Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cross Circulation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed1987

Left ventricular O2 consumption and pressure-volume area in puppies.

We studied the relation between O2 consumption (VO2) and systolic pressure-volume (PV) area (PVA) in the left ventricles of eight puppies (2-4 mo old). PVA is the area circumscribed by the end-systolic and end-diastolic PV curves and systolic PV trajectory. We assumed PVA to represent the total mechanical energy generated by ventricular contraction. We produced isovolumic contractions at different volumes in the left ventricles isolated and cross-circulated with adult dogs. VO2 closely correlated with PVA in each of control contractile state, an enhanced contractile state with epinephrine, and a depressed contractile state with propranolol in each heart. The slope of the regression line of VO2 on PVA was not significantly affected by epinephrine and propranolol. The regression line shifted upward with epinephrine and downward with propranolol. These characteristics of the puppy's VO2-PVA relation were comparable to those of the adult dog. These results suggest that similar relations hold between myocardial mechanics and energetics in both the puppy and adult dog despite the differences in the heart size and contractile properties.

Animals↗
PubMed1988

Oxygen-saving effect of negative work in dog left ventricle.

We compared left ventricular oxygen consumptions (VO2) of contractions performing negative external work (EW less than 0) and positive external work (EW greater than 0) that developed comparable peak systolic pressures in the excised cross-circulated dog hearts. We changed the polarity of ventricular work with volume servo-pump and measured both left ventricular VO2 and systolic pressure-volume area (PVA). PVA represents the total mechanical energy generated by contraction and is equal to the area circumscribed by the end-systolic and end-diastolic pressure-volume (PV) relation curves and the systolic PV trajectory. For comparable peak systolic pressures of approximately 90 mmHg, contractions performing negative EW of -834 +/- 327 mmHg.ml.100 g left ventricle-1 had 27 +/- 11% smaller VO2 and 62 +/- 12% smaller PVA than those performing positive EW of 851 +/- 329 mmHg.ml.100 g-1. The smaller VO2 for negative EW could be accounted for by the linear VO2-PVA relation regardless of the polarity and magnitude of work. The results indicate that negative work can save VO2 of contractions to develop a given peak systolic pressure.

Animals↗
PubMed1988

O2 consumption of dog heart under decreased coronary perfusion and propranolol.

We compared the effects of decreased coronary perfusion pressure (CP) and propranolol on the relation between left ventricular O2 consumption (VO2) and systolic pressure-volume area (PVA). PVA represents total mechanical energy generated by contraction and is the area under the end-systolic pressure-volume (PV) line and systolic PV trajectory. In excised cross-circulated dog hearts, a decrease in CP from 82 (mean) to 51 mmHg decreased ventricular contractility index Emax (slope of end-systolic PV relation) by 17% (P less than 0.05) and slightly (P less than 0.05 in 3 of 11 hearts) lowered the VO2-PVA relation in a parallel fashion. A further decrease in CP to 32 mmHg decreased Emax by 56% (P less than 0.05) and considerably (P less than 0.05) lowered the VO2-PVA relation by decreasing both the VO2-axis intercept by 26% (P less than 0.05) and the slope by 24% (P less than 0.05) from control. Propranolol decreased Emax by 48% (P less than 0.05) and the VO2-axis intercept by 25% (P less than 0.05) without changing the slope (P greater than 0.05). We attributed the different response of the VO2-PVA relation to the difference of the coronary O2 supply-demand balance between decreased CP and propranolol.

Animals↗
PubMed1988

Integrated regional work equals total left ventricular work in regionally ischemic canine heart.

To assess left ventricular (LV) regional work with physically correct dimensions, wall tension-regional area (T-A) loops were analyzed before and after coronary occlusion in the excised cross-circulated canine LV (n = 11) connected to a volume-servo pump. Wall tension was calculated with the force equilibrium equation for a sphere, and regional areas were determined from pairs of orthogonal sonomicrometers in ischemic and nonischemic regions. LV and regional stroke work were simultaneously assessed from the pressure-volume and T-A loops during one cardiac cycle at various end-diastolic and stroke volumes. After coronary occlusion, regional work of the ischemic region markedly decreased to near or even below zero. Although regional work of the nonischemic region moderately decreased at constant LV end-diastolic and stroke volumes, the contribution of the nonischemic region to LV stroke work increased. Globally integrated regional work calculated from regional work/unit area and estimates of the extent of ischemia closely agreed with measured LV stroke work either before (n = 119; r = 0.92) or after coronary occlusion (n = 141; r = 0.93) despite the marked changes in regional work in both regions. We conclude that the global integral of regional work equals the total LV work and that regional work of the LV can be reliably assessed from the T-A loop with the same dimensions as energy in both normal and regionally ischemic hearts.

Animals↗
PubMed1989

Minor preload dependence of O2 consumption of unloaded contraction in dog heart.

We studied whether end-diastolic volume (EDV) would affect myocardial oxygen consumption (VO2) of mechanically unloaded contraction in the cross-circulated dog heart, as expected from the concept of the myocardial length-dependent activation. We made preloaded but maximally unloaded contractions from different EDVs by quickly releasing ventricular volume to eliminate systolic pressure development and hence to minimize the VO2 for mechanical load during the contraction. We then studied the relation between VO2 and EDV. The VO2 of the almost unloaded contraction from a relatively large EDV slightly exceeded the VO2 of the isovolumic contraction at V0, where V0 is the volume at which peak isovolumic pressure was zero. However, the excess VO2 could be ascribed to the residual systolic pressure-volume area (PVA) adversely produced from the large EDV, where PVA is a measure of the total mechanical energy generated during contraction. Therefore, we considered that VO2 was practically little dependent on EDV. We interpreted this finding as an indication that an increase, if any, in VO2 due to the length-dependent activation of the excitation-contraction coupling was practically negligible in the whole heart preparation.

Animals↗
PubMed1991

Sensitivities of cardiac O2 consumption and contractility to catecholamines in dogs.

We studied the effects of plasma catecholamines from the adrenal gland on systolic pressure-volume area (PVA)-independent O2 consumption (VO2) and contractility index (Emax) in the left ventricle of excised cross-circulated dog hearts. PVA is a measure of the total mechanical energy of contraction. Under baseline conditions, the PVA-independent VO2 correlated with plasma catecholamine level in the hearts (r = 0.84). Plasma epinephrine and norepinephrine levels increased gradually from 0.3 and 0.4 ng/ml to 10.3 and 2.7 ng/ml on average during adrenal sympathetic nerve stimulation of support dogs. Simultaneously, Emax and PVA-independent VO2 increased by 240 +/- 127 (SD) and 75 +/- 24%. Although their increases were monotonic in a given heart, their sensitivities to catecholamines were considerably variable among hearts. However, these two sensitivities were correlated (r = 0.96) with each other in the hearts, and the interheart variation of the sensitivity of the PVA-independent VO2 to Emax (i.e., oxygen cost of Emax) was smaller. We conclude that the oxygen cost of Emax is less variable among hearts despite large interheart variations of Emax and VO2 responses to plasma catecholamines.

Animals↗
PubMed1991

Equivalent pressure-volume area accounts for oxygen consumption of fibrillating heart.

We attempted to find cardiac mechanical parameters to account for myocardial O2 consumption (VO2) during ventricular fibrillation (VF). We fully utilized the concept of pressure-volume (P-V) area (PVA), which is equivalent to the total mechanical energy generated by a ventricular contraction. We also utilized a multicompartment model consisting of multiple asynchronously contracting compartments, which we previously proposed to simulate the mechanics of a fibrillating ventricle. The model analysis had already validated the application of PVA to VF in terms of "equivalent PVA" (ePVA). ePVA is the area surrounded by the end-systolic and end-diastolic P-V relations in beating state and the isobaric P-V line at the VF pressure. ePVA is supposed to represent the total mechanical energy generated by single contractions of each compartment (or myocyte) in a fibrillating ventricle. We determined ePVA and correlated it with measured VO2 per minute (mVO2) at various ventricular volumes in electrically induced fibrillating left ventricles of the excised cross-circulated canine heart preparation. Correlation coefficient (r) of the mVO2-ePVA relation during VF was high (r = 0.95, P less than 0.01). Comparing mVO2 during VF with that in beating state at an unloaded ventricular volume, we calculated equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual compartments (myocytes). With the use of both ePVA and eHR, mVO2 during VF at various ventricular volumes was estimated. The relation between estimated mVO2 and directly measured mVO2 was highly linear (r = 0.88, P less than 0.01), and the regression line almost agreed with the identity line (regression coefficient = 1.05). We conclude that the new ePVA and eHR concepts can reasonably account for VO2 during VF.

Animals↗
PubMed1991

External mechanical work during relaxation period does not affect myocardial oxygen consumption.

We assessed the effect of external mechanical work (EW) during the relaxation period (RP) on myocardial oxygen consumption (VO2) and clarified the energetic significance of the potential energy (PE) portion of the pressure-volume area (PVA) in the cross-circulated dog left ventricle. We changed the course of the relaxation segment of the pressure-volume (P-V) trajectory by increasing or decreasing EW within a given PVA without changing the end-diastolic volume (EDV) and the systolic segment of the P-V trajectory while measuring VO2. Thus the ventricle underwent ejection or filling during RP. Although the percent fraction of EW in PVA (%EW/PVA) was markedly increased from 32 +/- 12 (SD) to 93 +/- 3% in ejecting contractions (8 hearts) and from 0 to 93 +/- 5% in isovolumic contractions (3 hearts), these marked changes in %EW/PVA did not significantly affect VO2. Moreover, the VO2-PVA data during these procedures fell on the reference VO2-PVA relation line obtained by changing EDV and PVA of isovolumic contractions. We conclude that EW during RP at a constant PVA does not affect VO2 and part of PE can be converted into EW in an energetically equivalent manner.

Animals↗
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↗
PubMed1993

Ejecting deactivation does not affect O2 consumption-pressure-volume area relation in dog hearts.

We studied the effects of ejection velocity and resistive properties of the left ventricle (LV) on myocardial oxygen consumption (VO2) in 13 excised cross-circulated dog hearts. Increases in peak ejection velocity (-dV/dt) from 4.0 +/- 1.3 (SD) end-diastolic volume (EDV)/s to 12.7 +/- 5.3 EDV/s with constant EDV and end-systolic volume (velocity run) induced systolic pressure deficit. This decreased pressure-volume area (PVA; a measure of ventricular mechanical energy) and LV end-systolic elastance (Emax) by 47 +/- 14 and 38 +/- 15%, respectively. Unchanged maximum rate of left ventricular pressure rise and time-varying elastance during the isovolumic contraction period at the same EDV indicated that these contractions started with the same contractile state although the quicker ejection caused the greater deactivation. If the PVA deficit due to systolic pressure deficit is attributable to an internal energy-dissipating resistive element, VO2 in the velocity run will not as much decrease in proportion to PVA as in the isovolumic or slowly ejecting control run. However, the decreases in PVA due to increased -dV/dt decreased VO2 to the same extent as in the control run. This result negated the possibility that the pressure and PVA deficits would be caused by a mechanical energy-losing process. The same results were obtained whether or not Emax was decreased by quick ejection. We conclude that the pressure and PVA deficits and the proportionally decreased VO2 during quick ejection are mainly attributable to suppression of a ventricular mechanical energy generation process, but not of mechanical energy-losing process, by ejecting deactivation.

Animals↗
PubMed1993

Resetting of regional preload due to ventricular shape change alters diastolic and systolic performance.

The diastolic and systolic pressure of one ventricle is increased by an increase in volume and/or pressure of the opposite ventricle; however, a mechanism for the ventricular interaction remains unclear. We hypothesized that the shape change of one ventricle elicited by the opposite ventricle would lead to resetting of the regional length, which may explain the ventricular interaction. We used 15 cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were independently controlled. Diastolic regional segment area was calculated by multiplying circumferential and longitudinal lengths on right ventricular free wall (RVFW; n = 6), interventricular septum (IVS; n = 11), and left ventricular (LV) FW (n = 12). The regional area at relatively small volumes of both ventricles were expressed as 100%. With constant RV volume, increasing LV from 7 to 19 ml increased RV diastolic and systolic pressures by 2.7 and 5.5 mmHg, respectively. Conversely, increasing RV volume increased LV diastolic and systolic pressures by 2.3 and 7.5 mmHg, respectively. Increasing LV volume increased RVFW regional area from 121.0 to 124.6% (P < 0.01) and increased IVS regional area from 103.3 to 108.7% (P < 0.01), whereas the RV volume was held constant. Increasing RV volume also increased LVFW and IVS regional areas from 109.9 to 111.6% (P < 0.01) and from 106.8 to 108.9% (P < 0.05), respectively. Ventricular shape change elicited by ventricular interaction will increase the regional wall area, even though the volume of the chamber is unchanged. The increase in the regional area alters the position of the tissue on its resting and active length-tension relations and, thus, leads to enhancement of the chamber pressure.

Animals↗
PubMed1994

Hypercapnic acidosis increases oxygen cost of contractility in the dog left ventricle.

The effect of acidosis on left ventricular (LV) mechanoenergetics was assessed in seven excised, cross-circulated dog hearts with the use of the frameworks of the contractility index (Emax) and the relationship between myocardial oxygen consumption (VO2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO2 and air in a membrane oxygenator in the coronary arterial perfusion circuit. Acidosis [pH: 6.98 +/- 0.09 (SD), PCO2: 91 +/- 25 mmHg in the coronary arterial blood] decreased Emax by 45 +/- 12% (P < 0.01) and PVA by 47 +/- 12% (P < 0.01) at a fixed LV volume. When the preacidosis Emax level was restored by Ca2+ infusion during acidosis, unloaded VO2 (the VO2 intercept of the VO2-PVA relation) exceeded the control value by 19 +/- 17% (P < 0.05), indicating that acidosis required higher VO2 for nonmechanical activities at a matched Emax. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded VO2 to Emax) was 1.53 +/- 0.40 times higher (P < 0.01) during acidosis than preacidosis. We conclude that acidosis results in LV contractile dysfunction accompanied by an increased oxygen cost of contractility. This increased energy cost of the excitation-contraction coupling can be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.

Acidosis↗
PubMed1996

Mechanoenergetics of negative inotropism of ventricular wall vibration in dog heart.

Mechanical vibration depresses cardiac contractility. We studied the mechanoenergetic effects of this negative inotropism in the left ventricle (LV) of an isolated, cross-circulated dog heart preparation. We took full advantage of the mechanoenergetic relationship among the LV end-systolic elastance (Emax, contractility index), systolic pressure-volume area (PVA), and myocardial oxygen consumption (VO2). PVA is a measure of the total mechanical energy that cardiac contraction generates. PVA correlates closely with VO2. The VO2 intercept of the VO2-PVA relation reflects the VO2 component for excitation-contraction (E-C) coupling plus basal metabolism (PVA-independent VO2). VO2 above the PVA-independent VO2 reflects the VO2 component for mechanical contraction (PVA-dependent VO2). When we applied 70-Hz vibration of 2-mm amplitude to a LV wall region, it instantly decreased Emax and PVA by 20%, followed by a 10% decrease in VO2 at a fixed volume. However, the vibration neither lowered the VO2-PVA relation obtained at different LV volumes, unlike ordinary negative inotropism, nor changed its slope (1.88 +/- 0.23 vs. 1.86 +/- 0.23 x 10(-5) ml O2.mmHg-1.ml-1). The virtually zero delta PVA-independent VO2/delta Emax with vibration indicates a much smaller O2 cost of Emax than that seen with calcium and propranolol inotropism. These mechanoenergetics support the hypothesis that mechanical vibration primarily suppresses cardiac contractility without suppressing E-C coupling.

Animals↗
PubMed1996

Decrease in oxygen cost of contractility during hypocapnic alkalosis in canine hearts.

Ca2+ sensitization of contractile machinery could theoretically enhance the mechanoenergetics of the heart. We studied the effects of alkalosis with Ca2+ sensitization on mechanoenergetics within the framework of the relationships of left ventricular pressure-volume area (PVA; a measure of the total mechanical energy), myocardial oxygen consumption per beat (VO2), and the contractility index [E(max) (slope of end-systolic pressure-volume relation)] in 10 excised, cross-circulated canine hearts. Alkalosis was stably maintained without hypoxia (mean pH 7.66). Alkalosis increased E(max) without changing the slope of the VO2-PVA relation, a reflected contractile efficiency. The incremental ratio of unloaded VO2 to E(max) in alkalosis was significantly lower than that in Ca2+ sensitization (0.0012 +/- 0.0010 vs. 0.0062 +/- 0.0030 ml O2 . mmHg-1 . ml . beat-1 . 100 g LV-2; P < 0.01). Basal metabolism under KCl arrest was unchanged by alkalosis, indicating the decreased energy cost of the excitation-contraction coupling by alkalosis. Compared with the control, alkalosis increased E(max) during the Ca2+ infusion of various concentrations without any further increase in unloaded VO2. Thus we demonstrated a decreased oxygen cost of contractility during alkalosis, presumably due to Ca2+ sensitization.

Alkalosis, Respiratory↗
PubMed1997

MCI-154, a Ca2+ sensitizer, decreases the oxygen cost of contractility in isolated canine hearts.

An increase in the responsiveness of the contractile machinery to Ca2+ could theoretically enhance the mechanoenergetics of the heart. To clarify this unresolved issue, we studied the effects of MCI-154, a Ca2+ sensitizer, on the mechanoenergetics in terms of the left ventricular contractility index [slope of end-systolic pressure-volume relationship (Emax)] and the relationship between myocardial oxygen consumption (VO2) and left ventricular pressure-volume area in excised cross-circulated canine hearts. MCI-154 increased Emax by 42 +/- 31% (SD), although the slope of the VO2-PVA relationship (an indicator of contractile efficiency) was unchanged by MCI-154. Despite equal increases in Emax, the relative increase in unloaded VO2 (delta VO2/delta Emax) during infusion of MCI-154 was, however, significantly less than that during CaCl2 infusion (0.0016 +/- 0.0018 vs. 0.0059 +/- 0.0054; P < 0.05). By contrast, delta VO2/delta Emax for milrinone was the same as that for CaCl2 (0.0043 +/- 0.0041 vs. 0.0039 +/- 0.0045; P > 0.05). Basal metabolism in KCl-arrested hearts was unchanged by MCI-154, indicating that MCI-154 consumes less energy than CaCl2 for excitation-contraction coupling. These findings suggest that MCI-154 acts energetically as a Ca2+ sensitizer in beating canine whole hearts.

Animals↗
PubMed1998

A new method to measure regional myocardial time-varying elastance using minute vibration.

We developed a new technique to evaluate regional myocardial elastance using minute vibration. In 13 isolated cross-circulated canine hearts, we applied small sinusoidal vibrations of displacement to the left ventricular surface at various frequencies (50-100 Hz). Using the measured displacement and force between the vibrator head and myocardium, we derived myocardial elastance on the basis of the equation of motion for a given moment of the cardiac cycle. Simultaneous solution of the equations of motion at different frequencies yielded a unique value of elastance. Time-varying myocardial elastance increased from diastole (0.028 +/- 0.211 x 10(6) dyn/cm) to systole (0.833 +/- 0.391 x 10(6) dyn/cm). The end-systolic elastance (ees) linearly correlated with end-systolic left ventricular elastance (r = 0.717, P < 0.001) and also with the end-systolic Young's modulus (r = 0.874, P < 0.0001). We also measured ees at both ischemic and nonischemic regions during coronary occlusion. Young's modulus, estimated by normalizing ees by the wall thickness and by the estimated mass, did not change significantly at the nonischemic regions, whereas it decreased significantly from 2.303 +/- 0.556 to 1.173 +/- 0.370 x 10(6) dyn/cm2 at the ischemic region after coronary occlusion (P < 0.005). We conclude that this technique is useful for the quantitative assessment of regional myocardial elastance.

Animals↗
PubMed1999

Novel method to estimate ventricular contractility using intraventricular pulse wave velocity.

We developed a novel technique for estimating ventricular contractility using intraventricular pulse wave velocity (PWV). In eight isolated, cross-circulated canine hearts, we used a fast servo pump to inject a volume pulse into the base of the left ventricular chamber at late diastole and at late systole. We measured the transit time of the volume pulse wave as it traversed the distance from base to apex and calculated the intraventricular PWV. The intraventricular PWV increased from diastole (2.3 +/- 0.4 m/s) to systole (11.7 +/- 2.4 m/s, P < 0.0001 vs. diastole). The square of the intraventricular PWV at late systole correlated linearly with the left ventricular end-systolic elastance (r = 0.939, P < 0.0001) and with the end-systolic Young's modulus (r = 0.901, P < 0.0001). Moreover, the intraventricular PWV was insensitive to preload. We conclude that the intraventricular PWV at late systole reflects left ventricular end-systolic elastance reasonably well. The fact that estimation of PWV does not require volume measurement or load manipulation makes this technique an attractive means of assessing ventricular contractility.

Animals↗
PubMed2000

Energy-wasteful total Ca(2+) handling underlies increased O(2) cost of contractility in canine stunned heart.

Postischemic myocardial stunning halved left ventricular contractility [end-systolic maximum elastance (E(max))] and doubled the O(2) cost of E(max) in excised cross-circulated canine heart. We hypothesized that this increased O(2) cost derived from energy-wasteful myocardial Ca(2+) handling consisting of a decreased internal Ca(2+) recirculation, some futile Ca(2+) cycling, and a depressed Ca(2+) reactivity of E(max). We first calculated the internal Ca(2+) recirculation fraction (RF) from the exponential decay component of postextrasystolic potentiation. Stunning significantly accelerated the decay and decreased RF from 0.63 to 0. 43 on average. We then combined the decreased RF with the halved E(max) and its doubled O(2) cost and analyzed total Ca(2+) handling using our recently developed integrative method. We found a decreased total Ca(2+) transport and a considerable shift of the relation between futile Ca(2+) cycling and Ca(2+) reactivity in an energy-wasteful direction in the stunned heart. These changes in total Ca(2+) handling reasonably account for the doubled O(2) cost of E(max) in stunning, supporting the hypothesis.

Animals↗