Increased myocardial contractility during endotoxin shock in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H715-H722 ◽  
Author(s):  
P. M. Kober ◽  
J. X. Thomas ◽  
R. M. Raymond

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

1988 ◽  
Vol 254 (6) ◽  
pp. H1051-H1058
Author(s):  
E. S. Myhre ◽  
A. Johansen ◽  
H. Piene

A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external stroke work, optimum values of stroke volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure, RAP) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10–1.20 (RAP 5–15 mmHg); Emax/mEmax 1.21–1.41; and Rp/mRp 0.84–0.69. After LV depression, SV/mSV was 0.80–0.83, Emax/mEmax was 0.78–0.71, and Rp/mRp was 1.56–1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.


2000 ◽  
Vol 278 (3) ◽  
pp. H698-H705 ◽  
Author(s):  
Sumanth D. Prabhu ◽  
Gregory L. Freeman

To test the hypothesis that alterations in left ventricular (LV) mechanoenergetics and the LV inotropic response to afterload manifest early in the evolution of heart failure, we examined six anesthetized dogs instrumented with LV micromanometers, piezoelectric crystals, and coronary sinus catheters before and after 24 h of rapid ventricular pacing (RVP). After autonomic blockade, the end-systolic pressure-volume relation (ESPVR), myocardial O2 consumption (MV˙o 2), and LV pressure-volume area (PVA) were defined at several different afterloads produced by graded infusions of phenylephrine. Short-term RVP resulted in reduced preload with proportionate reductions in stroke work and the maximum first derivative of LV pressure but with no significant reduction in baseline LV contractile state. In response to increased afterload, the baseline ESPVR shifted to the left with maintained end-systolic elastance ( E es). In contrast, after short-term RVP, in response to comparable increases in afterload, the ESPVR displayed reduced E es ( P < 0.05) and significantly less leftward shift compared with control ( P< 0.05). Compared with the control MV˙o 2-PVA relation, short-term RVP significantly increased the MV˙o 2 intercept ( P< 0.05) with no change in slope. These results indicate that short-term RVP produces attenuation of afterload-induced enhancement of LV performance and increases energy consumption for nonmechanical processes with maintenance of contractile efficiency, suggesting that early in the development of tachycardia heart failure, there is blunting of length-dependent activation and increased O2requirements for excitation-contraction coupling, basal metabolism, or both. Rather than being adaptive mechanisms, these abnormalities may be primary defects involved in the progression of the heart failure phenotype.


1996 ◽  
Vol 85 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier

Background The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs. Methods Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively. Results Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane. Conclusions The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (&lt; 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.


1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.


1962 ◽  
Vol 203 (6) ◽  
pp. 1141-1144 ◽  
Author(s):  
Jay M. Levy ◽  
Emmanuel Mesel ◽  
Abraham M. Rudolph

Simultaneous right and left ventricular stroke volumes were measured with electromagnetic flow probes in open-chest, anesthetized dogs. Atrial ectopic beats with normal ventricular depolarization produced differences between right and left ventricular stroke output, although the right and left ventricular pressures were proportionately reduced to an equal extent. This imbalance in volume ejected was a result of the differences in diastolic level, related to peak systolic pressure, in the aorta compared with pulmonary artery. With ventricular ectopic beats, the stimulated ventricle failed to develop the same percentage of control pressure as did the contralateral ventricle. The difference between aortic and pulmonary flow was thus less marked with right ventricular ectopic beats, and exaggerated with left ventricular ectopic beats.


1956 ◽  
Vol 186 (2) ◽  
pp. 365-368 ◽  
Author(s):  
D. M. MacCanon ◽  
Steven M. Horvath

Comparisons were made between the respiratory variations in right and left ventricular and femoral arterial pressures of anesthetized dogs before and after the administration of l-epinephrine and l-norepinephrine. These analyses revealed significant deviations from control patterns following administration of these pressor drugs, but only at isolated points in the respiratory cycle. Many of these alterations could only be explained on the basis of alterations in cardiac and/or vasomotor activity.


1978 ◽  
Vol 234 (3) ◽  
pp. H260-H265
Author(s):  
A. C. Kralios ◽  
T. J. Tsagaris

In pentobarbital-anesthetized, open-chest dogs with fixed heart rate, cardiac output, and systemic arterial pressure, ectopic ventricular activation originating from apical as compared to basilar regions of either ventricle was associated with small (3--5%) but significantly (P less than 0.005) lower myocardial O2 consumption (MVO2) and thus higher left ventricular (LV) efficiency without change in LV end-diastolic pressure (LVEDP), work index (LVWI), and LV dP/dt. Data obtained during epicardial and corresponding endocardial activation did not differ. During normal ventricular activation, MVO2 remained unchanged but LVEDP was significantly (P less than 0.005) lower, thus yielding higher LVWI and efficiency. MVO2 differences among ectopic sites were abolished after coronary artery occlusion, whereas data obtained during endocardial and epicardial on normal and ectopic activation were not affected. Thus, normal activation resulting in lower LVEDP is most efficient; apical ventricular activation is less efficient at the same MVO2P basilar is the least efficient, because both MVO2 and LVEDP are higher. Ventricular activation sequence changes do not constitute a substantial determinant of MVO2.


2005 ◽  
Vol 99 (4) ◽  
pp. 1422-1427 ◽  
Author(s):  
Titus Kuehne ◽  
B. Kelly Gleason ◽  
Maythem Saeed ◽  
Daniel Turner ◽  
Jochen Weil ◽  
...  

This study was conducted to determine the effects of chronic combined pulmonary stenosis and pulmonary insufficiency (PSPI) on right (RV) and left ventricular (LV) function in young, growing swine. Six pigs with combined PSPI were studied, and data were compared with previously published data of animals with isolated pulmonary insufficiency and controls. Indexes of systolic function (stroke volume, ejection fraction, and cardiac functional reserve), myocardial contractility (slope of the end-systolic pressure-volume and change in pressure over time-end-diastolic volume relationship), and diastolic compliance were assessed within 2 days of intervention and 3 mo later. Magnetic resonance imaging was used to quantify pulmonary insufficiency and ventricular volumes. The conductance catheter was used to obtain indexes of the cardiac functional reserve, diastolic compliance, and myocardial contractility from pressure-volume relations acquired at rest and under dobutamine infusion. In the PSPI group, the pulmonary regurgitant fraction was 34.3 ± 5.8%, the pressure gradient across the site of pulmonary stenosis was 20.9 ± 20 mmHg, and the average RV peak systolic pressure was 70% systemic at 12 wk follow-up. Biventricular resting cardiac outputs and cardiac functional reserves were significantly limited ( P < 0.05), LV diastolic compliance significantly decreased ( P < 0.05), but RV myocardial contractility significantly enhanced ( P < 0.05) compared with control animals at 3-mo follow-up. In the young, developing heart, chronic combined PSPI impairs biventricular systolic pump function and diastolic compliance but preserves RV myocardial contractility.


2018 ◽  
Vol 21 (4) ◽  
pp. E307-E310
Author(s):  
Peter Michael Rodgers-Fischl ◽  
Daniel L. Davenport ◽  
Sibu P. Saha ◽  
Maya E. Guglin

Introduction: The Framingham Studies revealed that diabetes mellitus (DM) predisposed subjects to a two- to eight-fold increase in the risk of developing heart failure (HF). However, there is much less information available about the reverse issue; namely, whether there is an increased risk of developing DM in patients with HF. We sought to determine if reversal or partial reversal of HF through aortic valve replacement (AVR) would improve glycemic control in patients with DM at our institution. Methods: The electronic medical records of 57 consecutive diabetic patients were retrospectively analyzed. These patients had undergone AVR at a medium-sized academic medical center from May 2005 through May 2015, and had glycated hemoglobin (HbA1C) measured before and after the procedure. The variables of interest included HbA1C, and echocardiographic parameters such as left ventricular ejection fraction (LVEF), tricuspid regurgitation velocity (TRV), and right ventricular systolic pressure (RVSP) before and after valve replacement. Results: HbA1C decreased significantly during the first year after replacement, from 7.1% (range 4.4 - 13.0%) before surgery to 6.5% in the first year (P < .05). In addition, the calculated RVSP decreased from 44 mmHg (20 - 79 mmHg) to 37 mmHg (P < .05 from the preoperative value). LVEF and TRV did not change significantly. Reductions in HbA1C and RVSP during the first year were greater in patients who experienced an increase of 5% or more in EF at their first postoperative measurement. Patients with higher baseline HbA1C values had a greater decline in glycated Hb during the first year (P < .01). Conclusion: AVR was associated with a reduction of HbA1C and a decrease in pulmonary artery systolic pressure within one year of the procedure.


1996 ◽  
Vol 24 (02) ◽  
pp. 169-176 ◽  
Author(s):  
Xi Huang ◽  
Yiming Zang ◽  
Yuming Wang ◽  
Guobao Niu ◽  
Aidong Wen ◽  
...  

Hemodynamic actions of intravenous (iv) administration of tetramethylpyrazine phosphate (TMPP) and sodium ferulate (SF) alone or in combination were studied in anesthetized dogs. When given alone, TMPP increased left ventricular systolic pressure (LVSP), peak positive first derivative of left ventricular pressure (+LVdp/dt), coronary blood flow (CBF) and heart rate (HR) while decreasing mean aortic pressure (mAoP). SF alone did not produce any significant hemodynamic changes. When the two were administered in combination, SF antagonized dose-dependently the hemodynamic actions of TMPP. Results of this study did not support the efficacy of combined treatment of Ligusticum wallichi and Angelica root, which contain TMPP and SF respectively.


Sign in / Sign up

Export Citation Format

Share Document