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Ann Thorac Surg 1997;63:1293-1297
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Myocardial Edema: Comparison of Effects on Filling Volume and Stiffness of the Left Ventricle in Rats and Pigs

Departments of Surgery and Pediatrics, Columbia University College of Physicians & Surgeons, New York, New York

Accepted for publication November 15, 1996.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Background. This study compared the adverse effects of crystalloid-induced myocardial edema on left ventricular (LV) compliance in small and large hearts.

Methods. Plegisol (289 mOsm/L) was perfused into the coronary arteries of pigs (n = 8) and 1:1 dilute Plegisol (145 mOsm/L) into the coronary arteries of rats (n = 6). Pressure-volume relations, heart weight, and water content were then determined. The pressure-volume relations were compared using an LV volume at a pressure of 10 mm Hg.

Results. Edema in rats was associated with significant (p < 0.05) increases in heart weight (1.1 ± 0.0 g versus 1.4 ± 0.1 g [average ± standard error of the mean]) and water content (76.8% ± 0.4% versus 81.3% ± 0.8%), but an increase in LV stiffness (7.91 ± 0.52 versus 9.27 ± 1.42) and a decrease in the LV volume at 10 mm Hg (0.25 ± 0.02 mL versus 0.14 ± 0.05 mL) were not statistically significant. Edema in pigs was associated with statistically significant (p < 0.05) increases in LV stiffness ß (0.050 ± 0.004 versus 0.072 ± 0.008), heart weight (207 ± 8 g versus 274 ± 9 g), and water content (79.8% ± 0.6% versus 85.3% ± 0.6%) and a significant decrease in the LV volume at 10 mm Hg (88.4 ± 5.8 mL versus 60.4 ± 6.8 mL).

Conclusions. Myocardial edema is associated with an increase in water content and LV stiffness and a decrease in the LV volume at 10 mm Hg in both species. In rats, however, the water content is smaller in the control state and a more hypotonic perfusate is needed to induce a given degree of edema.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Perfusion of the coronary arteries with hypotonic crystalloid cardioplegia solution causes myocardial edema in isolated hearts [1–6] and is associated with a decrease in left ventricular (LV) compliance in working and nonworking hearts [1–5, 7–12]. Such myocardial edema may impair systolic ventricular function through a reduction in diastolic filling.

It is known that myocardial edema resolves more quickly in rodents than in larger animals. Specifically, cardioplegia-induced myocardial edema resolves completely 15 minutes after blood reperfusion in rats [13] and after 45 minutes in pigs [14]. Because of this, resistance to edema formation in rats may also differ from that in larger animals.

Studies of myocardial protection in rat hearts are less expensive than studies in larger animals, but they are also often less predictive of clinical values. Incidental causes of edema are an important possible source of error in such studies, because edema after myocardial ischemia and reperfusion is an indicator of myocardial injury. Accordingly, the present study was designed to compare the effect of crystalloid coronary perfusion on myocardial edema in rats and pigs in an attempt to improve the relevance of studies in rats to the clinical situation.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the Institute of Laboratory Animal Resources and the "Guide for the Care and Use of Laboratory Animals" (NIH Publication 85-23, revised 1985). Serial measurements were performed in pigs, with each animal serving as its own control and thus allowing comparisons by paired t tests. The fragility of the hearts and relatively rapid onset of rigor mortis in rats necessitated the use of separate control and edema groups, with statistical comparisons done by unpaired t tests.

	Experimental Preparation (Rats)

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Twelve Sprague-Dawley rats (weight, 300 to 400 g) were anesthetized with intraperitoneally administered ketamine (40 to 80 mg/kg) and xylazine (5 to 10 mg/kg). After tracheostomy, mechanical ventilation was initiated with a small animal ventilator (Harvard Apparatus, Cambridge, MA). The abdomen was entered through a transverse incision placed just below the diaphragm. Two lateral thoracotomy incisions were made through the diaphragm, and the chest plate was reflected upward. The venae cavae and brachiocephalic vein were isolated and snared with 4-0 silk sutures. The aorta was dissected and isolated proximal to the brachiocephalic artery.

CONTROL GROUP.
After systemic heparinization in the rats in the control group (n = 6), venous snares were tightened and the aorta was cross-clamped. Diastolic cardiac arrest was produced by an injection of 0.1 mL (2 mEq/mL) of potassium chloride into the aortic root, proximal to the clamp. Hearts were rapidly excised and placed in cold (0° to 4°C) Stanford solution (380 mOsm/L). Wet heart weight (WHW), myocardial water content (MWC), and LV diastolic pressure-volume (P-V) relation were determined as described later.

EDEMA GROUP.
A 16-gauge angiocatheter connected to a three-way stopcock was placed into the aorta, just above the aortic valve, in the rats in the edema group (n = 6). The aortic root was tied around the catheter above the coronary ostia with 4-0 silk suture. Perfusion pressure was measured using a 5F micromanometer (Millar Instruments, Houston, TX) connected to the three-way stopcock. The third port of the stopcock was used for the volume infusion. Ten milliliters of dilute cold (0° to 4°C) 1:1 Plegisol (147 mOsm/L; Abbott Laboratories, Chicago IL) was infused into the aortic root and coronary arteries over 1.5 to 2 minutes, maintaining a perfusion pressure of less than 60 mm Hg. Left ventricular distention during Plegisol perfusion was avoided. The WHW, MWC, and LV diastolic P-V relation were determined as described later.

LEFT VENTRICULAR PRESSURE-VOLUME RELATION.
Excised hearts were kept submerged in cold solutions. An 18-gauge catheter connected to a three-way stopcock was placed into the left ventricle through the aortic valve. The aorta was then occluded around the catheter at the aortic root, thereby occluding the coronary arteries. Left ventricular pressures were measured using a 5F Millar micromanometer connected to the three-way stopcock. The third port of the stopcock was used for the volume infusion. The left ventricle was sealed by placing a small hemostat approximately 1 mm on the atrial side of the mitral annulus, thereby avoiding annular compression. Air was eliminated from the system. Volume was infused into the left ventricle in 0.05-mL increments while the pressure was recorded using an analog-to-digital convertor (MacLab; ADInstruments Inc, Milford, MA) and recorded on a digital computer (Macintosh Quadra 950; Apple Computer, Cupertino, CA) until an LV pressure of 20 mm Hg was reached. The P-V data were obtained in duplicate and analyzed only if 95% of the injected volume was recovered. Data were obtained within 15 minutes of the onset of ischemia to avoid rigor mortis [15–17]. Ventricular pressures corresponding to the volume injected were averaged to obtain a mean P-V relation for each animal.

	Experimental Preparation (Pigs)

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Eight domestic pigs (45 to 60 kg) were anesthetized with intramuscularly administered ketamine (20 mg/kg), xylazine (2 mg/kg), and atropine (0.02 mg/kg); intubated; and mechanically ventilated. Anesthesia was maintained with sodium pentobarbital (2 mg/kg) administered every 20 to 30 minutes. After a median sternotomy and systemic heparinization, the venae cavae were occluded and the pulmonary artery was incised to decompress the right heart. The aorta was cross-clamped, and the heart was arrested with intraaortically administered potassium chloride (80 mEq). Hearts were rapidly excised and immersed in cold (0° to 4°C) Stanford solution. Septal temperature was monitored with a needle thermistor (Fluke digital thermometer 2160A; Frigitronics, CT). Excised hearts were blotted, emptied of fluid, and placed on a beam balance (OHAUS; Dec-O-Gram, Florham, NJ) for determination of the WHW.

Three 1-liter coronary perfusions were carried out, using fluid precooled to 4°C and an aortic root cannula placed proximal to an aortic cross-clamp. Stanford solution (380 mOsm/L) was infused twice, followed by the Plegisol solution (294 mOsm/L). Coronary perfusion pressure was maintained at 60 mm Hg. The first Stanford perfusion was initiated 2.1 ± 0.8 minutes after excision to maximize the protective cooling and effect of cardioplegia. Transmural myocardial specimens were removed from the free wall of the right ventricle for determination of the MWC, as described later.

LEFT VENTRICULAR PRESSURE-VOLUME RELATION.
Two 16-gauge catheters were secured in the apex of the left ventricle for pressure monitoring and volume infusion. The mitral annulus was sealed with a Satinsky clamp placed across the atrioventricular groove. The clamp was placed 2 mm on the atrial side of the annulus to avoid distortion of the mitral annulus. The aorta was clamped close to the aortic valve annulus, thereby occluding the coronary ostia. The surrounding bath was filled with the same type of fluid as that used for the most recent perfusate, and the same solution was infused into the LV cavity in 5-mL increments at 3- to 5-second intervals to measure the P-V properties. Pressure was recorded with a Gould Statham P-23ID transducer, (Statham Instruments Inc, Hato Rey, Puerto Rico) and an optical oscillograph (DR-12; Electronics for Medicine Inc, White Plains, NY). Zero pressure was defined using a fluid-filled catheter immersed to the level of the mid-left ventricle. The P-V data were recorded from zero volume to 20 mm Hg pressure, and the left ventricle was then emptied. Recovery of 95% of the infused volume was used as the criterion for the absence of significant fluid leaks. All P-V curves were measured in duplicate. All P-V relation measurements were done within 100 minutes of the onset of ischemia to avoid the onset of rigor mortis [16]. The mean septal temperature during the experiments was 12° ± 3°C.

HEART WEIGHTS AND MYOCARDIAL WATER CONTENTS.
Specimens were gently blotted dry, placed in a preweighed Petri dish, and weighed on an analytical balance (H16; Mettler Instruments Corp, Highston, NJ) immediately after excision to obtain the wet weight. Each specimen was then dried to a constant weight in an oven at 60°C for 48 hours to obtain the dry weight. The MWC was calculated using the following equation:

(1)

VENTRICULAR STIFFNESS CONSTANT.
Diastolic pressure (P) and volume (V) from the P-V data were fitted to a exponential curve (e) of the form:

(2)

using a least-squares method and commercial software (Cricket Graph, Cricket Software, Malvern, PA) and omitting values below 0 mm Hg, where ß is an index of ventricular stiffness [18], and is the base constant.

LEFT VENTRICULAR VOLUME AT 10 MM HG.
The LV volume at 10-mm Hg LV pressure (LVV-10) was calculated for control and edema groups using equation 2 after determination of the base and ventricular stiffness constants.

NORMALIZED PRESSURE-VOLUME CURVES.
The LV volumes were normalized for differences in LV weight, as described previously [19]. Volumes were divided into six groups according to the pressure observed after infusion: 0 to 2.4 mm Hg, 2.5 to 7.4 mm Hg, 7.5 to 12.4 mm Hg, 12.5 to 17.4 mm Hg, 17.5 to 22.4 mm Hg, and 22.5 to 27.5 mm Hg. The average volume within each pressure range was normalized to a mean heart weight (MHW) of 1.2 g for rats and 240.5 g for pigs, using the following equation:

(3)

where WHW is the wet heart weight of each animal. The normalized volumes were averaged and plotted against average calculated pressures using commercial software (Cricket Graph).

	Results

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
The ventricular stiffness constants, LVV-10s, WHWs, and MWCs in rats are presented in Table 1. Compared with controls, the mean ventricular stiffness constants increased in the edema group (7.91 ± 0.52 [standard error of the mean] versus 9.27 ± 1.42) and the LVV-10s decreased 44% (0.25 ± 0.02 mL versus 0.14 ± 0.05 mL), but these changes were not significant. Statistically significant increases (p < 0.05) were observed in the WHWs (1.1 ± 0.0 g versus 1.4 ± 0.1 g, an increase of more than 27%) and the MWCs (76.8% ± 0.4% versus 81.3% ± 0.8%) in the edema group.

View larger version (25K): [in this window] [in a new window]   Fig 1. . Relation of filling pressure to average, normalized volume in arrested rat hearts before and after coronary perfusion with 1:1 dilute Plegisol. Standard errors are indicated by brackets. The illustrated decrease in the left ventricular (LV) volume at 10 mm Hg in the setting of edema is not statistically significant. (HW = heart weight.)

View larger version (23K): [in this window] [in a new window]   Fig 2. . Relation of filling pressure to average, normalized volumes in arrested pig hearts before and after coronary perfusion with full-strength Plegisol. The illustrated decrease in the left ventricular (LV) volume at 10 mm Hg in the setting of edema is statistically significant (p < 0.05; see Table 1). (HW = heart weight.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

The MWCs in the control state were also found to be smaller in rats (77%) than in pigs (80%). These data are similar to previously reported control MWCs of 76% to 78% in rats [13, 20, 21] and 78% to 80% in pigs, dogs, and humans [22–25]. Because a 3% increase in the water content in these circumstances is equivalent to a 15% increase in the LV mass [4], an MWC of 80% in a rat indicates a grossly edematous preparation, whereas this same value is characteristic of normal pig hearts.

Another important difference between rat and pig hearts is the rapidity with which rigor mortis occurs. The experimental design had to be modified in light of the rapid onset of ischemic contracture in rat left ventricle. The cardioplegia infusion took 2 minutes in rats, and measurement of the P-V curves took an additional 15 minutes. Diastolic LV stiffness increases in less than 30 minutes in rat hearts at 4°C (Starr et al, unpublished data). At 37°C, ischemic contracture is complete in 17 minutes in rats [15]. Separate groups of hearts (control and edema) were therefore employed for the studies in rats, but this was unnecessary in pig hearts, in which longitudinal studies could provide data on both conditions in less than 100 minutes. The diastolic properties of pig hearts are stable for more than 180 minutes at 4°C [3, 5, 16].

Because of these differences in experimental design, statistical significance was tested with paired t tests in pigs and with unpaired t tests in rats. This difference in statistical methods resulted in the finding of qualitatively similar changes in diastolic properties that were statistically significant in pigs (see Fig 2) but statistically insignificant in rats (see Fig 1).

Researchers at our laboratory have shown that myocardial edema causes a predictable [3, 5, 24] impairment of the diastolic filling volume in the isolated, arrested, hypothermic pig heart. Furthermore, we have found that myocardial edema in the beating heart does this by increasing diastolic LV stiffness but not by altering contractility [14].

In summary, coronary artery perfusion with crystalloid increases the wet weight and decreases the diastolic filling volume of the left ventricle in both rats and pigs. However, a 100% greater dilution of the Plegisol is needed in rats to produce the manifestations of edema similar to those observed in pigs. Any given absolute MWC is indicative of greater injury in rats than in larger animals, because of the fact that the "normal" myocardial water content is 77% in rats and 80% in pigs. The relevance of the rat model to clinical cardiac surgical procedures may be improved by the recognition that the myocardium is normally drier and more resistant to edema in the rat than it is in larger mammals.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Supported in part by USPHS #1 RO1 HL-48109-01 and American Heart Association Grant-in-Aid #92015230

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 
Address reprint requests to Dr Spotnitz, Department of Surgery, Columbia University, 622 W 168th St, PH 14-22 E, New York, NY 10032.

	References

Top Footnotes Abstract Introduction Material and Methods Experimental Preparation (Rats) Experimental Preparation (Pigs) Results Comment Acknowledgments References

 

1. Foglia RP, Lazar HL, Steed DL, et al. Iatrogenic myocardial edema with crystalloid primes: effects on left ventricular compliance, performance, and perfusion. Surg Forum 1978;29:312–5.[Medline]
2. Foglia RP, Steed DL, Follette DM. Iatrogenic myocardial edema with potassium cardioplegia. J Thorac Cardiovasc Surg 1979;78:217–22.[Abstract]
3. Weng ZC, Nicolosi AC, Detwiler PW, et al. Effects of crystalloid, blood, and University of Wisconsin perfusates on weight, water content, and left ventricular compliance in an edema-prone, isolated porcine heart model. J Thorac Cardiovasc Surg 1992;103:504–13.[Abstract]
4. Spotnitz HM, Hsu DT. Myocardial edema: importance in the study of left ventricular function. Adv Cardiac Surg 1994;5:1–25.[Medline]
5. Hsu DT, Weng Z-C, Nicolosi AC, Detwiler PW, Sciacca R, Spotnitz HM. Quantitative effects of myocardial edema on the left ventricular pressure-volume relation in the isolated stored pig heart. J Thorac Cardiovasc Surg 1993;106:651–7.[Abstract]
6. Boxt L, Hsu DT, Spotnitz HM, Katz J. Effect of perfusion induced myocardial edema on T2 relaxation time in vitro. Magn Res Imag 1993;11:375–83.
7. Salisbury PF, Cross CE, Rieben PA. Distensibility and water content of heart muscle before and after injury. Circ Res 1960;8:788–93.[Abstract/Free Full Text]
8. Cross CE, Rieben PA, Salisbury PF. Influence of coronary perfusion and myocardial edema on pressure-volume diagram of left ventricle. Am J Physiol 1961;201:102–8.[Abstract/Free Full Text]
9. Pogatsa G, Dubecz E, Gabor G. The role of myocardial edema in the left ventricular diastolic stiffness. Basic Res Cardiol 1976;71:263–9.[Medline]
10. Schaff HV, Gott VL, Goldman RA, Frederiksen JW, Flaherty JT. Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion. Am J Physiol 1981;240:H300–7.
11. Lazar HL, Haasler GB, Collins RH, Dubroff JM, Meisner J, Spotnitz HM. Compliance, mass, and shape of the canine left ventricle after global ischemia analyzed with two-dimensional echocardiography. J Surg Res 1985;39:199–208.[Medline]
12. Vogel WM, Cerel AW, Apstein CS. Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role of edema and effects of dextran. J Mol Cell Cardiol 1986;18:1207–18.[Medline]
13. Takoudes TG, Amirhamzeh MMR, Hsu DT, Wise BR, Odeh SO, Spotnitz HM. Time course of resolution of perfusion-induced myocardial edema in the rat heart. J Surg Res 1994;57:641–6.[Medline]
14. Amirhamzeh MMR, Dean DA, Jia CX, et al. Iatrogenic myocardial edema: increased diastolic compliance and time course of resolution in vivo. Ann Thorac Surg 1996;62:737–43.[Abstract/Free Full Text]
15. Iwasa Y, Onaya T. Postmortem changes in the level of calcium pumping adenosine triphosphate in rat heart sarcoplasmic reticulum. Forensic Sci Int 1988;39:13–22.[Medline]
16. Griggs DM Jr, Holt FR, Case RB. Serial pressure-volume studies in the excised canine heart. Am J Physiol 1960;198:336–40.[Abstract/Free Full Text]
17. Hearse DJ, Garlick PB, Humphrey SM. Ischemic contracture of the myocardium: mechanisms and prevention. Am J Cardiol 1977;39:986–93.[Medline]
18. Mirsky I. Assessment of passive elastic stiffness of cardiac muscle: mathematical concepts, physiologic and clinical considerations, directions of future research. Prog Cardiovasc Dis 1976;18:277–308.[Medline]
19. Auteri JS, Jeevanandam V, Bielefeld MR, Sanchez JA, Spotnitz HM. Effect of location of AICD patch electrodes on the diastolic pressure-volume curve in pigs. Ann Thorac Surg 1991;52:1052–7.[Abstract]
20. Amirhamzeh MMR, Jia C-X, Starr JP, et al. Diastolic function in the heterotopic rat heart transplant model: effects of edema, ischemia and rejection. J Thorac Cardiovasc Surg 1994;108:928–37.[Abstract/Free Full Text]
21. Sadeghi AM, Spotnitz HM, Thomas WA, et al. Cyclosporine increases rat heart weight in heterotopic transplants. Curr Surg 1987;44:51–2.[Medline]
22. Geffin GA, Vasu MA, O'Keefe D, et al. Ventricular performance and myocardial water content during hemodilution in dogs. Am J Physiol 1978;235:767–75.
23. Laks H, Standeven J, Blair O, Hahn J, Jellinek M, Willman VL. The effects of cardiopulmonary bypass with crystalloid and colloid hemodilution on myocardial extravascular water. J Thorac Cardiovasc Surg 1977;73:129–38.[Abstract]
24. Haasler GB, Rodrigas PC, Collins RH, et al. Two-dimensional echocardiography in dogs: variation of left ventricular mass, geometry, volume, and ejection fraction on cardiopulmonary bypass. J Thorac Cardiovasc Surg 1985;90:430–40.[Abstract]
25. Gross H. Water content of myocardium in hypertrophy and chronic congestive failure. J Lab Clin Med 1940;25:899–911.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Henry M. Spotnitz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Amirhamzeh, M. M. R. Articles by Spotnitz, H. M. Search for Related Content PubMed PubMed Citation Articles by Amirhamzeh, M. M. R. Articles by Spotnitz, H. M.