Assessment of donor heart viability during ex vivo heart perfusion

2015 ◽  
Vol 93 (10) ◽  
pp. 893-901 ◽  
Author(s):  
Christopher W. White ◽  
Emma Ambrose ◽  
Alison Müller ◽  
Yun Li ◽  
Hoa Le ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Ex Vivo ◽  
Lactate Concentration ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Myocardial Performance ◽  
Donor Heart ◽  
Functional Parameters ◽  
Heart Perfusion

Ex vivo heart perfusion (EVHP) may facilitate resuscitation of discarded donor hearts and expand the donor pool; however, a reliable means of demonstrating organ viability prior to transplantation is required. Therefore, we sought to identify metabolic and functional parameters that predict myocardial performance during EVHP. To evaluate the parameters over a broad spectrum of organ function, we obtained hearts from 9 normal pigs and 37 donation after circulatory death pigs and perfused them ex vivo. Functional parameters obtained from a left ventricular conductance catheter, oxygen consumption, coronary vascular resistance, and lactate concentration were measured, and linear regression analyses were performed to identify which parameters best correlated with myocardial performance (cardiac index: mL·min–1·g–1). Functional parameters exhibited excellent correlation with myocardial performance and demonstrated high sensitivity and specificity for identifying hearts at risk of poor post-transplant function (ejection fraction: R2 = 0.80, sensitivity = 1.00, specificity = 0.85; stroke work: R2 = 0.76, sensitivity = 1.00, specificity = 0.77; minimum dP/dt: R2 = 0.74, sensitivity = 1.00, specificity = 0.54; tau: R2 = 0.51, sensitivity = 1.00, specificity = 0.92), whereas metabolic parameters were limited in their ability to predict myocardial performance (oxygen consumption: R2 = 0.28; coronary vascular resistance: R2 = 0.20; lactate concentration: R2 = 0.02). We concluded that evaluation of functional parameters provides the best assessment of myocardial performance during EVHP, which highlights the need for an EVHP device capable of assessing the donor heart in a physiologic working mode.

Effect of acute edema on left ventricular function and coronary vascular resistance in the isolated rat heart

1994 ◽  
Vol 267 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
A. Rubboli ◽  
P. A. Sobotka ◽  
D. E. Euler
Keyword(s):  
Linear Relationship ◽  
Water Content ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Ventricular Performance ◽  
Developed Pressure ◽  
The Impact

The impact of acute myocardial edema on coronary flow and left ventricular performance was studied in isolated isovolumic rat hearts. After 15 min of aortic perfusion with Krebs-Henseleit buffer, hearts (10/group) were either removed for determination of water content or perfused for another 90 min. Three groups were perfused at a constant pressure of 60, 100, or 140 mmHg, and two groups were perfused at 60 or 140 mmHg with adenosine added. Compared with the 15-min group, there was a significant increase in water content in all groups except the 60-mmHg group (P < 0.005). There was a direct linear relationship between increases in coronary vascular resistance over time and water content (P < 0.0001). A decrease in developed pressure and peak +dP/dt was observed only in those groups that accumulated water. An inverse linear relationship was found between changes in developed pressure and water content (P = 0.0001). Water content had no effect on end-diastolic pressure below 5 ml/g; above 5 ml/g, a direct linear relationship was evident (P = 0.009). The results suggest that myocardial edema increases vascular resistance and decreases systolic performance. End-diastolic pressure is less influenced by edema than either systolic or coronary vascular function.

scholarly journals Description of a Novel Set-up for Functional Echocardiographic Assessment of Left Ventricular Performance During Ex Vivo Heart Perfusion

2018 ◽  
Vol 127 (3) ◽  
pp. e36-e39 ◽  
Author(s):  
Giulia Maria Ruggeri ◽  
Joshua Qua Hiansen ◽  
Emanuele Pivetta ◽  
Azad Mashari ◽  
Flavia Ballocca ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Left Ventricular ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
Heart Perfusion ◽  
Echocardiographic Assessment ◽  
Set Up

Myocardial capillary diffusion capacity in rat hearts with cardiac hypertrophy due to pressure and volume overload

1993 ◽  
Vol 265 (1) ◽  
pp. H61-H68 ◽  
Author(s):  
H. Wahlander ◽  
B. Haraldsson ◽  
P. Friberg
Keyword(s):  
Cardiac Hypertrophy ◽  
Vascular Resistance ◽  
Renal Hypertension ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Functional Adaptation ◽  
Arterial Stenosis ◽  
Coronary Vascular Resistance ◽  
Diffusion Capacity

The functional adaptation of the myocardial capillary bed in response to cardiac hypertrophy was studied in one volume overload (aortocaval fistula, ACF) and in one pressure overload model [left renal arterial stenosis, two-kidney, one-clip (2K,1C)]. Furthermore, a group where renal hypertension was reversed 1 wk before experimentation (UC-2K,1C) and a sham-operated (Sham) group were studied. Functional estimations of myocardial capillary diffusion capacity in terms of permeability surface area products (PS) per 100 g of myocardium were obtained by the single-injection indicator dilution technique in a Langendorff preparation. After 4 wk, ACF hearts, with 72% hypertrophy and normal minimal coronary vascular resistance (CVR), displayed an unchanged diffusion capacity, i.e., PS for Cr-EDTA and vitamin B12. This indicates a structural out-growth of the coronary vascular bed to match the increased demand of the tissue. 2K,1C hearts with marked elevations of minimal coronary vascular resistance and left ventricular hypertrophy (65%) showed higher PS values than Sham, implying that diffusion capacity was enhanced despite structural coronary vascular changes. These changes were completely reversed in UC-2K,1C. Thus the present data imply that myocardial capillary diffusion capacity was well maintained in volume overloaded cardiac hypertrophy and in contrast with earlier morphometric estimations, even enhanced in pressure overload hypertrophy.

Effects of short- and long-term left ventricular hypertrophy on coronary circulation

1981 ◽  
Vol 241 (3) ◽  
pp. H358-H362 ◽  
Author(s):  
M. L. Marcus ◽  
T. M. Mueller ◽  
C. L. Eastham
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Vascular Resistance ◽  
Ventricular Hypertrophy ◽  
Renal Hypertension ◽  
Time Frame ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Vascular Abnormalities ◽  
Coronary Vasodilator ◽  
Lv Mass

Although most studies suggest that coronary vasodilator responses are impaired in dogs with cardiac hypertrophy, the factors that contribute to this impairment have not been elucidated. To determine if the duration of hypertrophy was an important determinant, we studied coronary vasodilator responses in awake dogs with two-kidney renal hypertension of 6 wk (n = 11) and 6 mo (n = 8) duration. The dogs with hypertension (6 wk and 6 mo) and left ventricular hypertrophy (LVH) had about a 25% (P less than 0.05) increase in LV mass and mean arterial pressure. During maximal coronary vasodilation induced with 4.7 microM . kg-1 . min-1 iv adenosine, maximal flow was significantly decreased in both groups of hypertensive dogs, and minimal coronary vascular resistance was increased by about 50% (P less than 0.05). Minimal coronary vascular resistance was similar in dogs with 6 wk and 6 mo of hypertension and LVH. These experiments suggest that 1) mild LVH (25% increase in LV mass) can significantly decrease coronary dilator reserve and 2) within the time frame examined (6 wk to 6 mo), the duration of hypertension and LVH does not increase the coronary vascular abnormalities associated with cardiac enlargement.

Dynamics of myocardial oxygen consumption and coronary vascular resistance

1977 ◽  
Vol 233 (1) ◽  
pp. H34-H43 ◽  
Author(s):  
F. L. Belloni ◽  
H. V. Sparks
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Time Course ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Constant Flow

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

The Effect of Ethanol and Acetaldehyde on the Metabolism and Vascular Resistance of the Perfused Heart

1971 ◽  
Vol 49 (2) ◽  
pp. 227-233 ◽  
Author(s):  
L. Gailis ◽  
M. Verdy
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Anaerobic Glycolysis ◽  
Appreciable Effect ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Perfused Heart ◽  
Perfused Rat Heart ◽  
Ethanol Ethanol

The effect of ethanol and acetaldehyde on the perfused nonworking rat and guinea pig hearts was studied. Ethanol (100 mM) initially increased the coronary vascular resistance, but had no appreciable effect on oxygen consumption, glucose-U-14C oxidation, or anaerobic glycolysis. Acetaldehyde (1 mM) increased the heart rate and oxygen consumption, and decreased the coronary vascular resistance. The decrease in coronary resistance was not affected by propranolol but the increase in heart rate was partially blocked. The loss of amino acids or aspartate transminase activity from the heart was not affected by the presence of ethanol. Ethanol-1-14C, either at 10 or 100 mM, was not oxidized by the perfused rat heart.

scholarly journals Normothermic ex vivo Heart Perfusion Combined With Melatonin Enhances Myocardial Protection in Rat Donation After Circulatory Death Hearts via Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis

2021 ◽  
Vol 9 ◽  
Author(s):  
Jun Lu ◽  
Liwei Xu ◽  
Zifeng Zeng ◽  
Chuqing Xue ◽  
Jiale Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Nlrp3 Inflammasome ◽  
Ex Vivo ◽  
Left Ventricular ◽  
Warm Ischemia ◽  
Vehicle Group ◽  
Donation After Circulatory Death ◽  
Heart Perfusion ◽  
Circulatory Death

ObjectiveThe adoption of hearts from donation after circulatory death (DCD) is a promising approach for the shortage of suitable organs in heart transplantation. However, DCD hearts suffer from serious ischemia/reperfusion injury (IRI). Recent studies demonstrate that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis is a novel target to ameliorate myocardial IRI. Melatonin is shown to inhibit NLRP3 inflammasome-mediated pyroptosis. Therefore, this study is designed to verify the hypothesis that melatonin can protect the heart graft preserved with ex vivo heart perfusion (EVHP) against myocardial IRI via inhibiting NLRP3 inflammasome-mediated pyroptosis in a rat model of DCD.MethodsDonor-heart rats were randomly divided into three groups: (1) Control group: non-DCD hearts were harvested from heart-beating rats and immediately preserved with allogenic blood-based perfusate at constant flow for 105 min in the normothermic EVHP system; (2) DCD-vehicle group; and (3) DCD-melatonin group: rats were subjected to the DCD procedure with 25 min of warm ischemia injury and preserved by the normothermic EVHP system for 105 min. Melatonin (200 μmol/L) or vehicle was perfused in the cardioplegia and throughout the whole EVHP period. Cardiac functional assessment was performed every 30 min during EVHP. The level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis of heart grafts submitted to EVHP were evaluated.ResultsTwenty five-minute warm ischemia injury resulted in a significant decrease in the developed pressure (DP), dP/dtmax, and dP/dtmin of left ventricular of the DCD hearts, while the treatment with melatonin significantly increased the DP, dP/dtmax of the left ventricular of DCD hearts compared with DCD-vehicle group. Furthermore, warm ischemia injury led to a significant increase in the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis in the hearts preserved with EVHP. However, melatonin added in the cardioplegia and throughout the EVHP period significantly attenuated the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis compared with DCD-vehicle group.ConclusionEVHP combined with melatonin post-conditioning attenuates myocardial IRI in DCD hearts by inhibiting NLRP3 inflammasome-mediated pyroptosis, which might expand the donor pool by the adoption of transplantable DCD hearts.

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