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Biomedical subjects

S Birkeland

Publications and source records attributed to S Birkeland.

At least 19 recordsLinked to original sources
PubMed1992

[Multiple injuries and quality control].

A prospective registration was carried out of all patients with multiple injuries who were admitted to hospital in 1990 during the first 24 hours after the accident. The total number was 441, and included 47 patients with penetrating injuries. Such patients constituted 5% of a total of 9,000 admitted patients, and 19% of a total of 2,266 injured persons. The injuries were scored using the Trauma Score and Injury Severity Score and the probability for survival was calculated by the TRISS method. 148 patients were seriously injured, having an Injury Severity Score 16 or more. Traffic accidents were more common, and were the cause of injury in more than 50% of the patients. 15% of the patients with such injuries were under the influence of alcohol and 5% were drug abusers. The percentage under the influence of alcohol was three times as high, however, among patients injured by violence. Median ISS was 26 for the whole series, and 41 for the 41 patients who died. Mortality was significantly higher in patients older than 54 years of age than among younger patients. No patients were reduced to a vegetative state, but 13% of the surviving patients were considerably disabled. Among the 41 patients who died the main cause of death was haemorrhage in 17, and airway obstruction in five. Estimation of probability of survival showed that the mortality in this series compared well with the mortality in larger series of injured persons in America. None the less, improvement is still feasible.

Adult↗
PubMed1992

Transmural heterogeneity of postjunctional alpha 2 adrenergic coronary vasoconstriction in hypoperfused cat left ventricle.

OBJECTIVE: The aim was to analyse the influence of coronary postjunctional alpha 1 and alpha 2 adrenergic vasoconstriction in hypoperfused myocardium with special emphasis on transmural distribution of blood flow. METHODS: The left coronary artery was hypoperfused by means of a clamped shunt line. Sequential selective postjunctional alpha 1 (doxazosin) and alpha 2 (SK&F 104078) adrenergic antagonism was established following beta adrenergic antagonism with propranolol. Regional myocardial blood flow was measured with radiolabelled microspheres during equal coronary perfusion pressures. Experimental subjects were nine pentobarbitone anaesthetised open chest cats. RESULTS: Left coronary hypoperfusion decreased endocardial blood flow, whereas epicardial flow was unaltered. In this situation alpha 1 adrenergic antagonism did not affect myocardial blood flow. Subsequent alpha 2 antagonism impaired endocardial blood flow, whereas epicardial blood flow was augmented. Mean coronary vascular resistance declined following combined alpha 1 and alpha 2 adrenergic antagonism. CONCLUSIONS: Coronary alpha adrenergic vasoconstriction is localised mainly epicardially in hypoperfused myocardium and counteracts endocardial hypoperfusion distal to a fixed coronary stenosis. Furthermore, this vasoconstriction is of the postjunctional alpha 2 adrenergic subtype.

Adrenergic alpha-Antagonists↗
PubMed1992

Compensatory subendocardial hyperkinesis in the cat is abolished during coronary insufficiency outside an acutely ischaemic region.

OBJECTIVE: The aims were to determine (1) whether acute coronary occlusion provoked uniform hyperkinesis in remote non-ischaemic myocardium, and (2) how subsequent coronary stenosis affected such hyperkinesis. METHODS: Two pairs of ultrasonic crystals were placed in the anterior left ventricular midwall of nine pentobarbitone anaesthetised open chest cats. One pair (longitudinal) ran parallel to subendocardial fibres; the other pair (circumferential) was aligned with subepicardial and mid-myocardial fibres. Following circumflex coronary occlusion, subsequent hypoperfusion of the anterior wall was established by controlled constriction of a shunt line from the right subclavian artery to the left main coronary artery in two discrete steps. RESULTS: Following circumflex occlusion maximum systolic shortening of segments aligned to subendocardial fibres increased from 6.7(SEM 0.9)% to 11.5(1.4)% (p less than 0.001), whereas circumferential segment shortening was unchanged, at 12.2(0.8)% v 14.1(1.1)%. During mild shunt stenosis [delta P = 42(2) mm Hg] subendocardial tissue blood flow in the anterior wall decreased by 42(10)% (p less than 0.001), and longitudinal segment shortening decreased from 11.5(1.4)% to 6.9(1.1)% (p less than 0.001). Corresponding shortening of circumferential segments did not change. During severe shunt stenosis [delta P = 52(3) mm Hg] subendocardial tissue blood flow decreased further, and shortening of longitudinal segments approached zero value (p less than 0.001). CONCLUSIONS: Compensatory hyperkinesis of remote non-ischaemic myocardium following an acute coronary occlusion may depend mostly on augmented subendocardial contraction.

Animals↗
PubMed1992

Coronary artery stenosis provokes non-uniformity of two-dimensional deformation in the anterior wall of the feline left ventricle.

The effect of coronary stenosis on the uniformity of local left ventricular contraction was studied in 11 open-chest cats. Coronary artery stenosis was established by controlled constriction of a shunt line from the right subclavian artery to the left main coronary artery. Two pairs of ultrasonic crystals were placed in the midwall of the anterior left ventricular wall; one pair, circumferential (Circ), aligned with midwall and subepicardial fibres; the other, longitudinal (Long), aligned with subendocardial fibres. Three steps of coronary perfusion pressure (poststenotic) were studied; open shunt line (140 +/- 4 mmHg), light stenosis (94 +/- 2 mmHg), and severe stenosis (70 +/- 3 mmHg). Subendocardial tissue blood flow showed the most pronounced reduction (from 1.87 +/- 0.11 to 1.43 +/- 0.10 and 0.86 +/- 0.12 ml min-1 g-1, respectively) with coronary stenosis whereas subepicardial flow remained unchanged. Maximal systolic shortening deteriorated for both segments. However, it was most pronounced for longitudinal segments. Duration of shortening decreased in longitudinal segments during severe stenosis to 62% of duration with open shunt (P less than 0.05), but was unchanged in circumferential segments. Long/Circ ratio of maximal systolic shortening declined by 50% (P less than 0.05) with reduction of coronary perfusion pressure. The reduced uniformity of segment shortening, caused by a marked reduction of longitudinal segment shortening, may support the notion that the longitudinal segment reflects performance of subendocardial fibres. This study demonstrates local non-uniformity of two-dimensional deformation during coronary artery stenosis and subendocardial hypoperfusion.

Animals↗
PubMed1992

Compensatory regional contraction following coronary artery occlusion depends on subendocardial hyperaemia and hyperkinesis.

The effects of circumflex coronary artery occlusion on regional myocardial performance and blood flow in the left ventricular anterior wall was studied, using 16 thoracotomized pentobarbital-anaesthetized cats. Two pairs of ultrasonic crystals were placed in the midwall; one segment (longitudinal) parallel to the subendocardial fibres, the other (circumferential) being aligned to the fibres of the outer half-layer. A shunt line from the right subclavian artery to the main left coronary artery was unrestricted in eight cats (Group A) and clamped in another eight cats (Group B) until coronary perfusion pressure was clearly reduced with only a minor reduction in shunt flow, but without changes in global cardiac function. After circumflex coronary occlusion hyperkinesis was most pronounced in segments parallel to subendocardial fibres (longitudinal), also validated as a marked leftward shift in the end-systolic pressure-length relation of these segments. Such a shift may indicate decreased regional afterloading along the cardiac major axis. Hyperkinesis of longitudinal segments was attenuated in Group B where a fixed shunt stenosis hampered subendocardial and mid-myocardial hyperaemia. The lesser hyperkinesis of Group B was associated with decreased left ventricular systolic pressure and cardiac output. Thus, impaired compensatory contraction outside an acute ischaemic region was produced by a significant coronary stenosis which precluded the subendocardial hyperaemia and hyperkinesis of that region.

Animals↗
PubMed1992

Postjunctional alpha-adrenergic stimulation of inotropy in hypoperfused myocardium outside an acute infarct.

The functional significance of myocardial postjunctional alpha-adrenergic support of inotropy in the vicinity of an acute regional ischemic zone was addressed in pentobarbital-anesthetized, beta-adrenergic blocked cats with circumflex coronary artery occlusion. Regional myocardial performance was measured by ultrasonic crystals in the anterior wall perfused by the left anterior descending coronary artery (LAD) before and during postjunctional alpha-adrenergic antagonism (SK&F 104078 2 mg/kg). A group with unrestricted flow in the LAD (control group) was compared with a group perfused below the autoregulatory pressure range (stenosis group). End-systolic pressure-length relations during dynamic after-load elevation were calculated for assessment of regional contractility. Regional myocardial blood flow (RMBF) was measured by radioactive microspheres. SK&F 104078 did not alter regional myocardial shortening or the slope of end-systolic pressure-length relations in the control group. In the stenosis group, however, alpha-adrenergic antagonism produced significant deterioration of shortening as well as consistent reduction of the slope of the end-systolic pressure-length relations (p < 0.05). As a reflection of reduced demands for perfusion, impairment of midmyocardial and endocardial blood flow occurred in the stenosis group (p < 0.05). These findings imply a negative inotropic effect of SK&F 104078 in metabolically vasodilated myocardium in the vicinity of an acute ischemic region.

Adrenergic alpha-Agonists↗
PubMed1992

Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation.

Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK&F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventricular myocardial oxygen consumption (MVO2). alpha 1-Adrenergic antagonism alone did not significantly alter blood flow in any wall layer in either group. Subsequent alpha 2-adrenergic antagonism increased epicardial as well as composite transmural flow in the stenosis group (P < 0.025). The inverse correlation between coronary resistance and MVO2 vanished in the stenosis group following alpha 1- and alpha 2-adrenergic antagonism. Maximal first derivative of the left ventricular pressure-time relation (dP/dt) and cardiac output were reduced simultaneously (P < 0.001). Hence, the significance of alpha 1- and alpha 2-adrenergic stimulation of inotropy and cardiac performance are augmented by myocardial hypoperfusion. Furthermore, alpha 2-adrenergic receptors are responsible for epicardial vasoconstriction in hypoperfused myocardium.

Adrenergic alpha-Agonists↗
PubMed1992

Effect of afterload and beta-adrenergic blockade on nonischemic myocardial contraction pattern.

We studied how changes in afterload affect regional contraction in the anterior wall of the left ventricular after circumflex coronary arterial (CFX) occlusion and subsequent beta-adrenergic blockade in pentobarbital sodium-anesthetized cats. Regional function was determined by orthogonal sonomicrometry. CFX occlusion produced nonuniform hyperkinesis in the nonischemic anterior wall; shortening of circumferential segments increased from 10.1 to 14.1% (P < 0.001), whereas shortening of longitudinal segments increased from 3.0 to 9.6% (P < 0.001). Hyperkinesis of longitudinal segments was influenced neither by changes in afterload over a pressure range of +/- 30 mmHg nor by beta-adrenergic blockade, indicating that hyperkinesis of longitudinal segments does not rely on increased inotropic state or resistance to ventricular emptying. Hyperkinesis of longitudinal segments occurred at end-diastolic lengths equal to preocclusion conditions, whereas hyperkinesis of circumferential segments was dependent on activation of the Frank-Starling mechanism. Furthermore, shortening of circumferential segments decreased with increments in afterload, particularly after CFX occlusion and subsequent beta-adrenergic blockade. In conclusion, CFX occlusion alters the contraction pattern of the nonischemic anterior wall. The postocclusion contraction is sensitive to increased afterload in the cardiac minor axis direction. These initial alterations may well direct the following remodeling process in infarcted hearts.

Adrenergic beta-Antagonists↗
PubMed1992

[Multiple injuries and quality control].

A prospective registration was carried out of all patients with multiple injuries who were admitted to hospital in 1990 during the first 24 hours after the accident. The total number was 441, and included 47 patients with penetrating injuries. Such patients constituted 5 per cent of a total of 9,000 admitted patients, and 19 per cent of a total of 2,266 injured persons. The injuries were scored using the Trauma Score and Injury Severity Score (ISS) and the probability for survival was calculated by the TRISS method. 148 patients were seriously injured, having an Injury Severity Score 16 or more. Traffic accidents were most common, and were the cause of injury in more than 50 per cent of the patients. 15 per cent of the patients with such injuries were under the influence of alcohol and 5 per cent were drug abusers. The percentage under the influence of alcohol was three times as high, however, among patients injured by violence. Median ISS was 26 for the whole series, and 41 for the 41 patients who died. Mortality was significantly higher in patients older than 54 years of age than among younger patients. No patients were reduced to a vegetative state, but 13 per cent of the surviving patients were considerably disabled. Among the 41 patients who died the main cause of death was haemorrhage in 17, and airway obstruction in five. Estimation of probability of survival showed that the mortality in this series compared well with the mortality in larger series of injured persons in America. None the less, improvement is still feasible.

Adolescent↗
PubMed1991

Dyssynchrony of segment shortening in the anterior wall of the feline left ventricle.

Non-uniformity of regional contraction may be both spatial and temporal. This study was undertaken to deal with the temporal aspects of shortening and to quantify non-uniformity with regard to timing. Nine cats were anaesthetized and artificially ventilated. Two pairs of ultrasonic crystals were situated in the anterior midwall of the left ventricle to measure regional shortening. One pair, longitudinal segment, was oriented to align with midwall fibres. The other pair, transverse segment, was placed perpendicular to the first one. Registrations in control state, during caval occlusion, and during aortic constriction were carried out with and without isoprenaline infusion. Cyclic events were analysed in terms of phase angle, 0-2 pi representing one heart cycle. Transverse segments showed marked shift of duration of shortening, from 1.19 pi +/- 0.06 pi (mean +/- SEM) in the control state to 0.40 pi +/- 0.14 pi during caval occlusion with isoprenaline infusion. Duration of shortening of longitudinal segments showed less prominent shift with mean values between 1.38 pi and 1.11 pi. Regional uniformity of timing, expressed as synchronization index, varied markedly with interventions (P less than 0.0005). Dyssynchrony was most prominent during caval occlusion with mean values less than 0.6. A simple model of force generation for the two segments visualizes that segment shortening of the transverse segment is of shorter duration than the longitudinal segment and a common mechanism for temporal and spatial non-uniformity within a region could be elaborated. This study quantifies both the time course of shortening and temporal non-uniformity of two cross-oriented segments within the same myocardial region.

Animals↗
PubMed1991

Myocardial contractile performance during acute coronary occlusion with special emphasis on nonoccluded regions.

Ischaemia of the left ventricle caused by coronary artery occlusion generally leads to less changes in overall ventricular performance than would be expected from the amount of ischaemic, noncontracting tissue. Ischaemic myocardium shows elongation of segment lengths and paradoxial movement during contraction of the left ventricle. Compensation for the loss of contractile tissue is most likely related to increased performance of the nonischaemic myocardium and the most likely mechanisms involved are discussed. The effect of increased preload, brought about by increased left ventricular end-diastolic pressure following coronary occlusion, on nonischaemic parts appear to be the most important mechanism of compensation.

Adaptation, Physiological↗
PubMed1990

Gradual reduction of coronary perfusion pressure in cats: changes in transmural distribution of blood flow.

We evaluated a model for regional myocardial hypoperfusion in cats with an extracorporeal shunt line to the left main coronary artery, and investigated the effects of reduced coronary perfusion pressure on the transmural distribution of left ventricular blood flow measured with radioactive microspheres. Shunt establishment did not alter cardiac function, myocardial tissue blood flow, or its transmural distribution. An artificial shunt stenosis, which clearly reduced coronary perfusion pressure without changing cardiac function, caused reduced endocardial blood flow, slight flow reduction in mid-myocardium, and no flow change in the epicardium. When a severe stenosis was applied, causing increased end-diastolic pressure and reduced shunt flow, endocardial and mid-myocardial flow further decreased whereas epicardial blood flow remained essentially unchanged. These results demonstrate a transmural profile of the coronary autoregulation capacity.

Animals↗
PubMed1990

Regional perfusion in hearts with acute coronary artery occlusion and subsequent beta 2- and alpha 1-adrenergic blockade.

Blockade of cardiac adrenoceptor subtypes, coronary or myocardial, might elicit compensatory interaction from remaining unblocked subtypes. An attempt to explore this interplay was made by studying regional myocardial blood flow alterations associated with beta 2-adrenergic blockade followed by alpha 1-adrenergic blockade in anaesthetized cats with acute coronary occlusion. In order to maintain constant needs for perfusion, atrial pacing was established and the aortic blood pressure was kept constant. In myocardium remote from the ischaemic region, beta 2-adrenergic blockade produced higher endocardial blood flow whereas no flow changes were observed close to the ischaemic region. With subsequent alpha 1-adrenergic blockade, blood flow increased endocardially in non-ischaemic regions, but remained unchanged in epicardial tissue. Control experiments without coronary ligation revealed no increase in left ventricular oxygen consumption during the experiments and support the theory that the observed blood flow increase in the coronary ligation group, following drug interventions, was not caused by increased cardiac work. This study indicates that combined beta 2- and alpha 1-adrenergic blockade alters the balance between receptor subtypes. Unopposed beta 1-mediated vasodilation is the most likely candidate to explain why endocardial flow was increased.

Adrenergic alpha-Antagonists↗
PubMed1989

Does alpha 1-adrenergic blockade influence regional blood flow regulation in hearts with coronary artery occlusion?

The effects of selective alpha 1-adrenergic blockade with doxazosin on regional myocardial tissue blood flow was studied in anaesthetized cats with acute coronary artery occlusion. Reflex tachycardia was prevented by selective beta 1-adrenergic blockade with atenolol and coronary perfusion pressure was kept constant by partial stenosis of the descending aorta. Administration of atenolol reduced cardiac mechanical work-load by its negative inotropic and chronotropic effects, and reduced myocardial tissue blood flow in normally perfused myocardium. This reduction was most pronounced in the endocardial half-layer of the myocardium adjacent to the ischaemic region. Administration of doxazosin in this situation clearly reduced peak systolic and coronary perfusion pressure. But when coronary perfusion pressure was raised to pre-administration values, measurements of regional blood flow revealed no changes either in ischaemic or non-ischaemic myocardium. Also, there was no sign of redistribution of blood flow between endocardial and epicardial tissue in any area. This study, therefore, indicates that alpha 1-adrenoceptors play a minor role in the regulation of coronary blood flow in normal myocardium as well as ischaemic myocardium.

Animals↗
PubMed1989

Nonuniform shortening of the anterior wall of feline left ventricles.

Recorded performance of segments between implanted ultrasonic crystals placed at midwall position of the left ventricle reportedly depends almost exclusively on midwall function and alignment with fibers. Accordingly, one would expect the ratio between performance of a segment perpendicular to midwall fiber direction (transverse) and a parallel segment (longitudinal) to be constant and independent of changes in preload, afterload, and the inotropic state. We tested this hypothesis by implanting cross-oriented crystal pairs in nine open-chest cats and studied their performance during preload and afterload changes with and without isoproterenol infusion. Fiber orientation across the ventricular wall was determined by serial histological sectioning. The ratio between performance of transverse and longitudinal segments (trans/long) changed with interventions. Increased end-diastolic pressure leads to increased segment performances as well as trans/long. Inotropic stimulation produced increased sensitivity to preload changes both for individual segment performances and for trans/long. These results suggest that longitudinal segments represent the function of midwall fibers, whereas transverse segments may well represent the function of sub-endocardial fibers, which run closer to this orientation. Thus trans/long provides a way to quantify nonuniformity of local myocardial contraction.

Animals↗
PubMed1988

[Lung abscess].

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Adolescent↗