanded during saline infusion and pericardiotomy. The interventricular septum behaves as part of the left ventricle during aortic and pulmonary artery constriction. The pericardium imposes a restraint on the interventricular septum and free walls of the ventricles during volume loading, but not during pressure loadings, because dilation of one ventricle is associated with shrinkage of the other.

Animals↗