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Biomedical subjects

O M Sejersted

Publications and source records attributed to O M Sejersted.

At least 91 records · Page 5Linked to original sources
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

Anaerobic capacity determined by maximal accumulated O2 deficit.

We present a method for quantifying the anaerobic capacity based on determination of the maximal accumulated O2 deficit. The accumulated O2 deficit was determined for 11 subjects during 5 exhausting bouts of treadmill running lasting from 15 s to greater than 4 min. The accumulated O2 deficit increased with the duration for exhausting bouts lasting up to 2 min, but a leveling off was found for bouts lasting 2 min or more. Between-subject variation in the maximal accumulated O2 deficit ranged from 52 to 90 ml/kg. During exhausting exercise while subjects inspired air with reduced O2 content (O2 fraction = 13.5%), the maximal O2 uptake was 22% lower, whereas the accumulated O2 deficit remained unchanged. The precision of the method is 3 ml/kg. The method is based on estimation of the O2 demand by extrapolating the linear relationship between treadmill speed and O2 uptake at submaximal intensities. The slopes, which reflect running economy, varied by 16% between subjects, and the relationships had to be determined individually. This can be done either by measuring the O2 uptake at a minimum of 10 different submaximal intensities or by two measurements close to the maximal O2 uptake and by making use of a common Y-intercept of 5 ml.kg-1.min-1. By using these individual relationships the maximal accumulated O2 deficit, which appears to be a direct quantitative expression of the anaerobic capacity, can be calculated after measuring the O2 uptake during one exhausting bout of exercise lasting 2-3 min.

Adenosine Triphosphate↗
PubMed1988

Motor drive and metabolic responses during repeated submaximal contractions in humans.

Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.

Adenosine Triphosphate↗
PubMed1987

Determination of ionic metabolites from ethylene glycol in human blood by isotachophoresis.

Conditions for isotachophoretic determination of anionic metabolites in blood from ethylene glycol in poisoned humans were established. Leading electrolytes with 5 mM chloride and and 2.5 gave good separation. Optimal separation was found with leading electrolytes at pH 2.5, and 10 mM acetic acid as terminating electrolyte. Separation and quantification of four out of six metabolites were possible. The four were glycolic acid, glyoxylic acid, oxalic acid and formic acid. Besides these compounds, citric acid, lactic acid, and alpha- and beta-hydroxybutyric acid were separated and quantified. The formation of mixed zones did not give any serious problems, although in samples with high amounts of glycolic acid we had to reduce the maximum injected amount from 3 to 1 microliter. This method might be valuable in further studies of the mechanism of ethylene glycol toxicity and as an important supplement in the diagnosis of late stages of ethylene glycol poisoning in which the glycol has been metabolized to glycolic acid.

Electrolytes↗
PubMed1987

Effect of duration of exercise on excess postexercise O2 consumption.

This study was undertaken to determine the effect of exercise duration on the time course and magnitude of excess postexercise O2 consumption (EPOC). Six healthy male subjects exercised on separate days for 80, 40, and 20 min at 70% of maximal O2 consumption on a cycle ergometer. A control experiment without exercise was performed. O2 uptake, respiratory exchange ratio (R), and rectal temperature were monitored while the subjects rested in bed 24 h postexercise. An increase in O2 uptake lasting 12 h was observed for all exercise durations, but no increase was seen after 24 h. The magnitude of 12-h EPOC was proportional to exercise duration and equaled 14.4 +/- 1.2, 6.8 +/- 1.7, and 5.1 +/- 1.2% after 80, 40, and 20 min of exercise, respectively. On the average, 12-h EPOC equaled 15.2 +/- 2.0% of total exercise O2 consumption (EOC). There was no difference in EPOC:EOC for different exercise durations. A linear decrease with exercise duration was observed in R between 2 and 24 h postexercise. No change was observed in recovery rectal temperature. It is concluded that EPOC increases linearly with exercise duration at a work intensity of 70% of maximal O2 consumption.

Adult↗
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↗
PubMed1986

Magnitude and duration of excess postexercise oxygen consumption in healthy young subjects.

Postexercise oxygen consumption was investigated in eight healthy subjects. The subjects exercised for about 80 minutes at 70% of their maximum VO2. Following the exercise the subjects rested in bed for 24 hours. Oxygen uptake was measured continuously during the first hour after exercise, then hourly for the next 11 hours, and finally at 24 hours after exercise. Heart rate and rectal temperature were recorded continuously during the first 12 hours and then at 24 hours after exercise. Blood was sampled hourly after exercise. The results were compared with those of an identical control experiment in which the subjects rested instead of exercising. Oxygen uptake of each time point in each subject was greater after exercise compared with the control experiment. Mean total oxygen consumption after exercise was 211 +/- 16 L/12 h as compared to 185 +/- 13 L/12 h in the control experiment (P less than 0.001). Also, the heart rate was higher during the first 12 hours following exercise than in the control study. No significant differences were observed in rectal temperature in the two experiments after the initial 30 minutes following exercise. The first meal taken after the cessation of exercise increased markedly the rate of oxygen consumption in comparison to the increase observed following the same meal in the control experiment. The respiratory exchange ratios were lower following exercise than in the control study. In conclusion, we have demonstrated that the excess postexercise oxygen consumption (EPOC), may persist for at least 12 hours, and possibly for 24 hours. Also, exercise caused enhancement of the stimulation in oxygen uptake seen after a meal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Magnitude of myocardial potassium changes during acute alterations in pacing frequency in the in situ pig heart.

A transient loss of potassium from cardiac tissue during increments in stimulation frequency has been found in different isolated preparations, but there is no agreement as to the magnitude and time course of this loss. In the present study myocardial potassium balance was determined during changes in heart rate in pigs with an intact circulation. The left azygos vein, which drains into the coronary sinus in this species, was cannulated and a shuntline to the right atrium established. Coronary sinus blood was thus continuously drawn from the shunt by a pump, without admixture of systemic venous blood, and myocardial release and uptake of potassium were determined before, during, and after periods of pacing tachycardia. A transient mean(SEM) loss of potassium (13.0(5.6) mumol X 100 g-1 or about 0.25 mumol per beat change in heart rate) occurred during the first 90 s after increasing heart rate by a mean(SEM) of 53(4) beats X min-1. By discontinuing pacing heart rate returned to control values (mean(SEM) -43(7) beats X min-1), and myocardial potassium uptake ensued (mean(SEM) 9.8(3.3) mumol X 100 g-1 or 0.23 mumol per beat change in heart rate). The peak changes in coronary sinus potassium concentrations occurred 30 s after heart rate). The potassium lost during the periods of pacing tachycardia represented only about 0.2% of total myocardial potassium, equivalent to a reduction in intracellular potassium concentration of 0.3 mmol X litre-1. Since intracellular sodium and calcium concentrations are closely linked to the potassium concentration, the observed changes in potassium concentrations, although small, may be related to the positive inotropic effect of pacing tachycardia (the positive staircase phenomenon).

Animals↗
PubMed1986

Renal Na,K-adenosine triphosphatase transport rate limits transcellular NaCl reabsorption in distal nephrons of volume-expanded dogs.

To examine whether the adenosine triphosphatase (Na,K-ATPase) transport rate regulates transcellular NaCl reabsorption, experiments were performed on anesthetized volume-expanded dogs. Ouabain was injected into the renal artery in doses inhibiting 10 to 80% of the renal Na,K-ATPase activity. Acetazolamide was administered before ouabain to render the NaHCO3 reabsorption and associated NaCl reabsorption constant during variations in the glomerular filtration rate. Ouabain reduced sodium reabsorption significantly after inhibiting 20% of the Na,K-ATPase. By inhibiting 80% of the Na,K-ATPase, NaCl reabsorption was reduced by 40 to 50% without affecting NaHCO3 reabsorption. During mechanical constriction of the suprarenal aorta, the remaining NaCl reabsorption was constant until the glomerular filtration rate was lowered by about 50%. Bound ouabain and the remaining Na,K-ATPase activity were distributed between the cortex and medulla in proportion to the Na,K-ATPase activity before ouabain injection. The reduction in NaCl reabsorption and ouabain binding were correlated (r = 0.90), the slope suggesting a turnover for ATP similar to the in vitro turnover of 5700 ATP min-1 estimated from the relationship between the remaining Na,K-ATPase activity and bound ouabain (r = 0.95). We conclude that transcellular reabsorption of NaCl in the distal nephron reaches a maximum in volume-expanded dogs by saturating the sodium sites of Na,K-ATPase because even a small dose of ouabain inhibits NaCl reabsorption and because the calculated turnover for Na,K-ATPase activity is similar to in vitro maximum estimates. The Na,K-ATPase transport rate, therefore, limits transcellular NaCl reabsorption in volume-expanded dogs.

Absorption↗
PubMed1986

Muscle fluid and electrolyte balance during and following exercise.

During shortlasting exhausting exercise plasma volume is decreased by up to 20%. Water is probably taken up by muscle cells since the concentration of small plasma solutes like Na+ and Cl- increases in parallel with the hemoglobin concentration. During the first 4 min of the recovery phase the extracellular distribution volume for NaCl seems to be restored as evidenced by normalization of the plasma sodium and chloride concentrations. However, the plasma volume is restored at a much slower rate by recapture of isotonic fluid. Interestingly, arterial lactate concentrations are normalized at the same rate. We propose that immediately after end of shortlasting exercise the swollen muscle cells rapidly reduce their volume. Fluid will accumulate in the interstitium since reuptake of fluid into the capillaries is a much slower process.

Blood Volume↗
PubMed1985

Dependency of renal potassium excretion on Na,K-ATPase transport rate.

Potassium secretion may depend on the transport rate of Na, K-ATPase in basolateral cell membranes of distal tubular cells. To examine this hypothesis experiments were performed in anaesthetized dogs during inhibition of proximal potassium reabsorption by acetazolamide or mannitol (fractional potassium excretion 1.2 - 1.4) or additional stimulation of potassium secretion by ethacrynic acid (fractional potassium excretion 2.1). Ouabain in a dose which inhibits 70-80% of the Na, K-ATPase activity reduced fractional potassium excretion to 0.8 - 0.9 by an effect on distal tubular secretion since potassium transport in the proximal tubules was not affected. Ouabain-sensitive potassium excretion varied in proportion to ouabain-sensitive sodium reabsorption during variation in glomerular filtration rate, even at urinary sodium concentrations exceeding 80 mmol X 1(-1). In experiments without ouabain, saline infusion raised potassium excretion and sodium reabsorption until maximal Na,K-ATPase transport rate was reached, as judged from heat production measurements, but not during further increments in urine flow. After inhibition of Na,K-ATPase activity by hypokalaemia, potassium excretion and cortical heat production remained constant over a wide range of urine flow and sodium excretion. We conclude that potassium secretion is dependent on intact Na,K-ATPase activity and is stimulated by sodium delivery to the distal nephron until maximal transport rate of the enzyme is reached.

Animals↗
PubMed1985

Effects of digitoxin and hypokalaemia on pancreatic NaHCO3 secretion and pancreatic Na,K-ATPase activity.

To study the role played by Na,K-ATPase in the pancreatic secretion of NaHCO3, experiments were performed in 20 anaesthetized, secretin-infused pigs (3.0 clinical units X kg b. wt. X h-I). The relationship between pancreatic NaHCO3 secretion and arterial pH was obtained before and during Na,K-ATPase inhibition by digitoxin and hypokalaemia. Na,K-ATPase activity in pancreatic tissue homogenate averaged 5.45 (5.02-6.68) mumol Pi X mg X protein X h-I. Retrograde injection of 0.5 ml 1.4 X 10(-4) mol X l-I digitoxin into pancreatic ducts reduced pancreatic Na,K-ATPase activity by 3I(I8-47)%, while intra-arterial injection of 0.2 mg X kg b. wt-I digitoxin reduced pancreatic Na,K-ATPase activity by 50(45-56)%. Digitoxin and hypokalaemia reduced the rate of pancreatic NaHCO3 and shifted the normal, proportional relationship between NaHCO3 secretion and arterial pH towards higher pH. Hypokalaemia reduced Na,K-ATPase activity and NaHCO3 secretion in proportion. These effects indicate that Na,K-ATPase helps to sustain the requisite electrochemical potential gradients for driving H+ ions, and hence HCO-3 ions, out of secretory cells.

Animals↗
PubMed1985

Haemodynamic conditions for renal PGE2 and renin release during alpha- and beta-adrenergic stimulation in dogs.

Constriction of the renal artery and infusion of an alpha-adrenergic agonist induce autoregulated vasodilation and increase prostaglandin E2 (PGE2) and renin release. The enhancement of renin release during autoregulated vasodilation might be mediated by prostaglandins. To examine this hypothesis, experiments were performed in three groups of anaesthetized dogs. In six dogs constriction of the renal artery to a perfusion pressure below the range of autoregulation raised renin release from 2 +/- 1 to 27 +/- 6 micrograms AI X min-1 and PGE2 release from 1 +/- 1 to 10 +/- 2 pmol X min-1. After administration of indomethacin (10 mg X kg-1 b.wt), PGE2 release was effectively blocked and constriction of the renal artery raised renin release only from 0.1 +/- 0.1 to 6 +/- 1 micrograms AI X min-1. During subsequent continuous infusion of a beta-adrenergic agonist, isoproterenol (0.2 micrograms X kg-1 X min-1), constriction of the renal artery raised renin release from 0.1 +/- 0.1 to 52 +/- 11 micrograms AI X min-1, although there was no rise in PGE2 release. In six dogs, intrarenal infusion of phenylephrine, an alpha- adrenergic agonist, increased PGE2 and renin release before, but not after, indomethacin administration. In six other dogs, phenylephrine infused during isoproterenol infusion increased renin release equally before and after indomethacin administration. Thus the enhancing effect of constricting the renal artery or infusing an alpha-adrenergic agonist is not dependent upon prostaglandins. We propose that autoregulated dilation enhances renin release whether the stimulatory agent is a prostaglandin or a beta-adrenergic agonist.

Adrenergic alpha-Agonists↗
PubMed1985

Acid-base and electrolyte balance after exhausting exercise in endurance-trained and sprint-trained subjects.

High ability to perform strenuous exercise of short duration is accompanied by a large lactate formation in the exercising muscles, but the disturbances in extracellular acid-base and electrolyte balance might be attenuated compared to subjects with less ability to perform intense exercise. To study this, oxygen deficit, changes in arterial blood acid-base status and plasma electrolytes were studied in six-endurance trained (ET) and six sprint-trained (ST) subjects who exercised on a treadmill at a speed which led to exhaustion within 1 min. During exercise the ET and ST subjects developed an oxygen deficit of 41 and 56 ml oxygen units kg-1 respectively, whereas peak blood lactate concentration post exercise averaged 12.5 and 16.7 mmol l-1. Blood pH followed lactate concentration closely, reaching nadir values of 7.175 and 7.065 for ET and ST subjects respectively. Respiratory compensation and changes in blood bicarbonate and standard base deficit (SBD) concentrations for a given lactate concentration were the same for the two groups, amounting to a change in PCO2 of 0.12 kPa, in bicarbonate concentration of 1.09 mmol l-1 and in SBD of 1.44 mmol l-1 mM-1 change in blood lactate concentration. During exercise the increase in haematocrit, from to 43 to 45% for the ET subjects and from 46 to 50% for the ST subjects, was accompanied by almost parallel relative changes in plasma chloride and sodium concentrations. Whereas haematocrit continued to increase post exercise and followed blood lactate concentration closely, plasma sodium and chloride concentrations decreased to pre-exercise values within 9 min of recovery. The anion gap increased significantly more than blood lactate concentration. Thus, ST subjects were capable of accumulating more lactate in blood compared with ET subjects, but at the expense of a lower pH, since the buffer capacity seemed to be the same for the two groups. The acidosis, which was larger than could be accounted for by lactic acid, was associated with an inexplicably large anion gap.

Acid-Base Equilibrium↗
PubMed1985

Distribution of ouabain-binding sites along the dog nephron.

To quantify the relative amount of ouabain bound to different segments of the nephron after in vivo injection of the drug, an autoradiographic (ARG) study was carried out. After intrarenal injection of [3H]ouabain (120 nmol kg-1 body wt, 0.9-1.2 Ci mol-1) to intact kidneys of three anaesthetized dogs, 69-89% of renal Na,K-ATPase activity was inhibited. Sodium reabsorption decreased by 21-54%. Sections for ARG were obtained from tissue slices frozen in liquid Freon, freeze-dried and embedded in resin. Almost no loss of activity occurred during processing and background activity was negligible after 23-36 days' exposure. The density of [3H]ouabain grains per mu 2 of tubular walls was 3.8 times higher over medullary ascending limbs of Henle's loop (MAL) and distal cortical tubules (DT) as compared to proximal tubules (PT). In terms of tubular length, the grain density of MAL exceeded that of PT by merely 35% since the cross-sectional area of the MAL was only 25% of that of PT. In DT, grain density in terms of tubular length was lower than in PT by 10%. Based on previous estimate of the absolute ouabain-binding capacity in MAL of 60 fmol mm-1 tubule, the ouabain-binding capacity in PT and DT would equal 45 and 40 fmol mm-1, respectively. From composite microphotographs, the relative volume of PT was estimated to be 42% of the total renal volume. This means that 47% of the total renal ouabain-binding sites are localized to PT, whereas MAL and DT together contain 51%.

Animals↗
PubMed1985

Autoregulatory vasodilation enhances renal prostaglandin E2 and associated renin release during arachidonic acid infusion in dogs.

To examine whether autoregulatory dilation of preglomerular vessels enhances prostaglandin (PG)E2 and renin release during arachidonic acid infusion, the ureter was occluded or the renal artery constricted in anesthetized dogs. Intrarenal arachidonic acid infusion (40 micrograms X kg-1 X min-1) increased PGE2 release by 41 +/- 17 pmol/min at control pressures and by 149 +/- 60 pmol/min during ureteral occlusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) increased PGE2 release by 149 +/- 60 pmol/min at control pressures, by 505 +/- 211 pmol/min during ureteral occlusion and by 581 +/- 201 pmol/min during renal arterial constriction. Thus, PGE2 release during arachidonic acid infusion was trebled by autoregulatory dilation. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renin release by 6 +/- 2 micrograms of angiotensin I per min at control pressures, by 25 +/- 9 micrograms of angiotensin I per min during renal arterial constriction and during ureteral occlusion by 16 +/- 4 micrograms of angiotensin I per min, which was not significantly higher than induced by the lower rate of infusion. Arachidonic acid infusion (160 micrograms X kg-1 X min-1) raised renal blood flow by 54 +/- 5% at control pressures but exerted no vasoactive effect during ureteral occlusion and renal arterial constriction. We conclude that autoregulatory dilation enhances the stimulatory effects of arachidonic acid on renal PG synthesis. Both increased intrarenal PG concentration and autoregulatory dilation may contribute to enhancement of renin release. The stimulatory effects of arachidonic acid on PG synthesis and renin release are independent of the vasoactive effects of arachidonic acid.

Animals↗
PubMed1985

Potassium balance and ouabain binding sites in intact porcine hearts during isoproterenol infusion.

A pacing-induced tachycardia causes a net loss of K+ from the myocardium whereas adrenergic stimulation at constant heart rate will cause a net K+ accumulation. In the intact heart, isoproterenol (ISO) will, as expected, exert both effects, but the net result with regard to K+ balance is unknown. In the experiments on intact porcine hearts presented herein, a shunt from the coronary sinus to the right atrium allowed continuous monitoring of the myocardial K+ balance. ISO caused heart rate, dP/dt, and peak aortic flow to increase to a new steady state in less than 10 sec. There was an initial K+ loss lasting 1 min followed by a 10- to 15-times larger net uptake subsiding after 7 min. Overall, tissue K+ increased by 140.5 +/- 60.0 mumole/100 g, corresponding roughly to a 3 mM increase in intracellular concentration during ISO infusion. Ouabain binding sites determined in intact biopsies from the left ventricle remained unchanged. Thus, ISO has a biphasic effect on myocardial K+ balance, eventually causing a net increase of tissue K+ content probably unrelated to the inotropic effects. Direct stimulation of the Na+, K+-ATPase without changing the number of enzymes is possible.

Animals↗