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).

Variations in left ventricular volume alter myocardial oxygen consumption more at low than at high inotropy.

Variations in left ventricular (LV) wall tension during changes in LV end-diastolic volume significantly affect myocardial oxygen consumption (MVO2). In the present study we examined if the reduction in MVO2 per beat accompanying a decline in LV end-diastolic volume at constant LV systolic pressure (LVSP) is dependent on the level of myocardial inotropy. In six anaesthetized open-chest pigs, the blood volume was expanded by i.v. infusion of a Ringer solution. At constant heart rate (by atrial pacing) and LVSP (by adjustments of a proximal aortic snare), LV end-diastolic volume was reduced in steps by withdrawals of blood. This procedure was performed at high inotropy (during a continuous intracoronary infusion of isoproterenol, 0.40 +/- 0.08 micrograms min-1), and at low inotropy (after i.v. injection of 3.4 +/- 0.2 mg propranolol). LVSP was about 25 mmHg higher at high than at low inotropy. The fall in LV tension was therefore greater during blood volume reductions at high than at low inotropy because the fall in LV end-diastolic volume was almost identical and was initiated from the same level at both high and low inotropy. Nevertheless, the slope of the MVO2/LV end-diastolic volume relationship was significantly (P less than 0.05) less steep at high (1.26 +/- 0.30 mumol 100 g-1 mm-1) than at low inotropy (2.06 +/- 0.48 mumol 100 g-1 mm-1).(ABSTRACT TRUNCATED AT 250 WORDS)

A model for quantitative sampling of myocardial venous blood in the pig.

A lack of good models for studies of myocardial metabolism prompted us to develop a model which allows the continuous measurement of myocardial blood flow and sampling of adequate amounts of coronary sinus (c.s.) blood without admixture of blood from the right atrium, with the working heart in situ. In the pig the left azygos vein drains into the c.s. and can easily be cannulated after thoracotomy. Thus, a shunt to the right atrium can be established by closing the entrance of the c.s. into the right atrium by a stitch ligature. More than 90% of shunt flow originates from the left ventricular myocardium. It is presently shown that establishing the shunt does not compromise myocardial flow, and there are no observable changes in left ventricular pressure, flow or dimensions. Myocardial flow in the drained and adjacent regions, as determined by injections of microspheres, and flow determined by electromagnetic flowmetry on the shunt are all identical. The model is stable during aortic constriction and isoproterenol infusion which induce expected changes in myocardial flow- and oxygen consumption. Thus, the model described is suitable for hemodynamic and metabolic studies of the left ventricular myocardium with the working heart in situ.

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.

Isoprenaline augments total myocardial K+ influx of the in-situ beating porcine heart.

To determine the total rate of K+ flux into myocardial cells of the in-situ beating heart and how this influx is affected by beta-adrenoceptor stimulation, we measured 42K+ content in myocardial biopsies taken at intervals after an intra-atrial infusion of 42K+ before and during an i.v. isoprenaline infusion (20 micrograms min-1) in six anaesthetized, open-chest pigs. Determination of the total K+ influx during beta-adrenoceptor stimulation was initiated 10 min after the start of isoprenaline infusion, when the transient net myocardial K+ uptake had subsided. Total K+ influx increased from a control value of 414 +/- 42 to 1086 +/- 246 mumol 100 g-1 min-1 during isoprenaline infusion. A quantitatively smaller increase in K+ influx carried by the Na(+)-K+ pump has previously been demonstrated during isoprenaline infusion. Left ventricular dP/dt rose from 1350 +/- 146 to 4833 +/- 150 mmHg s-1, stroke volume remained unchanged, but heart rate and peak left ventricular systolic pressure rose as expected, by 52 +/- 4 and 32 +/- 4% respectively during isoprenaline stimulation. All haemodynamic parameters, total plasma K+ concentration and plasma 42K+ activity remained stable throughout each experimental period. The number of ouabain binding sites was 65.5 +/- 1.0 before and 66.9 +/- 1.6 nmol 100 g-1 during isoprenaline infusion (difference n.s.). The present data indicate that not only the K+ influx carried by the ouabain-sensitive Na(+)-K+ pump but also the influx through ouabain-insensitive pathways is increased during beta-adrenoceptor stimulation of the in-situ beating pig heart.

Myocardial oxygen consumption during atrial pacing at various inotropic levels.

In anaesthetized open-chest pigs (n = 15) we examined whether myocardial oxygen consumption (MVO2) per min increased in proportion to heart rate during right atrial pacing at control, high and low inotropy. By modulating aortic constriction and the circulating blood volume, left ventricular (LV) systolic blood pressure, stroke volume and LV dimensions were kept constant. Examinations at control inotropy (n = 7) showed a linear relationship between increments in MVO2 beat-1 and LV dP/dt when heart rate was increased in four steps, each of 10 beats min-1 from 130 +/- 3 beats min-1 (r = 0.76 +/- 0.08). In a second series (n = 8) heart rate was increased by 36-37 beats min-1 in control experiments, during intracoronary isoproterenol infusion (high inotropy) and after propranolol administration (low inotropy). The increments in MVO2 min-1 during pacing tachycardia were not significantly different at control, high or low inotropy. At high inotropy MVO2 beat-1 and LV dP/dt did not rise significantly during pacing tachycardia. Myocardial oxygen consumption beat-1 increased more at control (6.3 +/- 2.0%) than at high inotropy (diff: P less than 0.02). At low inotropy MVO2 beat-1 increased even more (17.4 +/- 2.8%) than at control inotropy (diff: P less than 0.05). Thus, the increase in MVO2 beat-1 during pacing tachycardia is related to the increase in LVdP/dt and is dependent on the level of inotropy; great increments during tachycardia after propranolol administration and no changes during intracoronary isoproterenol infusion.

[Outbreak of food-borne gastroenteritis caused by a Norwalk-like virus. Evaluation of methods for confirmation of the etiology in suspected viral gastroenteritis]. / Utbrudd av naeringsmiddelbåren gastroenteritt forårsaket av Norwalk-liknende virus. Vurdering av metoder for påvisning av etiologi ved mistenkt virusgastroenteritt.

Acute gastroenteritis is a common disease and can be food-borne. We describe an outbreak of acute gastroenteritis, probably caused by Norwalk-like virus, which struck 250 people in the course of one week in a small Norwegian community. The source of the infection was probably an infected food handler in a bakery who contaminated cream cakes with the virus. The sensitivity of electronmicroscopy and analyses of IgG antibodies in serum to detect the etiologic agent was very low. The sensitivity to Norwalk Virus Polymerase Chain Reaction was much higher, and this was a considerable diagnostic benefit during the epidemic. Close cooperation between the local health authorities, the food control authorities, the bakery and the public was necessary to diagnose the etiology, source and spread of this food-borne infection.

Dopamine release from the porcine myocardium.

Dopamine is a catecholamine with profound influence on cardiac function and known to be present in adrenergic nerve terminals as a precursor of noradrenaline. However, no previous study has examined whether dopamine is produced by myocardial tissue. During stable hemodynamic conditions in 13 young, thoracotomized pigs with the heart in situ, we found a net release of dopamine into the coronary sinus amounting to 1.39 +/- 0.36 ng/min X 100 g of left ventricular muscle mass (p less than 0.01). Dopamine was released from the myocardium whether the v-a difference for noradrenaline was positive or negative. This observation indicates a release of dopamine from the heart independent of sympathetic noradrenergic activity. Regulation of myocardial dopamine release remains unknown.