Abstract 2329: Donor Pretreatment with Hypertonic Saline Attenuates Primary Cardiac Allograft Dysfunction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Mitesh V Badiwala ◽  
Danny Ramzy ◽  
Laura C Tumiati ◽  
Elissa D Tepperman ◽  
Rohit Sheshgiri ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Heart Arrest ◽  
Myocardial Function ◽  
Left Ventricular ◽  
Cardiac Allograft ◽  
Stroke Work ◽  
Donor Heart ◽  
Ventricular Performance ◽  
Post Transplant ◽  
Donor Pretreatment

Objective: Hypertonic saline (HTS) has been previously demonstrated to have immune modulatory and vascular protective effects. We assessed the effect of donor pretreatment with HTS on allograft myocardial function in a porcine model of orthotopic heart transplantation. We hypothesized that HTS infusion prior to donor heart arrest and storage would limit ischemia-reperfusion injury and improve myocardial performance following transplantation. Methods: Orthotopic transplants were performed after 6 hours of ischemic allograft storage. Donor pigs were randomly assigned to pretreatment with (n = 7) or without (n = 6) HTS (4.5 ml/kg of 7.5% NaCl) administered 1 hour prior to donor heart arrest. Left ventricular performance was determined after caval occlusion using a Millar micromanometer and conductance catheter. Hemodynamic measurements were obtained using a Swan-Ganz catheter. Results: Administration of hypertonic saline increased serum sodium level from 138 ± 2 mmol/L to 154 ± 4 mmol/L, which normalized to 144 ± 3 mmol/L 1 hour post-infusion. Weaning from CPB and LV performance after transplantation was improved after donor HTS treatment. Successful weaning from CPB was significantly greater in HTS treated hearts (6/7 versus 1/6, p < 0.05). Preload recruitable stroke work post-transplantation was improved compared to control (88 ± 21% versus 35 ± 8% of baseline, p < 0.01). Similarly, maximal elastance was improved compared to control (85 ± 17% versus 42 ± 12% of baseline, p = 0.03). No significant differences in post-transplant central venous, pulmonary artery or pulmonary capillary wedge pressures were observed between groups. However, post-transplant systolic blood pressure was significantly higher in the donor HTS group (60 ± 9 mmHg versus 35 ± 6 mmHg, p = 0.04). Conculsions: Donor HTS pretreatment attenuates post-transplant cardiac allograft myocardial function and improves post-transplant systemic hemodynamic function. HTS may be a novel organ donor intervention to prevent primary graft dysfunction. Further clinical evaluation of this simple and potentially cost-effective intervention is warranted.

Abstract 3292: Cardiac Dysfunction Induced By Chronic Restrain Stress Is Mediated By Opioid Receptors

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jinping Gao ◽  
Chu C Chua ◽  
Deling Yin ◽  
Hong Wang ◽  
Ronald C Hamdy ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Chronic Stress ◽  
Opioid Receptors ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
Opioid Antagonist ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Major Health Problem ◽  
Stressed Group

Psychological and physical stressors are a major health problem in our society. The effect of chronic stress on myocardial function has not been assessed. Our hypothesis is that chronic stress induces cardiac dysfunction and that its effect is mediated by activation of opioid receptors (OPR). Six week-old male ICR mice were restrained for 12 h with no food and water. This was followed by 12 h of rest with food and water provided ad labium. Unstressed (control) mice were kept in the original cage and were not given food and water during the stress period of the experimental group. Left ventricular performance was analyzed in mice anesthetized with 2% isoflurane using an ARIA pressure-volume conductance system (Millar Instruments). Our studies demonstrated for the first time that cardiac function was significantly depressed in restrained mice, as evidenced by a significant decrease in body weight (9%), heart rate (21%), stroke volume (38%), cardiac output (52%), ejection fraction (27%) and preload recruitable stroke work (43%). Systolic function (control vs. stressed group) (P<0.05), was 88 ± 2.2 vs. 68 ± 2.8 mmHg for end-systolic pressure, 6.1 ± 0.15 vs. 7.6 ± 0.15 μl for end-systolic volume, and 11,471 ± 913 vs. 5,860 ± 761 mmHg/s for +dP/dt. Diastolic function (control vs. stressed group) (P<0.05), was 2.9 ± 0.3 vs. 5.0 ± 0.5 mmHg for end-diastolic pressure, 17.1 ± 0.4 vs. 14.4 ± 0.5 μl for end-diastolic volume, 7,678 ± 419 vs. 4,195 ± 358 mmHg/s for -dP/dt, and 7.1 ± 0.5 vs. 10.8 ± 1.1 ms for tau (time constant of isovolumic relaxation). Peripheral vascular resistance (Ea) increased from 7.7 ± 0.2 in the control group to 9.8 ± 0.7 mmHg/μ l in the stressed group (P<0.05). Administration of an opioid antagonist naltrexone (8 mg/kg, i.p.) during each cycle of stress completely restored the cardiac function of stressed mice. Naltrexone alone had no effect on cardiac function in unstressed mice. These intriguing data suggest that opioid receptors are involved in the chronic stress-induced cardiac dysfunction and that treatment with an opioid antagonist can prevent this cardiac dysfunction.

Ventricular performance and myocardial water content during hemodilution in dogs

1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  
Keyword(s):  
Water Content ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Lv Mass ◽  
Right Heart Bypass ◽  
Water Gain

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

scholarly journals Left ventricular dysfunction after two hours of polarizing or depolarizing cardioplegic arrest in a porcine model

Perfusion ◽  
2018 ◽  
Vol 34 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Terje Aass ◽  
Lodve Stangeland ◽  
Christian Arvei Moen ◽  
Atle Solholm ◽  
Geir Olav Dahle ◽  
...  
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Myocardial Function ◽  
Blood Flow Rate ◽  
Left Ventricular ◽  
Tissue Blood Flow ◽  
Myocardial Tissue ◽  
Stroke Work ◽  
Cardioplegic Arrest ◽  
Blood Cardioplegia

Introduction: This experimental study compares myocardial function after prolonged arrest by St. Thomas’ Hospital polarizing cardioplegic solution (esmolol, adenosine, Mg2+) with depolarizing (hyperkalaemic) St. Thomas’ Hospital No 2, both administered as cold oxygenated blood cardioplegia. Methods: Twenty anaesthetized pigs on tepid (34°C) cardiopulmonary bypass (CPB) were randomised to cardioplegic arrest for 120 min with antegrade, repeated, cold, oxygenated, polarizing (STH-POL) or depolarizing (STH-2) blood cardioplegia every 20 min. Cardiac function was evaluated at Baseline and 60, 150 and 240 min after weaning from CPB, using a pressure-conductance catheter and epicardial echocardiography. Regional tissue blood flow, cleaved caspase-3 activity and levels of malondialdehyde were evaluated in myocardial tissue samples. Results: Preload recruitable stroke work (PRSW) was increased after polarizing compared to depolarizing cardioplegia 150 min after declamping (73.0±3.2 vs. 64.3±2.4 mmHg, p=0.047). Myocardial tissue blood flow rate was high in both groups compared to the Baseline levels and decreased significantly in the STH-POL group only, from 60 min to 150 min after declamping (p<0.005). Blood flow was significantly reduced in the STH-POL compared to the STH-2 group 240 min after declamping (p<0.05). Left ventricular mechanical efficiency, the ratio between total pressure-volume area and blood flow rate, gradually decreased after STH-2 cardioplegia and was significantly reduced compared to STH-POL cardioplegia after 150 and 240 min (p<0.05 for both). Conclusion: Myocardial protection for two hours of polarizing cardioplegic arrest with STH-POL in oxygenated blood is non-inferior compared to STH-2 blood cardioplegia. STH-POL cardioplegia alleviates the mismatch between myocardial function and perfusion after weaning from CPB

Deleterious effect of ouabain on myocardial function during hypoxia

1989 ◽  
Vol 256 (3) ◽  
pp. H681-H687
Author(s):  
M. J. Cunningham ◽  
C. S. Apstein ◽  
E. O. Weinberg ◽  
B. H. Lorell
Keyword(s):  
Myocardial Function ◽  
Diastolic Pressure ◽  
Lactate Production ◽  
Treated Group ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Fiber Tension ◽  
Coronary Vasodilatation ◽  
Developed Pressure ◽  
Ventricular Distensibility

The effect of cardiac glycosides on myocardial function during hypoxia is controversial. Accordingly, we studied left ventricular performance during hypoxia and reoxygenation in the presence of a mildly inotropic, nontoxic dose of ouabain using isolated, isovolumic, buffer-perfused rabbit hearts. After 15 min of hypoxia, left ventricular developed pressure was less in the ouabain-treated group than in controls (35 +/- 4 vs. 55 +/- 3 mmHg, P less than 0.025). Left ventricular end-diastolic pressure (LVEDP) increased more during hypoxia in the presence of ouabain (9 +/- 1 to 32 +/- 7 with ouabain vs. 9 +/- 1 to 14 +/- 3 mmHg without ouabain, P less than 0.005) despite comparable degrees of coronary vasodilatation and myocardial lactate production in the two groups. When coronary flow was abruptly reduced to zero to eliminate the coronary turgor contribution to diastolic pressure, LVEDP after 15 min of hypoxia in the presence of ouabain was greater than that in control hearts that did not receive ouabain (13 +/- 4 vs. 4 +/- 1 mmHg, P less than 0.05), implicating greater diastolic myocardial fiber tension in the ouabain group during hypoxia. With reoxygenation, recovery of developed pressure was less and end-diastolic pressure remained elevated in the ouabain-treated group when compared with controls. We conclude that a modestly inotropic dose of ouabain exacerbates the decrease in diastolic ventricular distensibility induced by hypoxia, worsens the decline in developed pressure during hypoxia, and impairs recovery during reoxygenation.

Left ventricular performance characteristics in trained and sedentary dogs

1980 ◽  
Vol 48 (1) ◽  
pp. 130-138 ◽  
Author(s):  
T. F. Ritzer ◽  
A. A. Bove ◽  
R. A. Carey
Keyword(s):  
Exercise Group ◽  
Left Ventricular ◽  
Contractile Element ◽  
Lv Function ◽  
Stroke Work ◽  
Shortening Velocity ◽  
Ventricular Performance ◽  
Pump Performance ◽  
Pressure Transducers ◽  
Sedentary Group

Training effects on left ventricular (LV) performance were studied in 14 dogs. Nine had chronically implanted LV pressure transducers, five dogs had sham operations. Ventriculographic evaluation of LV function was performed initially in all animals. The sham-operated dogs were killed. The remaining nine dogs were divided into an exercise group (n - 5) and a sedentary group (n = 4). The exercise group ran on a treadmill for 10 wk with a progressively more rigorous routine. The trained dogs had a decreased heart rate response to graded exercise after 10 wk. At similar heart rates, LV end-diastolic volume (pre: 30.3 +/- 3.0, post: 41.8 +/- 2.4 ml) increased significantly after training (P less than 0.05), but ejection fraction was unchanged (pre: 0.68 +/- 0.03, post: 0.67 +/- 0.06). Stroke work (pre: 1848 +/- 199 X 103, post: 4968 +/- 168 X 103 dyn-cm, P less than 0.05) also increased after training. In the presence of a tachycardia, peak dP/dt and peak contractile element shortening velocity showed increases after training. No significant changes in LV volumes, pump performance, or contractility indices were found in the sedentary group. Chronic endurance training alters the size, and appears to improve pump performance of the LV.

Interaction of aortic pressure and left ventricular end-diastolic pressure in the dog

1977 ◽  
Vol 232 (6) ◽  
pp. H697-H704
Author(s):  
J. R. Foster ◽  
E. R. Powers ◽  
W. J. Powell
Keyword(s):  
Performance Improvement ◽  
Fiber Length ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure ◽  
Right Heart Bypass

Fiber length (preload) is an important determinant of left ventricular performance. Mean aortic blood pressure also influences ventricular performance. The present study was undertaken to examine the influence of mean aortic pressure on the fiber length-ventricular performance relationship. Fifteen anesthetized, adrenergically blocked dogs were studied on right-heart bypass at constant heart rate and coronary blood flow. An increase in mean aortic pressure permitted a greater improvement in performance as evaluated by stroke work for a given increase in left ventricular end-diastolic pressure. A given increase in mean aortic pressure at a constant stroke volume produced a greater rise in stroke work over intermediate ranges of left ventricular end-diastolic pressure than occurred with higher or lower left ventricular end-diastolic pressure. Thus, the degree of afterload-induced performance improvement depended on the magnitude of the preload. External circumference-left ventricular end-diastolic pressure data suggested a possible relationship between isovolumic systolic circumferential expansion and the improvement of ventricular performance at higher mean aortic pressures.

Effect of vasopressin on left ventricular performance

1993 ◽  
Vol 264 (1) ◽  
pp. H53-H60
Author(s):  
C. P. Cheng ◽  
Y. Igarashi ◽  
H. S. Klopfenstein ◽  
R. J. Applegate ◽  
Z. Shihabi ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
End Systolic Volume ◽  
The Right

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Nonlinearity of indexes of left ventricular performance: effects on estimation of slope and diameter axis intercepts

1991 ◽  
Vol 260 (6) ◽  
pp. H1802-H1809
Author(s):  
C. F. Toombs ◽  
J. Vinten-Johansen ◽  
H. Yokoyama ◽  
W. E. Johnston ◽  
J. S. Julian ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Accurate Estimation ◽  
Stroke Work ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Wide Range ◽  
Performance Effects ◽  
Linear Fit

The slope and diameter axis intercept (D0) of the linear indexes end-systolic pressure-diameter relation (ESPDR), maximum of the first derivative of left ventricular pressure (dP/dtmax)-end-diastolic diameter relation (dP/dtmax-Ded), and dimensional preload-recruitable stroke work relation (PRDSW) are used to describe left ventricular performance. We tested the hypothesis that nonlinearity in these indexes would preclude accurate estimation of slope and D0. In nine pentobarbital-anesthetized dogs, right heart bypass was used to obtain a wide range of pressure-minor axis diameter (sonomicrometry) points from which the three indexes were derived. For ESPDR and dP/dtmax-Ded, a nonlinear fit (y = ax2 + bx + c) approximated the data better than a linear fit, with significant nonlinearity toward the diameter axis (a = -10.28 +/- 3.42 and -111.2 +/- 26.2, respectively, P less than 0.05). Although linear D0 was significantly less than nonlinear D0, this difference was overcome by the diameter intercept at a midrange value of end-systolic pressure or dP/dtmax. PRDSW demonstrated no significant nonlinearity (a = -4.40 +/- 3.53, P = 0.86) but extrapolation to D0 demonstrated linear and nonlinear differences. We conclude that 1) ESPDR and dP/dtmax-Ded demonstrate significant nonlinearity, while PRDSW is well-approximated by a linear fit over a large range of data points; and 2) extrapolation of D0 is inaccurate in all three indexes, while a midrange intercept is independent of the model used to fit the data. Left ventricular performance may be more accurately described by linear slope and midrange diameter intercept over comparable ranges of data.

Frequency-dependent left ventricular performance in women and men

2012 ◽  
Vol 302 (11) ◽  
pp. H2363-H2371 ◽  
Author(s):  
Rodrigo V. Wainstein ◽  
Zion Sasson ◽  
Susanna Mak
Keyword(s):  
Mechanical Performance ◽  
Left Ventricular ◽  
Right Atrial ◽  
Stroke Work ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Specific Manner ◽  
And Function ◽  
Inotropic Responses ◽  
The Relationship

We aimed to determine whether sex differences in humans extend to the dynamic response of the left ventricular (LV) chamber to changes in heart rate (HR). Several observations suggest sex influences LV structure and function in health; moreover, this physiology is also affected in a sex-specific manner by aging. Eight postmenopausal women and eight similarly aged men underwent a cardiac catheterization-based study for force-interval relationships of the LV. HR was controlled by right atrial (RA) pacing, and LV +dP/d tmax and volume were assessed by micromanometer-tipped catheter and Doppler echocardiography, respectively. Analysis of approximated LV pressure-volume relationships was performed using a time-varying model of elastance. External stroke work was also calculated. The relationship between HR and LV +dP/d tmax was expressed as LV +dP/d tmax = b + mHR. The slope ( m) of the relationship was steeper in women compared with men (11.8 ± 4.0 vs. 6.1 ± 4.1 mmHg·s−1·beats−1·min−1, P = 0.01). The greater increase in contractility in women was reproducibly observed after normalizing LV +dP/d tmax to LV end-diastolic volume (LVVed) or by measuring end-systolic elastance. LVVed and stroke volume decreased more in women. Thus, despite greater increases in contractility, HR was associated with a lesser rise in cardiac output and a steeper fall in external stroke work in women. Compared with men, women exhibit greater inotropic responses to incremental RA pacing, which occurs at the same time as a steeper decline in external stroke work. In older adults, we observed sexual dimorphism in determinants of LV mechanical performance.

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