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

1994 ◽  
Vol 266 (2) ◽  
pp. H730-H740 ◽  
Author(s):  
K. Hata ◽  
Y. Goto ◽  
O. Kawaguchi ◽  
T. Takasago ◽  
A. Saeki ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Left Ventricular ◽  
Oxygen Cost ◽  
Membrane Oxygenator ◽  
Arterial Perfusion ◽  
Control Value ◽  
Arterial Blood ◽  
Total Mechanical Energy ◽  
Lv Volume ◽  
The Relationship

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.

Negative inotropism of hyperthermia increases oxygen cost of contractility in canine hearts

2000 ◽  
Vol 279 (6) ◽  
pp. H2855-H2864 ◽  
Author(s):  
Akio Saeki ◽  
Yoichi Goto ◽  
Katsuya Hata ◽  
Toshiyuki Takasago ◽  
Takehiko Nishioka ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Baseline Level ◽  
Myocardial Oxygen Consumption ◽  
Myocardial Metabolism ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Lv Function ◽  
Oxygen Cost ◽  
Negative Inotropism ◽  
Total Mechanical Energy

Heart temperature affects left ventricular (LV) function and myocardial metabolism. However, how and whether increasing heart temperature affects LV mechanoenergetics remain unclear. We designed the present study to investigate effects of increased temperature by 5°C from 36°C on LV contractility and energetics. We analyzed the LV contractility index ( Emax) and the relation between the myocardial oxygen consumption (MV˙o2) and the pressure-volume area (PVA; a measure of LV total mechanical energy) in isovolumically contracting isolated canine hearts during normothermia (NT) and hyperthermia (HT). HT reduced Emaxby 38% ( P < 0.01) and shortened time to Emaxby 20% ( P < 0.05). HT, however, altered neither the slope nor the unloaded MV˙o2of the MV˙o2-PVA relation. HT increased the oxygen cost of contractility (the incremental ratio of unloaded MV˙o2to Emax) by 49%. When Ca2+infusion restored the reduced LV contractility during HT to the NT baseline level, the unloaded MV˙o2in HT exceeded the NT value by 36%. We conclude that HT-induced negative inotropism accompanies an increase in the oxygen cost of contractility.

Mechanoenergetics of the Negative Inotropism of Isoflurane in the Canine Left Ventricle 

1997 ◽  
Vol 87 (1) ◽  
pp. 82-93 ◽  
Author(s):  
Yasunori Nakayama ◽  
Miyako Takaki ◽  
Kunihisa Kohno ◽  
Junichi Araki ◽  
Hiroyuki Suga
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Mechanical Energy ◽  
Contractile Proteins ◽  
Left Ventricular ◽  
Free Calcium ◽  
Canine Heart ◽  
Inotropic Effects ◽  
Total Mechanical Energy ◽  
Lv Volume

Background The mechanisms underlying the negative inotropic effects of isoflurane are incompletely understood. One suggested mechanism is that isoflurane may decrease Ca2+ sensitivity of contractile proteins. If so, more free calcium would be needed to activate contractile proteins to the same degree, which would impose a greater requirement for myocardial oxygen consumption used in the cycling of calcium. In this study, the authors use the excised, cross-circulated, canine heart model and the volume servopump technique to measure the effects of isoflurane on Emax (a contractile index) and on the relationship between pressure-volume area (PVA, a measure of total mechanical energy) and myocardial oxygen consumption per beat (VO2). Methods Effects of intracoronary isoflurane infused via a precoronary oxygenator on myocardial mechanoenergetics were studied during isovolumic contractions. The authors measured left ventricular (LV) pressure, LV volume, coronary flow, and arteriovenous oxygen content difference and computed Emax, VO2 and PVA at 0, 1.0, 1.5, and 2.0% isoflurane. From these data, the authors obtained oxygen costs of PVA and Emax in control subjects and in those receiving 2.0% isoflurane. Results Emax, PVA, and VO2 dose-dependently decreased by similar degrees (P &lt; 0.05). Isoflurane did not change the oxygen costs at 1.5% and 2.0% concentration (P &lt; 0.05). Conclusions These mechanoenergetic findings suggest that the primary method by which isoflurane decreases contractility is not by decreasing Ca2+ sensitivity of contractile proteins but mainly by decreasing Ca2+ handling in the excitation-contraction coupling without myocardial oxygen wasting effect.

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

1996 ◽  
Vol 270 (6) ◽  
pp. H1905-H1913
Author(s):  
K. Onishi ◽  
K. Sekioka ◽  
R. Ishisu ◽  
H. Tanaka ◽  
M. Nakamura ◽  
...  
Keyword(s):  
Energy Cost ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Oxygen Cost ◽  
Contraction Coupling ◽  
Total Mechanical Energy ◽  
Volume Relation ◽  
Hypocapnic Alkalosis

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.

O2cost of contractility but not of mechanical energy increases with temperature in canine left ventricle

1999 ◽  
Vol 277 (1) ◽  
pp. H65-H73 ◽  
Author(s):  
Takeshi Mikane ◽  
Junichi Araki ◽  
Shunsuke Suzuki ◽  
Ju Mizuno ◽  
Juichiro Shimizu ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Left Ventricular ◽  
Beating Heart ◽  
Canine Heart ◽  
Oxygen Cost ◽  
Temperature Dependent ◽  
Total Mechanical Energy ◽  
Myocardial Temperature ◽  
Linear Manner ◽  
Dependent Processes

We investigated the effects of myocardial temperature on left ventricular (LV) mechanoenergetics in the excised, cross-circulated canine heart. We used the framework of the LV contractility ( Emax)-pressure-volume area (PVA; a measure of total mechanical energy)-myocardial oxygen consumption (Vo2) relationship. We have shown this framework to be useful to integrative analysis of the mechanoenergetics of a beating heart. In isovolumic contractions at a constant pacing rate, increasing myocardial temperature from 30 to 40°C depressed Emaxand increased the oxygen cost of Emax, which was enhanced by dobutamine, in a linear manner. However, the slope of the Vo2-PVA relation (reciprocal of contractile efficiency) and its Vo2intercept remained constant. Q10values of Emax, the oxygen cost of Emax, and the oxygen cost of PVA were 0.4, 2.1 and 1.0, respectively, around normothermia. We conclude that the temperature-dependent processes of cross-bridge cycling and Ca2+handling integratively depress Emaxand augment its oxygen cost without affecting the oxygen cost of PVA as myocardial temperature increases by 10°C around normothermia.

NHE-1 participates in isoproterenol-induced downregulation of SERCA2a and development of cardiac remodeling in rat hearts

2011 ◽  
Vol 301 (5) ◽  
pp. H2154-H2160 ◽  
Author(s):  
Munetaka Shibata ◽  
Daisuke Takeshita ◽  
Koji Obata ◽  
Shinichi Mitsuyama ◽  
Haruo Ito ◽  
...  
Keyword(s):  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Beneficial Effects ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Male Wistar Rats ◽  
Lv Volume

Impaired Ca2+ handling is one of the main characteristics in heart failure patients. Recently, we reported abnormal expressions of Ca2+-handling proteins in isoproterenol (ISO)-induced hypertrophied rat hearts. On the other hand, Na+/H+ exchanger (NHE)-1 inhibitor has been demonstrated to exert beneficial effects in ischemic-reperfusion injury and in the development of cardiac remodeling. The aims of the present study are to investigate the role of NHE-1 on Ca2+ handling and development of cardiac hypertrophy in ISO-infused rats. Male Wistar rats were randomly divided into vehicle [control (CTL)] and ISO groups without or with pretreatment with a selective NHE-1 inhibitor, BIIB-723. ISO infusion for 1 wk significantly increased the ratios of heart to body weight and left ventricle (LV) to body weight and collagen accumulation. All of these increases were antagonized by coadministration with BIIB-723. The ISO-induced significant increase in LV wall thickness was suppressed significantly ( P < 0.05) by BIIB-723. ISO-induced decreases in cardiac stroke volume and a total mechanical energy per beat index, systolic pressure-volume area at midrange LV volume, were normalized by BIIB-723. The markedly higher expression of NHE-1 protein in the ISO group than that in CTL group was suppressed ( P < 0.05) by BIIB-723. Surprisingly, ISO induced downregulation of the important Ca2+-handling protein sarcoplasmic reticulum Ca2+-ATPase 2a, the expression of which was also normalized by BIIB-723 without changes in phosphorylated phospholamban (PLB)/PLB expression. We conclude that NHE-1 contributes to ISO-induced abnormal Ca2+ handling associated with cardiac hypertrophy. Inhibition of NHE-1 ameliorates cardiac Ca2+-handling impairment and prevents the development of cardiac dysfunction in ISO-infused rats.

Intrathoracic pressures and left ventricular configuration with respiratory maneuvers

1989 ◽  
Vol 66 (1) ◽  
pp. 481-491 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown ◽  
K. G. Warner ◽  
S. Khuri
Keyword(s):  
High Volume ◽  
Intermittent Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Lateral Dimension ◽  
Mueller Maneuver ◽  
Pericardial Pressure ◽  
Lv Volume ◽  
The Relationship ◽  
Phrenic Stimulation

In 12 dogs, we examined the correspondence between esophageal (Pes) and pericardial pressures over the anterior, lateral, and inferior left ventricular (LV) surfaces. Pleural pressure was decreased by spontaneous inspiration, Mueller maneuver, and phrenic stimulation and increased by intermittent positive pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). To separate effects due to blood flow, we analyzed beating and nonbeating hearts. In beating hearts, there were no significant differences between changes in Pes and pericardial pressures. In arrested hearts, increasing LV pressure by 8 Torr increased pericardial pressures by only 3.6 Torr. With IPPV and PEEP, increases in Pes and pericardial pressures were equal in live hearts and in low-volume arrested hearts (LV pressure = 4 Torr). In high-volume arrested hearts (LV pressure = 12 Torr), the increase in pericardial pressure over the anterior LV surface was less than Pes, whereas that over the lateral and inferior LV surfaces was the same as Pes. At high LV volume, in arrested hearts pericardial pressures decreased less than Pes during negative pressure maneuvers. In another six dogs, external LV configuration and volume were measured. In beating hearts during spontaneous inspiration, Mueller maneuver, and phrenic stimulation (endotracheal tube open), septal-lateral dimension and LV volume decreased by approximately 3% (P less than 0.05). This was also true for PEEP. In arrested hearts, septal-lateral dimension and LV volume decreased only with PEEP. We conclude that 1) the relationship between Pes and pericardial pressures is complex and depends on LV volume, local pericardial compliance, and the means by which Pes is changed, 2) changes in measured pericardial pressures did not completely explain changes in LV configuration, and 3) during different respiratory maneuvers, different forces account for the same observed changes in LV volume and configuration.

Left ventricular function of isoproterenol-induced hypertrophied rat hearts perfused with blood: mechanical work and energetics

2009 ◽  
Vol 297 (5) ◽  
pp. H1736-H1743 ◽  
Author(s):  
Chikako Nakajima-Takenaka ◽  
Guo-Xing Zhang ◽  
Koji Obata ◽  
Kiyoe Tohne ◽  
Hiroko Matsuyoshi ◽  
...  
Keyword(s):  
Relaxation Rate ◽  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Mechanical Work ◽  
Linear Relations ◽  
Rat Hearts ◽  
Total Mechanical Energy ◽  
Heart Preparation

We investigated left ventricular (LV) mechanical work and energetics in the cross-circulated (blood-perfused) isoproterenol [Iso 1.2 mg·kg−1·day−1 for 3 days (Iso3) or 7 days (Iso7)]-induced hypertrophied rat heart preparation under isovolumic contraction-relaxation. We evaluated pressure-time curves per beat, end-systolic pressure-volume and end-diastolic pressure-volume relations, and myocardial O2 consumption per beat (V̇o2)-systolic pressure-volume area (PVA; a total mechanical energy per beat) linear relations at 240 beats/min, because Iso-induced hypertrophied hearts failed to completely relax at 300 beats/min. The LV relaxation rate at 240 beats/min in Iso-induced hypertrophied hearts was significantly slower than that in control hearts [saline 24 μl/day for 3 and 7 days (Sa)] with unchanged contraction rate. The V̇o2-intercepts (composed of basal metabolism and Ca2+ cycling energy consumption in excitation-contraction coupling) of V̇o2-PVA linear relations were unchanged associated with their unchanged slopes in Sa, Iso3, and Iso7 groups. The oxygen costs of LV contractility were also unchanged in all three groups. The amounts of expression of sarcoplasmic reticulum Ca2+-ATPase, phospholamban (PLB), phosphorylated-Ser16 PLB, phospholemman, and Na+-K+-ATPase are significantly decreased in Iso3 and Iso7 groups, although the amount of expression of NCX1 is unchanged in all three groups. Furthermore, the marked collagen production (types I and III) was observed in Iso3 and Iso7 groups. These results suggested the possibility that lowering the heart rate was beneficial to improve mechanical work and energetics in isoproterenol-induced hypertrophied rat hearts, although LV relaxation rate was slower than in normal hearts.

Sensitivities of cardiac O2 consumption and contractility to catecholamines in dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H196-H205 ◽  
Author(s):  
Y. Ohgoshi ◽  
Y. Goto ◽  
S. Futaki ◽  
H. Yaku ◽  
H. Suga
Keyword(s):  
Mechanical Energy ◽  
Plasma Catecholamines ◽  
Systolic Pressure ◽  
Plasma Catecholamine ◽  
Catecholamine Level ◽  
Oxygen Cost ◽  
O2 Consumption ◽  
Total Mechanical Energy ◽  
Plasma Catecholamine Level ◽  
Stimulation Of

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.

Oxygen-wasting effect of inotropy  in the “virtual work model”

1999 ◽  
Vol 276 (4) ◽  
pp. H1339-H1345 ◽  
Author(s):  
Christian Korvald ◽  
Odd P. Elvenes ◽  
Lars M. Ytrebø ◽  
Dag G. Sørlie ◽  
Truls Myrmel
Keyword(s):  
Virtual Work ◽  
Mechanical Energy ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Chemomechanical Coupling ◽  
Total Mechanical Energy ◽  
Work Model ◽  
Inotropic Stimulation

In the “virtual work model,” left ventricular total mechanical energy (TME) is linearly related to myocardial oxygen consumption (MV˙o2). This relationship (MV˙o2-TME) is supposedly independent of inotropic stimulation, vascular loading, and heart rate variations. We reexamined the effect of inotropic stimulation (dopamine) on the metabolic to mechanical energy transfer in nine open-chest anesthetized pigs. Left ventricular mechanical energy was calculated using TME (mean ejection pressure × end-diastolic volume + stroke work), TMEW(end-diastolic volume reduced by unstressed ventricular volume), and the pressure-volume area (PVA). A highly linear relationship between MV˙o2and mechanical energy was found for all three indexes during control and dopamine runs ( r = 0.87–0.99). The slopes were unaltered by dopamine. y-Axis intercepts were (control vs. dopamine) as follows (in J ⋅ beat−1⋅ 100 mg−1; means ± SD): TME, 0.36 ± 0.12 vs. 0.61 ± 0.30 ( P< 0.02); TMEW, 0.43 ± 0.16 vs. 0.72 ± 0.32 ( P < 0.02); and PVA, 0.34 ± 0.13 vs. 0.60 ± 0.30 ( P < 0.02). We conclude that the virtual work model is dependent on inotropic stimulation and that new insight into myocardial chemomechanical coupling is not added by this concept.

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