Relationship between myocardial K+ balance, O2 consumption, and contractility

Sarnoff, S.J.; Jp, Gilmore; Rh, McDonald; Wm, Daggett; Weisfeldt, M. L.; Mansfield, P. B.

doi:10.1152/ajplegacy.1966.211.2.361

Cited by 42 publications

(11 citation statements)

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“…Implied in this discussion, needless to say, is the assumption that these AP changes may be initiated by other types of ionic flux. The primacy of K + is invoked here only because it is compatible with the experimental observations of others (15)(16)(17)(18) and because repolarization is generally conceived to be generated by the efflux of K + ions.…”

Section: Physiologic Considerationsmentioning

confidence: 82%

“…The studies of Langer and Brady (15), as well as Hajdu (16), are consonant with such a hypothesis, demonstrating K + efflux in association with positive inotropic responses. Moreover, Samoff et al (17,18) have recently observed an association between augmentation of contractility and a net loss of K + from the isolated canine heart. Our studies are also in accord with the above hypothesis, demonstrating post-extrasystolic action potential changes which are quite consistent with increased K + efflux.…”

Section: Physiologic Considerationsmentioning

confidence: 97%

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The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Greenspan

Edmands

Fisch

1967

Circulation Research

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Simultaneous recordings of contractile tension and transmembrane potentials from canine ventricular tissue yielded a consistent correlation of action potential (AP) alteration with contractile change associated with abrupt rate change. The AP terminating a relative prolongation of the cycle-length manifested shortening of phase 2 with lengthening of phase 3 and was associated with potentiation of contractile force. Conversely, the AP terminating a relative abbreviation of cycle-length displayed a broader phase 2 with a more precipitous phase 3, while the associated contraction was less forceful than the control. In each circumstance, the relative magnitude of cycle-length change correlated with the extent of both AP change and contractile alteration. Changes in AP configuration may reflect changes in transmembrane flux of K + during repolarization consistent with the findings of prior workers who have related K* efflux to increased contractility. Mechanical altemans, in addition, was frequently observed in association with abrupt rate change and was consistently associated with an electrical altemans manifested by action potentials with alternately wide and narrow plateaus (phase 2). As above, the more forceful contractions were associated with action potentials which displayed a narrower "phase 2. Mechanical altemans initiated by abrupt fate change may represent an adaptive phenomenon prior to the establishment of a stable contractile state, as reflected by a stable AP configuration. ADDITIONAL KEY WORDScardiac repolarization and contractility cardiac contractility cardiac action potentials post-extrasystolic potentiation compensatory pause and repolarization mechanical and electrical altemans rest potentiation cycle-length, repolarization and contractility• Augmentation of cardiac contraction associated with abrupt rate change has been noted repeatedly in a variety of mammals (1) as well as the human (2) since first described by Langendorff in 1875. The mechanism by which such a phenomenon occurs has, nevertheless, remained obscure and of little more than academic concern until recently. With

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Section: Physiologic Considerationsmentioning

confidence: 82%

Section: Physiologic Considerationsmentioning

confidence: 97%

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Greenspan

Edmands

Fisch

1967

Circulation Research

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“…There are other, nonspatial ways, however, in which propranolol may decrease the deflection. As suggested by the work of Sarnoff et al (75), Parker et al (66), and Polimeni and Vassalle (76), decreases in oxygen consumption will also decrease the rate of potassium leakage and accumulation in the ischemic region. This in turn will limit the development of AVm and the TQ-ST deflection magnitude will decline.…”

Section: +++mentioning

confidence: 88%

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Holland¹,

Brooks²,

Lidl³

1977

J. Clin. Invest.

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A B S T R A C T Spatial and nonspatial aspects ofTQ-ST segment mapping were studied with the solid angle theorem and randomly coded data from 15,000 electrograms of 160 anterior descending artery occlusions each of 100-s duration performed in 18 pigs. Factors analyzed included electrode location, ischemic area and shape, wall thickness, and increases in plasma potassium (K+). Change from control in the TQ-ST recorded at 60 s (ATQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, ATQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) ATQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) ATQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123+18%, ATQ-ST at IS sites decreased (-38.1+3.6%), and sum of ATQ-ST at IS sites increased by only 67.3±10.3%. In RV NIS Pos ATQ-ST became Neg. With increased K+, ATQ-ST decreased proportionately to log K+ (r = 0.97±0.01) at IS and NIS sites on the epicardium and precordium. TQ-ST at 60 s was obliterated when K+ = 8.7+0.2 mM. All findings were significant (P < 0.005) and agreed with the solid angle theorem. Thus, a transmembrane potential difference and current flow at the IS boundary alone are responsible for the TQ-ST. Nonspatial factors affect the magnitude of transmembrane potential difference, while spatial factors alter the position of the boundary to the electrode site.

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“…Several theoretical possibilities besides a direct action of H + or CO 2 upon the contractile machinery can be contemplated. The first hypothesis devolves from the fact that interventions that increase myocardial contractility are frequently associated with changes in myocardial potassium balance (25,26), a release of potassium from the cell occurring during an increase in performance. This hypothesis is related to the findings of Brown and Goot (27), who demonstrated that a decrease of the ratio of intracellular to extracellular H + activity promotes a net loss of potassium from the skeletal muscle cell; on the other hand, the demonstration that hypercapnia is associated with an uptake of potassium by the myocardium gives support to this theory (28).…”

Section: Summary Of the Changes In Developed Tension And Maximal Dt/dmentioning

confidence: 99%

Contractility in Isolated Mammalian Heart Muscle after Acid-Base Changes

Cingolani

Mattiazzi

Blesa

et al. 1970

Circulation Research

111

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In-vitro experiments performed in cat papillary muscles and strips of rat right ventricle suggest that the changes in myocardial contractility that follow acid-base disturbances are not a function of extracellular pH. Simultaneous changes in Pco 2 and NaHCO 8 concentration, with extracellular pH constant, decreased developed tension and maximal rate of rise of the tension (dT/dt) without significant changes in the time to peak tension when the muscle was exposed to the solution with higher Pco 2 and NaHCO 8 concentration. At an extracellular pH of 7.40, developed tension decreased 0.51 ± 0.13 g/mm 2 (P<0.02) and dT/dt decreased 1.29 ± 0.50 g/sec (P < 0.05) with no significant change in time to peak tension (0.038 ± 0.022 sec). Changes in pH produced by increasing Pco 2 at constant NaHCO 3 concentration were followed by a significant decrease in contractility. A change of Pco 2 from 20 to 90 Tnm Hg that produced a change in extracellular pH from 7.60 to 7.00 was accompanied by a decrease in developed tension of 0.67 ± 0.14 g/mm 2 (P<0.01), in dT/dt of 2.63±0.54 g/sec (P<0.01) with no changes in time to peak tension (0.0017 ± 0.10 seconds). We were unable to show significant variations in contractility when extracellular pH was changed at a constant Pco 2 of approximately 21 mm Hg (NaHCO 8 7.5, 15, and 30 DIM) or at a Pco 2 of approximately 95 mm Hg (NaHCO 3 15, 30, 60, 80 and 120 HIM). Only when extracellular pH reached a value as high as 8.0 (Pco 2 21 mm Hg, NaHCO 3 80 HIM) a small but significant increase in contractility was evidenced. Either Pcoj or intracellular pH could be the major determinants of the changes in myocardial contractility that follow acid-base alterations. gest that contractility is a function of external pH and independent of the way in which a change in pH took place. These authors concluded that the observed changes were most closely associated with external pH. Changes in P002 alone had no significant effect. On the other hand, Lorkovic (3), using an in-vitro preparation of isolated frog ventricular muscle, concluded that both intra-and extracellular pH play a role in the observed changes in contractility. It is difficult to ascertain whether the changes in cardiac performance observed in isolated blood-perfused hearts, heart-lung, or more intact preparations are due to variation in blood pH, Pco 2 , or both (3-10).Recent experiments in our laboratory on heart-lung preparations or perfused dog hearts have demonstrated that heart performance is affected by changes in Pco 2 but not by changes in pH when Pco 2 is kept constant (11).Considering the discrepancies between our results and those obtained with in-vitro preparations by other authors, experiments were undertaken on cat papillary muscles and strips of rat right ventricle to supply information about the effect of Pco 2 , pH, and NaHCO 3 concentration on mammalian ventricular contractility. Evidence will be presented that in changing ventricular contractility during extracellular pH alterations, the way in which a change in ex...

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Relationship between myocardial K+ balance, O2 consumption, and contractility

Cited by 42 publications

References 0 publications

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

The Relation of Contractile Enhancement to Action Potential Change in Canine Myocardium

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

Contractility in Isolated Mammalian Heart Muscle after Acid-Base Changes

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