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O Ellingsen

Publications and source records attributed to O Ellingsen.

36 records · Page 2Linked to original sources
PubMed1989

Myocardial K+ repletion and rise in contractility after brief ischemic periods in the pig.

Potassium loss from the myocardium during brief ischemic periods is well documented, but whether intrinsic myocardial mechanisms restore this loss during reperfusion is unclear. To address this question, we established a shunt from the coronary sinus to the right atrium in seven open-chest pigs. Shunt flow and arterial and coronary sinus potassium concentrations were measured continuously in order to determine myocardial potassium balance. Thirty, 60 and 120 s occlusions of the mid-LAD coronary artery were repeated four times each at 10 min intervals with reproducible metabolic and hemodynamic responses. A myocardial K+ reuptake amounting to 51 to 77% of K+ release during ischemia occurred between 20 and 140 s of reperfusion. The maximal rate of K+ reuptake was 1.4 (0.7 to 3.6), (median and 95% confidence interval), 4.3 (2.5 to 9.6) and 7.3 (4.9 to 13.4) mumol/100 g min after occlusion periods of 30, 60 and 120 s, respectively. Concomitant with the K+ reuptake a progressive rise in LV dP/dt occurred. Adrenoceptor stimulation could not explain these findings since catecholamine release declined during occlusion and reperfusion. We suggest that increased intracellular Na+ concentration in early reperfusion stimulates the Na,K-pump and favours Ca++ entry through Na+/Ca++ exchange, thereby mediating K+ reuptake and the rise in contractility.

Animals↗
PubMed1989

Effects of hemodynamic variables on myocardial K+ balance during and after shortlasting ischemia.

Ischemia-induced myocardial potassium loss and post-ischemic potassium reuptake was quantitated in 8 open chest pigs during control conditions and during hemodynamic alterations which have been shown to increase steady state sarcolemmal potassium fluxes. Myocardial K+ balance was continuously computed before, during and after a 90 s occlusion of a branch of the circumflex artery during control (CTR), during pacing tachycardia (PACE: 34% increase in heart rate), during proximal aortic constriction (AC; 28% increase in LVSP), and during isoprenaline infusion (ISO; 135% increase in LVdP/dt and 35% increase in heart rate). Ischemia-induced potassium loss increased significantly (40%) during ISO only. Higher basal metabolic rate, increased sarcolemmal K+ conductance, or ischemia-induced depression of a more active Na/K-pump during ISO are possible explanations to why increased K+ loss appeared in this situation. The maximal rate of post-ischemic potassium reuptake was not different from CTR during PACE and ISO, but it was reduced during AC, which might be due to persisting subendocardial ischemia in early reperfusion when ventricular wall stress is high. The extent of potassium restoration was not different from CTR during AC, PACE and ISO.

Animals↗
PubMed1989

Factors reducing left and right ventricular output during simultaneous atrioventricular activation in the pig heart.

Forward stroke volume fell by 26% (23-30%) (median and 95% confidence interval) when simultaneous atrioventricular (AV) pacing was induced at constant heart rate in 10 anaesthetized open-chest pigs. To assess the relative importance of factors which could cause this reduction in right and left ventricular (RV and LV) output, we compared cardiac dynamics when either ventricular filling or forward stroke volume was equally reduced by caval constriction and simultaneous AV pacing. We estimated the degree of ventricular filling by recording segment lengths (SL) in the free walls of both ventricles. Our analysis revealed that abolished active LV filling by the left atrium reduced forward stroke volume by 11% (8-14%). The remaining fall in output could be attributed to mitral regurgitation. In the right side of the heart the response was different. The drop in RV filling during simultaneous AV pacing accounted for approximately one-half of the fall in forward RV stroke volume. Estimates based on SL recordings demonstrated that forward RV stroke volume fell by 7% (2-25%) because of tricuspidal regurgitation. Pulmonary artery pressure was 4.5 (3.4-5.7) mmHg higher during simultaneous AV pacing than during caval constriction, representing a relative rise in afterload that reduced the RV stroke volume by 6-8%. Thus, reduced ventricular filling during simultaneous AV pacing accounted for approximately one-half of the drop in forward output from both ventricles. Slightly more than one-half of the reduction in forward LV stroke volume could be attributed to mitral regurgitation. In the right side of the heart tricuspidal regurgitation and a relative rise in pulmonary artery pressure each accounted for about one-quarter of the fall in forward RV output.

Animals↗
PubMed1989

In-vivo quantification of myocardial Na-K pump rate during beta-adrenergic stimulation of intact pig hearts.

Maintenance of adequate electrical activity of the heart depends critically on the ability of the Na-K pump to compensate for normal passive sodium and potassium fluxes. Using sudden injections of [3H]ouabain into the left coronary artery in anaesthetized open-chest pigs, we monitored transient changes in myocardial potassium balance by PVC-valinomycin mini-electrodes. When related to the number of pumps blocked and fractional inhibition, these data provided estimates of total Na-K pump capacity as well as actual pump rate and perturbations of the Na-K balance. Experiments were performed in hearts with and without intracoronary isoprenaline infusion (2.5 nmol min-1). After injection of 120 nmol [3H]ouabain into the left coronary artery, myocardial [3H]ouabain concentrations were 118 (74-178) and 103 (76-145) pmol g-1 and total concentrations of [3H]ouabain binding sites were 893 (752-1076) and 785 (691-877) pmol g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (differences not significant). The [3H]ouabain injection caused a net potassium release of 81 (56-132) and 43 (23-75) mumol 100 g-1 (median, 95% confidence interval) in isoprenaline-treated and control hearts respectively (n = 6-8; significance of difference, P = 0.03). Na-K pump rate estimated from mono-exponential release curves was 6363 (3942-10,858) K+ ions min-1 site-1 during beta-adrenoceptor stimulation and 2514 (1380-4322) in control (significance of difference, P = 0.03). This corresponds to 40 and 16%, respectively, of the maximum possible pump rate determined from ATP hydrolysis. Comparison of accumulated potassium release and relative Na-K pump rate indicates that catecholamines enhance the sensitivity of the Na-K pump for intracellular sodium.

Adrenergic beta-Agonists↗
PubMed1989

Different oxygenators for cardiopulmonary bypass lead to varying degrees of human complement activation in vitro.

Complement activation was studied in vitro with six different membrane and bubble oxygenators for cardiopulmonary bypass. There was a similar increase in terminal (C5 to C9) activation with all oxygenators (p less than 0.001), ranging from 281% (117% to 444%) to 453% (225% to 680%) after 60 minutes (median and 95% confidence intervals). C3 activation was not observed with a hollow fiber membrane and a soft shell bubble oxygenator. On the other hand, a capillary membrane, a sheet membrane, a nonporous membrane, and a hard shell bubble oxygenator all induced a similar increase in C3 activation (p less than 0.01), ranging from 107% (23% to 346%) to 272% (88% to 395%) after 60 minutes. The differences in C3 activation could not be explained by the blood contact materials or any other single factor known to induce activation, which suggests that overall complement activation during cardiopulmonary bypass is a multifactorial effect. The tubing set per se induced only minor C3 activation but contributed to the overall formation of terminal complement complex. The study further indicates that an arterial line blood filter prevents activated neutrophils from being reinfused to the patient and should be used regardless of type of oxygenator.

Cardiopulmonary Bypass↗
PubMed1988

Significance of right atrial function during right sided inotropic stimulation of pig hearts in situ.

Cardiac adjustments to inotropic stimulation of the right side of the heart were examined in anaesthetised, open chest pigs by calcium chloride infusion (80 mumol.min-1) into the right coronary artery. At stable haemodynamic conditions and at constant heart rate, right ventricular (RV) pre-ejection segment length increased by 4.6 (2.7-7.2) % (median, 95 % confidence interval) (p less than 0.01), RV end diastolic pressure rose from 5.3 (3.4-7.7) to 6.0 (3.6-8.8) mm Hg (p less than 0.05), and stroke volume rose by 6.8 (4.2-10.8) % (p less than 0.001). When the effect of right atrial contraction on RV filling was excluded by simultaneous pacing of atria and ventricles, the RV pre-ejection segment length no longer increased, and stroke volume rose by only 3.5 (0.1-9.5) % (p less than 0.05) during right side inotropic stimulation. Right atrial inotropic stimulation improves right ventricular filling, and may cause redistribution of blood from the systemic to the pulmonary circulation. This redistribution would raise the pulmonary vascular pressures, and thereby also improve left ventricular filling. The improved right ventricular filling partly accounts for the rise in RV output.

Animals↗
PubMed1988

Temporal relationship of contractility and myocardial potassium balance following beta-adrenergic stimulation of the in situ pig heart.

Lower intracellular Na+ during beta-adrenergic stimulation provides an increased driving force for Na-Ca exchange, which might attenuate the inotropic response. Since (1) Na+ reduction is coupled to K+ uptake, and (2) K+ uptake lags behind the positive inotropic response to isoproterenol, we could examine the effect of Na-Ca exchange by comparing cardiac contractility and K+ balance following intracoronary isoproterenol infusion (0.6-0.8 microgram min-1). In 8 open-chest pigs, potassium concentrations were continuously measured by PVC-valinomycin mini-electrodes in arterial blood (a), and in myocardial venous blood in a shunt from the coronary sinus (cs) to the right atrium. Shunt flow, aortic flow, a left ventricular segment length and left ventricular pressure (LVP) were also continuously recorded. 64 (41-85)% (median and 95% confidence interval) of the LV dP/dt increase occurred within 1 min; thereafter contractility rose slowly. During the first minute of isoproterenol infusion, there was a small net myocardial K+ release, which then reversed to K+ accumulation. A maximum a-cs K+ concentration difference of 0.20 (0.09-0.39) mM occurred at 3.0 (2.0-4.25) min, falling to 0.05 (0.01-0.10) mM after 6.5 (3.75-8.75) min, at which point accumulated myocardial K+ uptake was 135 (27-219) mumol 100 g-1. Heart rate remained unchanged and intramural ECG indicated no sign of ischemia during the first 1.5 min of isoproterenol infusion. At 6.25 (5.0-8.0) min after stop of isoproterenol, LV dP/dt was 12 (9-24)% lower than before infusion (P less than 0.02) whereas myocardial K+ content remained higher than control. Thus, the monovalent cation shift succeeding the positive inotropic response was not associated with reduced contractility, but could explain the undershoot of LV dP/dt after stopping isoproterenol.

Adrenergic beta-Agonists↗
PubMed1988

Forward diastolic flow in pulmonary artery induced by right atrial contraction of pig hearts.

To study whether right atrial contraction can forward blood into the pulmonary artery during diastole, blood volume was expanded in anesthetized open-chest pigs until mean right atrial pressure was 13-20 mmHg (range). In the control situation, blood flow in the pulmonary artery was only observed during ventricular systole. Forward diastolic pulmonary artery flow, coinciding with right atrial contraction, was observed when diastolic pulmonary artery pressure was reduced during selectively increased left-side contractility, during bradycardia after propranolol injection (0.5 mg/kg body wt iv), and during the prolonged diastolic interval after spontaneously occurring atrial extrasystoles. The prolongation of the diastolic interval in all three series caused the diastolic pulmonary artery pressure to decline and the filling of the right atrium to increase, thus further stimulating the right atrial Frank-Starling mechanism. The diastolic blood flow in the pulmonary artery constituted 11% of the stroke volume during increased left-side inotropic stimulation, 8% during bradycardia, and 6% in beats preceded by a prolonged diastolic interval. Thus, in the normal heart, blood can be ejected into the pulmonary artery during right atrial contraction.

Animals↗
PubMed1987

Myocardial potassium uptake and catecholamine release during cardiac sympathetic nerve stimulation.

To determine whether sympathetic nerve stimulation induces a significant potassium uptake in the myocardium, the changes in myocardial potassium balance, catecholamine release, lactate uptake, and oxygen consumption were recorded in eight anaesthetised open chest pigs during electrical stimulation of the right intermediate cardiac nerve at 10 Hz. Potassium concentrations were continuously measured by polyvinylchloride valinomycin minielectrodes in arterial and coronary sinus blood. Potassium concentration in coronary sinus blood fell to a nadir 0.42(0.21-0.61) mmol.litre-1 below control values (median and 95% confidence interval) and resulted in a peak potassium uptake of 65(38-102) mumol.min-1 100 g-1 after 2.5(2.0-3.0) min, which correlated (r = 0.94, p less than 0.001) with cardiac noradrenaline release. Accumulated myocardial potassium uptake amounted to 139(82-241) mumol.100 g-1 when a stable potassium concentration difference between arterial and coronary sinus blood was reached after 5.5(4.25-6.50) min. Cardiac contractility (LV dP/dt), myocardial oxygen consumption, and lactate uptake rose from control to peak potassium uptake (p less than 0.001) by 140%, 158%, and 92% respectively. Coronary sinus blood noradrenaline and adrenaline concentrations rose significantly (p less than 0.01) from 58(44-87) pg.ml-1 at control to 2208(1159-5627) pg.ml-1 at peak uptake and from 15(11-19) pg.ml-1 to 85(64-230) pg.ml-1 respectively. Arterial noradrenaline increased from 29(19-41) pg.ml-1 to 374(176-640) pg.ml-1 and arterial adrenaline rose from 15(11-23) pg.ml-1 to 31(24-52) pg.ml-1 (p less than 0.001). It is concluded that sympathetic nerve stimulation induces a substantial myocardial potassium uptake in a dose dependent relation to cardiac noradrenaline release and alters the contractile and metabolic state of the heart substantially with only minor changes in arterial catecholamine concentration.

Animals↗
PubMed1987

Cardiac adjustments to left-side inotropic stimulation of in situ pig hearts.

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.

Animals↗
PubMed1987

Myocardial potassium uptake during alpha- and beta-adrenoceptor stimulation.

The changes in myocardial K+ balance during alpha- and beta-adrenoceptor stimulation were compared in 10 anesthetized open-chest pigs by intracoronary isoproterenol and phenylephrine infusions. K+ concentration was continuously recorded by polyvinyl chloride catheter-valinomycin minielectrodes in arterial and coronary sinus blood. The arterial-coronary sinus difference and accumulated myocardial K+ uptake were calculated after computerized data sampling. Isoproterenol (2.5 nmol/min ic) reduced coronary sinus K+ transiently to a nadir of 0.37 (0.23-0.53) mM (median and 95% confidence interval) below control. The accumulated K+ uptake amounted to 139 (63-215) mumol/100 g. After beta-blockade by propranolol, phenylephrine (100 nmol/min ic) induced a transient coronary sinus K+ lowering of 0.16 (0.13-0.21) mM and an accumulated K+ uptake of 30 (20-41) mumol/100 g, both values less than those of isoproterenol (P less than 0.001). Myocardial contractility increased only during isoproterenol infusion, arterial blood pressure rose slightly by phenylephrine, but changes in myocardial O2 extraction and lactate uptake did not indicate cardiac ischemia. We conclude that both alpha- and beta-adrenoceptor stimulation induce a myocardial K+ uptake presumably due to increased Na-K pump activity, the latter more efficiently.

Adrenergic alpha-Agonists↗
PubMed1987

Catecholamine-induced myocardial potassium uptake mediated by beta 1-adrenoceptors and adenylate cyclase activation in the pig.

The myocardial potassium uptake during intracoronary isoproterenol stimulation was characterized in 12 anesthetized pigs. The beta-receptor subtype specificity and the effect of adenylate cyclase activation were determined. Potassium concentrations were continuously recorded by PVC-valinomycin minielectrodes in the left atrial cavity and in coronary sinus blood diverted through a shunt to the right atrium. The difference in potassium concentration between the left atrial cavity and coronary sinus, and the accumulated myocardial potassium uptake were calculated after computerized data sampling. By intracoronary drug infusion, changes in heart rate and systemic effects were minimized. Isoproterenol (0.6-0.8 microgram/min), a nonspecific beta-agonist, reduced coronary sinus potassium concentration transiently to a nadir of 0.28 (0.15-0.43) mM (median and 95% confidence interval) below control values (n = 12). The potassium uptake, which amounted to 140 (79-202) mumol/100 g tissue, corresponding to an intracellular potassium increase of about 3 mM, was abolished after selective beta 1-blockade by pafenolol. The specific beta 1-agonist dobutamine (40 micrograms/min) caused a similar potassium uptake before and after selective beta 2-blockade by ICI 118, 551. Salbutamol (2 micrograms/min), a specific beta 2-agonist, induced a minor potassium uptake of 4 (1-20) mumol/100 g, blocked by pafenolol. After nonselective beta-blockade by propranolol the adenylate cyclase stimulator forskolin caused a myocardial potassium uptake of similar magnitude to that of isoproterenol before beta-blockade. We conclude that a myocardial potassium uptake ensues during beta 1-adrenoceptor stimulation and adenylate cyclase activation.

Adenylyl Cyclases↗
PubMed1987

Spontaneous pneumothorax in chronic obstructive pulmonary disease: complications, treatment and recurrences.

Data from 303 patients with 389 admissions for spontaneous pneumothorax from 1970 to 1980 at Ullevaal Hospital, Oslo, Norway, were reviewed. Spontaneous pneumothorax carried a significantly higher complication and mortality rate in patients suffering chronic obstructive pulmonary disease (COPD). Their higher median age compared to non-COPD patients contributed to this, but did not account for the increased mortality. The risk of developing wound infection and/or pneumonia was significantly higher after 7 days of chest tube treatment in both patient groups, independent of age. There was no association between recurrence rate and COPD/non-COPD, age or duration of chest tube treatment (1-7 days, 8 days or more). Complications were not more frequent after thoracotomies performed in COPD patients. Therefore operative treatment for both primary and COPD-related spontaneous pneumothorax should be considered if tube treatment is not successful after 1 week and there are no contraindications.

Adolescent↗
PubMedDate not supplied

Myocardial potassium balance during adrenergic stimulation.

1) The primary receptor mechanism of catecholamine-induced myocardial potassium uptake is beta 1-adrenoceptor stimulation. Thus, K+ uptake seems to be a general effect of beta-adrenergic stimulation, dominated by beta 1-receptors in heart and by beta 2-receptors in skeletal muscle according to subtype preponderance in either tissue. In the myocardium there is also an effect of alpha 1-adrenoceptor stimulation which causes a significantly smaller uptake and requires higher catecholamine concentrations. 2) Both humoral and nervous adrenergic stimulation of the heart induce a significant potassium uptake which transiently reduces coronary sinus K+ concentration. It is likely that these changes affect cardiac functioning in vivo. During intense endogenous sympathetic activity and by high dose pharmacological interventions, the magnitude of change in coronary sinus concentration suggests that the reduction in extracellular K+ within the myocardium could be up to 1 mM. Under vulnerable conditions like hypokalemia and localized ischemia such changes might contribute to the risk for malignant arrhythmias. 3) Presumably net myocardial K+ accumulation is accompanied by a reciprocal reduction of intracellular Na+ concentration, which tends to reduce myocardial contractility and contribute to impaired cardiac function after a period of strong adrenergic stimulation. In vivo the negative inotropic effect could not be detected as long as catecholamines were supplied, but it occurred after stimulation was stopped. 4) In the intact beating heart beta-adrenergic stimulation increases Na,K-pumping 2.5 fold, from 15% of the maximum possible pump rate in control to 40% of maximum at high inotropy. These findings imply the presence of a substantial spare Na,K-pump capacity of the non-ischemic myocardium, even during intense sympathetic activity. Comparison of changes in pump rate and accumulated ionic shifts indicates that catecholamine-induced stimulation of Na,K-ATPase might be due to increased sensitivity for intracellular sodium.

Animals↗