Biomedical subjects

B K Slinker

Publications and source records attributed to B K Slinker.

At least 37 records · Page 2Linked to original sources

PubMed1994

Previous beat contraction history alters mechanical restitution in the isolated left ventricle.

OBJECTIVE: The aim was to test directly the hypothesis that the magnitude of previous beat contraction history will be greatest for short pulse intervals, will become smaller as pulse interval is lengthened, and will vanish when pulse interval is long enough to allow complete restitution. METHODS: Experiments were performed in isolated rabbit and ferret left ventricles in which pressure and volume were controlled with a servo-motor system. Two restitution curves were generated, each constructed from isovolumetric beats that were preceded by a beat with differing amounts of ejection: one curve was constructed from isovolumetric beats preceded by non-ejecting beats, while the other was constructed from isovolumetric beats preceded by a beats that had a high level of ejection (ejection fraction approximately 50%). RESULTS: When the isovolumetric beats used to construct a restitution curve were preceded by ejecting beats, the restitution curve was shifted upward (that is, higher activation at a given interval between beats) when compared to a restitution curve constructed from isovolumetric beats that were preceded by non-ejecting beats. CONCLUSIONS: Mechanical restitution is affected by the mechanical events of preceding contractions, implying that previous beat contraction history and restitution share a common mechanism and that restitution sets the stage for previous beat contraction history. Hence restitution is not simply a useful tool for assessing calcium cycling or interval dependent behaviour and should be viewed more broadly as a fundamental process in the beat to beat regulation of cardiac contraction.

Animals↗

PubMed1994

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts.

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Use of 2,3-butanedione monoxime to estimate nonmechanical VO2 in rabbit hearts.

The purpose of the present study was to evaluate the feasibility of partitioning myocardial O2 consumption (VO2) into mechanical and nonmechanical components in the whole heart preparation using a negative inotrope, 2,3-butanedione monoxime (BDM), which has been reported to have a selective effect on the contractile proteins in a low concentration range (< 6 mM). In six isolated bovine red blood cell-perfused rabbit hearts, VO2 and force-time integral (FTI) were measured during infusion of varying concentrations of BDM at a constant left ventricular volume chosen such that control left ventricular peak isovolumic pressure was approximately 100 mmHg. The VO2-FTI relation with BDM concentrations < or = 5 mM was highly linear (median r = 0.98). Its VO2-axis intercept at zero FTI had a positive value (mean 23% of control, 0.014 ml O2.beat-1 x 100 g-1). To confirm the selective effect of BDM on the contractile proteins, the intracellular free Ca2+ transient was measured with the fluorescent indicator indo 1 in three isolated buffer-perfused rabbit hearts. The amplitude of the Ca2+ transient was not altered by BDM at concentrations < or = 10 mM, although left ventricular developed pressure was markedly depressed. This finding indicates that BDM < or = 10 mM does not affect excitation-contraction coupling. We conclude that the VO2-axis intercept value of the VO2-FTI relation during BDM infusion in a low concentration range represents VO2 for nonmechanical energy utilization. The BDM method to partition VO2 into mechanical and nonmechanical components is thus feasible in the whole rabbit heart.

Animals↗

PubMed1992

The sinus node inhibitor UL-FS 49 lacks significant inotropic effect.

UL-FS 49 is a sinus node inhibitor that has been reported to reduce heart rate and may be useful in improving myocardial oxygen supply vs. demand. However, previous studies performed in a variety of preparations have produced mixed results regarding the independent inotropic effect of UL-FS 49. To determine whether UL-FS 49 has an inotropic effect, we measured both steady-state hemodynamic responses and transient hemodynamic responses to random preload and afterload changes, both with and without UL-FS 49. We found that under steady-state conditions, the effect of UL-FS 49 is so small that it would be of doubtful physiologic significance: a 3% increase in stroke volume (p = 0.007) and 7% increase in peak positive dP/dt (p = 0.051), in the presence of no statistically significant differences in end-diastolic pressure, end-diastolic volume, peak systolic pressure, end-systolic pressure, or heart rate. The more powerful multiple linear regression modeling of hemodynamic transient sequences resulting from random preload and afterload changes showed that UL-FS 49 is without a statistically significant direct effect on left ventricular function. We conclude that UL-FS 49 has no physiologically important direct effect on left ventricular pump function.

Algorithms↗

PubMed1992

Effects of amrinone and isoproterenol on mechanoenergetics of blood-perfused rabbit heart.

To compare the effects of amrinone (AMR) and isoproterenol (Iso) on left ventricular contractility and energetics, we assessed Emax (ventricular contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA, a measure of left ventricular total mechanical energy) in isolated cross-circulated (blood-perfused) rabbit hearts during infusion of AMR or Iso in either a constant-flow (CF) or constant-pressure (CP) perfusion mode. Both Emax and the VO2 intercept of the linear VO2-PVA relation increased significantly during AMRCP (increase in Emax 15% and increase in VO2 intercept 11%), ISOCF (49 and 43%), and ISOCP (55 and 54%) but not during AMRCF. However, neither drug changed the slope of the VO2-PVA relation (reciprocal of contractile efficiency) in either perfusion mode. Furthermore, with both drugs the relation between increases in Emax and the VO2 intercept fell on a single regression line (r = 0.92). We conclude that 1) although the mechanism of action and inotropic potency of the two drugs differ, their effects on cardiac energetic cost are essentially the same, i.e., both drugs increase the nonmechanical oxygen cost in proportion to the increase in contractility without changing contractile efficiency, and 2) a significant portion of the inotropic effect of AMR in the whole ventricle is likely due to increased coronary blood flow, i.e., Gregg's phenomenon.

Amrinone↗

PubMed1992

Single perturbed beat vs. steady-state beats for assessing systolic function in the isolated heart.

Single-beat and steady-state techniques for evaluating end-systolic pressure-volume relationship (ESPVR) and Frank-Starling mechanism (FSM) in the crystalloid-perfused isolated rabbit heart were compared. In the single-beat technique, a train of stable isovolumic beats was interrupted with a single perturbed beat that either ejected against various levels of imposed isobaric load (ESPVR protocol) or beat isovolumically against various levels of end-diastolic volume (V(ED); FSM protocol). In steady-state technique, sustained beating was established, isobarically, at each of various loads (ESPVR protocol) or, isovolumically, at each of various V(ED) values (FSM protocol). ESPVR from steady-state technique lay above and to the left of that from single-beat technique. Contractile state was not uniform within steady-state technique, whereas it was uniform within single-beat technique. In the FSM protocol, single-beat technique exhibited the following features relative to steady-state technique: 1) greater range of developed pressures, 2) steeper ascending limb and more sharply defined maxima, 3) higher maximal developed pressure (Pdmax), and 4) greater volume at Pdmax(Vmax). Again. a common contractile state existed within single-beat technique but not within steady-state technique. It was concluded that single-beat technique was preferable to steady-state technique for evaluating ESPVR and FSM because 1) single-beat technique required less time for obtaining data, 2) single-beat technique allowed identification of uncomplicated values of Pdmax and Vmax, and 3) single-beat technique provided a common contractile-state reference for all data, whereas steady-state technique did not.

Animals↗

PubMed1992

Absence of right ventricular isovolumic relaxation in open-chest anesthetized dogs.

During the left ventricular (LV) pump cycle, peak negative first derivative of pressure vs. time (dP/dt) occurs very close to the end of LV ejection, and there is a well-defined isovolumic relaxation period. Despite similarities between the right ventricular (RV) and LV pump cycles, recent studies indicate uncertainty as to whether peak negative RV dP/dt occurs simultaneously with RV end ejection and whether there is an isovolumic relaxation period during the RV pump cycle. To study these questions, we recorded relative timing of peak negative RV dP/dt, RV end ejection, and right atrial-RV pressure crossover in the open-chest anesthetized dog. The data demonstrate that peak negative RV dP/dt occurs an average of 60 ms before end ejection and that there is no RV isovolumic relaxation period. These findings have implications for the possible use of peak negative RV dP/dt as a marker of RV end ejection and for how time constants of pressure decay obtained during RV relaxation can be interpreted.

Anesthesia↗

PubMed1992

2,3-Butanedione monoxime increases contractile efficiency in the rabbit ventricle.

The efficiency of chemomechanical energy transduction (contractile efficiency) of the left ventricle (LV) has been calculated from the linear correlation of the systolic pressure-volume area (PVA) of the LV and its O2 consumption (VO2). Thus far, a wide range of acute interventions, including adrenergic agents, Ca(2+)-sensitizing drugs, and Ca2+ channel blockers have not altered contractile efficiency. In contrast, hyperthyroidism has been reported to decrease contractile efficiency, an effect attributed at the cross-bridge level to an increase in the V1/V3 myosin isoenzyme ratio. We hypothesized that an acute intervention which directly alters cross-bridge cycling would also change contractile efficiency. Accordingly, 2,3-butanedione monoxime (BDM), a negative inotropic agent that is thought to directly inhibit cross-bridge formation, was administered to seven excised, red blood cell-perfused, isovolumically beating rabbit LVs. At 3-4 mM perfusate concentration, BDM resulted in the following reversible mechanical and energetic effects compared with control. Contractility, assessed by the slope (Emax) of the end-systolic pressure-volume relation, decreased by 11% (196.6 +/- 25.9 vs. 222 +/- 28 mmHg/ml). Both the time to end systole (Tmax) and relaxation half time (T1/2) decreased. The slope of the VO2-PVA relation decreased by 20% (1.55 +/- 0.44 x 10(-5) vs. 1.95 +/- 0.52 x 10(-5) ml O2 x mmHg-1 x ml-1), equivalent to an increase in contractile efficiency from 36.5 +/- 10.4 to 46.4 +/- 14.4%, while the O2 costs of the mechanically unloaded LV decreased by 12% (0.0258 +/- 0.0060 vs. 0.0292 +/- 0.0064 ml O2 x beat-1 x 100 g-1). Finally, BDM also produced coronary vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Stability of myocardial O2 consumption-pressure-volume area relation in red cell-perfused rabbit heart.

We evaluated the mechanical and energetic stability of the isolated rabbit heart perfused with a suspension of bovine red cells in Krebs-Henseleit buffer in terms of the pressure-volume area (PVA) concept. PVA, the area surrounded by the end-systolic and end-diastolic pressure-volume (P-V) relations and the systolic P-V trajectory of the P-V diagram, represents the total mechanical energy generated by each cardiac contraction. Myocardial O2 consumption (VO2) per beat has been reported to be highly linearly correlated with PVA. We used the slope and VO2-axis intercept of the VO2-PVA relation as energetic parameters and the maximum P-V ratio (Emax) as a contractility index of the left ventricle (LV) and compared them every 30 min for 120 min. Emax, the slope, and VO2 intercept of the VO2-PVA relation did not change significantly over 120 min compared with their control values [7.3 +/- 2.9 mmHg.ml-1.100 g LV, (1.67 +/- 0.40) x 10(-5) ml O2.mmHg-1.ml-1, and (3.26 +/- 1.01) x 10(-2) ml O2.beat-1.100 g LV-1, respectively]. However, the goodness of the linear fit of the VO2-PVA relation decreased after 90 min (r = 0.94 control, 0.62 at 90 min, and 0.64 at 120 min). Therefore, we conclude that the isolated bovine red cell-perfused rabbit heart preparation is stable for mechanical and energetic studies for at least 60 min.

Animals↗

PubMed1991

Effect of coronary hyperemia on Emax and oxygen consumption in blood-perfused rabbit hearts. Energetic consequences of Gregg's phenomenon.

To assess the relation between increases in contractile function and oxygen consumption (VO2) during increased coronary flow (Gregg's phenomenon), we measured the end-systolic pressure-volume relation and the relation between VO2 and left ventricular systolic pressure-volume area (PVA, a measure of total mechanical energy output) in blood-perfused, isovolumically contracting rabbit hearts during control and intracoronary adenosine infusion. During adenosine infusion at a constant perfusion pressure (93 +/- 11 mm Hg), coronary flow increased by 99 +/- 76% (p less than 0.01), and the slope of the end-systolic pressure-volume relation, Emax (ventricular contractility index), increased by 18 +/- 15% (p less than 0.01). When compared at the same left ventricular volume, PVA increased by 20 +/- 14% (p less than 0.01) and VO2 by 19 +/- 15% (p less than 0.01) with adenosine. The VO2-PVA relation was linear under each condition (both median r = 0.98). With increased coronary flow, the VO2-intercept of the VO2-PVA relation (unloaded VO2) increased by 22 +/- 18% (p less than 0.01) without a change in the slope; that is, a parallel upward shift was observed, indicating that the contractile efficiency (energy conversion efficiency of the contractile machinery) remained constant. These increases in Emax and unloaded VO2 were not eliminated by beta-adrenergic blockade with propranolol. We conclude that increased coronary flow with adenosine at a constant perfusion pressure augments both Emax and the nonmechanical energetic cost for excitation-contraction coupling and basal metabolism via nonadrenergic mechanisms, without changing contractile efficiency.

Adenosine↗

PubMed1991

Cardiac cycle length modulates cardiovascular regulation that is dependent on previous beat contraction history.

Previous studies of the beat-to-beat regulation of left ventricular performance in the intact cardiovascular system have shown that the performance of the left ventricle on any one beat is influenced by the mechanical events of the previous beat, so-called previous beat contraction history. The general hypothesis investigated in this study is that previous beat contraction history occurs because of the perturbation of one or more biochemical processes with time courses that are long relative to one cardiac cycle. If this is true, then previous beat contraction history should depend on the interval between beats and, therefore, should extend beyond the previous beat to two, or even three, previous beats as heart rate is increased. Hemodynamic responses to random preload and afterload changes were measured in 11 anesthetized open-chest dogs on right heart bypass at three paced heart rates. Multiple linear regression was used to analyze these hemodynamic sequences and identify variables from the previous one, two, or three beats that were important in the mechanical history dependence of left ventricular function. The results of this analysis showed that under baseline conditions, all 11 hearts showed one beat of history dependence, with only two of 11 hearts showing a dependence on the previous two or three beats. At the highest heart rate, all 11 hearts still showed one beat of history dependence, but 10 of 11 hearts showed two beats of history dependence, and four of 11 showed three beats of history dependence (p less than 0.05). A general framework for the mechanism underlying these findings, which relates previous beat contraction history to the interval-dependent mechanical restitution phenomenon, is proposed and discussed.

Animals↗

PubMed1991

Left ventricular function depends on previous beat ejection but not previous beat pressure load.

Previous beat contraction history, in which the performance of the left ventricle on any one beat is influenced by the mechanical events of the previous beat, may be important in the beat-to-beat regulation of left ventricular performance in the intact cardiovascular system. Prior studies of this phenomenon have established that mechanical events of the previous beat influence the function of the current beat, but it is not known whether the important mechanical influence is exerted by previous beat ejection or previous beat pressure. In addition, the magnitude of the effect of previous beat contraction history on left ventricular performance is unknown. To make these determinations, we performed experiments in six isolated rabbit left ventricle preparations buffer perfused at 30 degrees C. Left ventricular pressure and volume were controlled precisely with a servo-controlled linear motor system. After steady-state ejecting conditions were established by clamping left ventricular ejection pressure at 60% of peak isovolumic pressure, single test beats, which were pressure clamped at 40%, 60%, 80%, and 100% of peak isovolumic pressure, were introduced and followed by an isovolumic reference beat. As the level of pressure clamp decreased from 100% to 40%, developed pressure on the isovolumic beat following the single test beats increased from 139 +/- 15 (mean +/- SD) to 151 +/- 13 mm Hg. Similarly, peak positive left ventricular dP/dt increased from 1,718 +/- 209 to 1,864 +/- 181 mm Hg.sec-1 (both p less than 0.01). Multiple regression analysis showed that this increase in left ventricular function was related to previous beat ejection but not to previous beat pressure load or relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Missing data in two-way analysis of variance.

We previously described a regression approach to analysis of variance computations that permitted analysis of unbalanced designs and experiments with missing data in two-way (or higher) analyses of variance Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R353-R367, 1988. That approach can only be used correctly under a set of narrow, and relatively uninteresting, circumstances. In fact, in the example we worked, we extended that approach beyond its intended scope and incorrectly computed F statistics for testing hypotheses about the main effects of strain of rat and nephron site in a study of renal Na(+)-K(+)-adenosinetriphosphatase. This paper presents the correct approach, which can be generalized to most situations likely to be encountered when two-way, or higher, analyses of variance are used.

Adenosine Triphosphatases↗

PubMed1990

Decreased contractile efficiency and increased nonmechanical energy cost in hyperthyroid rabbit heart. Relation between O2 consumption and systolic pressure-volume area or force-time integral.

Both systolic pressure-volume area (PVA) and force-time integral (FTI) have been used as measures of oxygen consumption per beat (VO2) in the isolated left ventricle. The reciprocal of the slope of the VO2-PVA relation has been considered to reflect the chemomechanical energy transduction efficiency of the contractile machinery (contractile efficiency), whereas its VO2 intercept consists of energy cost of excitation-contraction coupling and basal metabolism. To examine whether the increase in myosin isoform V1/V3 ratio in hyperthyroid rabbits decreases contractile efficiency and to determine overall mechanisms of higher oxygen consumption in hyperthyroid hearts, the VO2-PVA and VO2-FTI relations as well as the end-systolic pressure-volume relation were assessed in cross-circulated, isovolumically beating hearts isolated from normal, hyperthyroid, and hypothyroid rabbits. Normalized initial slopes of the rising limb of the curvilinearly fitted end-systolic pressure-volume relation (E'max, ventricular contractility index) were similar for normal and hyperthyroid groups. However, the slopes and VO2 intercepts of the VO2-PVA and VO2-FTI relations were greater in hyperthyroid hearts than in normal hearts. Accordingly, in the hyperthyroid hearts, the contractile efficiency (27 +/- 6%) was lower and left ventricular VO2 for excitation-contraction coupling (0.028 +/- 0.004 ml O2/beat/100 g) was higher than in normal hearts (40 +/- 4% and 0.021 +/- 0.005 ml O2/beat/100 g, respectively). This decreased contractile efficiency in the hyperthyroid hearts was attributable to myosin isoform alteration rather than to increased beta-adrenoceptors because isoproterenol did not affect the slope of the VO2-PVA relation in all groups. In contrast, the slope of the VO2-FTI relation was significantly increased by isoproterenol in all groups. Neither the VO2-PVA nor the VO2-FTI relations in hypothyroid hearts were different from those in normal hearts except for significantly lower VO2 for basal metabolism. We conclude that in hyperthyroid rabbits, the left ventricle has decreased contractile efficiency and increased energy cost of excitation-contraction coupling and that the decreased contractile efficiency in hyperthyroid hearts is probably due to the increased V1/V3 ratio of the myosin isoform component. In addition, this study demonstrates that the VO2-PVA and VO2-FTI relations dissociate depending on the intervention, even in the same isovolumic contraction mode.

Animals↗

PubMed1990

Pentoxifylline (Trental) does not inhibit dipyridamole-induced coronary hyperemia: implications for dipyridamole-thallium-201 myocardial imaging.

Dipyridamole-thallium-201 imaging is often performed in patients unable to exercise because of peripheral vascular disease. Many of these patients are taking pentoxifylline (Trental), a methylxanthine derivative which may improve intermittent claudication. Whether pentoxifylline inhibits dipyridamole-induced coronary hyperemia like other methylxanthines such as theophylline and should be stopped prior to dipyridamole-thallium-201 imaging is unknown. Therefore, we studied the hyperemic response to dipyridamole in seven open-chest anesthetized dogs after pretreatment with either pentoxifylline (0, 7.5, or 15 mg/kg i.v.) or theophylline (3 mg/kg i.v.). Baseline circumflex coronary blood flows did not differ significantly among treatment groups. Dipyridamole significantly increased coronary blood flow before and after 7.5 or 15 mm/kg i.v. pentoxifylline (p less than 0.002). Neither dose of pentoxifylline significantly decreased the dipyridamole-induced hyperemia, while peak coronary blood flow was significantly lower after theophylline (p less than 0.01). We conclude that pentoxyifylline does not inhibit dipyridamole-induced coronary hyperemia even at high doses.

Animals↗

PubMed1989

Direct diastolic ventricular interaction gain measured with sudden hemodynamic transients.

Changes in right ventricular volume affect left ventricular function via direct ventricular interaction mediated by the septum, common myocardial fibers in the free wall, and the pericardium, and also via series interaction mediated by changes in right ventricular output reaching the left ventricle through the pulmonary circulation. To study direct interaction, series interaction must be held constant or removed from the experimental preparation. Because there has been no way to directly measure direct ventricular interaction in the intact circulation, we developed a new method to experimentally separate these two components of ventricular interaction by combining abrupt occlusion of both venae cavae and quick withdrawal of 10-15 ml of blood from the right ventricle. This procedure decreased right ventricular end-diastolic pressure (RVEDP) on the next beat without changing pulmonary venous flow, left ventricular end-diastolic segment lengths, or left ventricular systolic function. The direct interaction gains, quantified as delta LVEDP/delta RVEDP, where LVEDP is left ventricular end-diastolic pressure, and delta refers to the change between the beats before and after reducing right ventricular volume, were (means +/- SD) 0.32 +/- 0.32 at steady-state LVEDP = 5 mmHg, 0.38 +/- 0.23 at LVEDP = 10 mmHg, and 0.28 +/- 0.32 at LVEDP = 15 mmHg. These gains were not significantly different (P greater than 0.50). Therefore, we calculated an overall average gain by pooling data from the three base-line LVEDP conditions. This value is 0.33 with 95% confidence interval 0.16-0.51. This 95% confidence interval indicates our data are consistent with many previous reports of diastolic direct interaction.

Animals↗

PubMed1989

Beat-to-beat regulation of left ventricular function in the intact cardiovascular system.

A variety of regulatory mechanisms have evolved to control the heart's pump function because the cardiovascular system must continually adapt to the changing demands that body functions place on it. This regulation takes place through many physiological systems; however, fine adjustments in cardiac pumping probably require adaptations more quickly than external control mechanisms (such as the autonomic nervous system) can compensate. Thus cardiac pumping is also regulated by mechanisms intrinsic to the heart. To better understand these intrinsic control mechanisms, we studied the beat-to-beat response of left ventricular function to continually varying changes in loading conditions produced by transiently occluding the pulmonary artery, venae cavae, and aorta. We used multiple linear regression to identify and quantify the important beat-to-beat determinants of left ventricular systolic function, quantified as stroke work. We could not adequately explain or predict beat-to-beat changes in stroke work with traditional determinants of ventricular function, preload, afterload, and heart rate, because a large systematic error remains after taking these traditional determinants of function into account. To eliminate this systematic error, we had to include some function of previous beat stroke volume and end-systolic size and pressure. This additional information significantly improved both our ability to model the observed transient changes in left ventricular stroke work and to predict additional observations that were not used to develop our model. We conclude that previous beat contraction history is an important determinant of left ventricular function and implies an important regulatory mechanism whereby the left ventricle can fine tune its function from beat to beat in response to continually changing loading conditions.

Animals↗

PubMed1989

Nonhomogeneous left ventricular regional shortening during acute right ventricular pressure overload.

Acute right ventricular pressure overload shifts the interventricular septum leftward and decreases systolic shortening of the left ventricular (LV) septal-lateral diameter. These changes should alter regional shortening in the LV minor axis. To test this hypothesis, LV minor axis circumferential segment lengths of the septum and anterior, lateral, and posterior walls were measured during pulmonary artery or venae caval constriction in seven open-chest dogs with intact pericardia. Starting at an end-diastolic pressure of 10 mm Hg, venae caval constriction decreased LV end-systolic pressure by 19 +/- 6% and stroke volume by 40 +/- 15% and produced uniform decreases in systolic shortening and end-diastolic length around the minor axis. However, during pulmonary artery constriction resulting in similar decreases in end-systolic pressure (22 +/- 7%) and stroke volume (39 +/- 11%), decreases in systolic shortening were significantly larger in the anterior (-34 +/- 10%) and posterior (-33 +/- 21%) walls than in the septum (-10 +/- 9%) or lateral wall (-8 +/- 13%). The mechanisms of these large anterior and posterior shortening decreases differed: anterior end-diastolic length decreased more than posterior and lateral end-diastolic lengths, while posterior end-systolic length decreased less than anterior and lateral end-systolic lengths. Similar changes were seen at starting end-diastolic pressures of 5 and 15 mm Hg. Propranolol did not alter this nonuniform response, while pericardiectomy attenuated the regional variations. Thus, changes in LV geometry during acute right ventricular pressure overload are associated with nonuniform regional changes in systolic shortening in the LV minor axis that are enhanced by the pericardium.

Animals↗