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Ann Thorac Surg 1997;63:84-87
© 1997 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Hyperkalemia Exposure Impairs EDHF-Mediated Endothelial Function in the Human Coronary Artery

Cardiovascular Research Laboratory, Department of Surgery, University of Hong Kong, Grantham Hospital, Hong Kong

Accepted for publication July 11, 1996.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. My colleagues and I have found in the porcine coronary artery that the pathway other than the nitric oxide (N^G-nitro-L-arginine [L-NNA]-sensitive) and cyclooxygenase (indomethacin-sensitive) pathways of endothelium-dependent relaxation, related to the endothelium-derived hyperpolarizing factor (K⁺ channel–related), are altered after exposure to hyperkalemia. The present study was designed to examine whether this effect exists in the human coronary artery.

Methods. Coronary artery rings obtained from explanted fresh human hearts were studied in organ chambers under physiologic pressure. The endothelium-dependent relaxation in response to calcium ionophore A23187 was studied in U46619 (30 nmol/L)-induced precontraction in the presence of the cyclooxygenase inhibitor indomethacin (7 µmol/L) and the nitric oxide biosynthesis inhibitor L-NNA (300 µmol/L). The effect of incubation with 20 mmol/L K⁺ for 1 hour on the relaxation was examined in other coronary rings.

Results. In control rings, A23187 induced a maximal relaxation of 50.7% ± 3.2% (n = 6). After 1 hour of exposure to 20 mmol/L K⁺, the relaxation was reduced to 30.4% ± 4.6% (n = 6; p = 0.005). Incubation with hyperkalemia also significantly reduced the sensitivity (increased effective concentration that caused 50% of maximal relaxation) of the indomethacin- and L-NNA–resistant relaxation (-7.37 ± 0.17 versus -8.28 ± 0.27 log mol/L; p = 0.019).

Conclusions. Exposure to hyperkalemia reduces the indomethacin- and L-NNA–resistant, endothelium-dependent (endothelium-derived hyperpolarizing factor–related) relaxation in the human coronary artery. This suggests that the previously proposed mechanism of coronary dysfunction after exposure to cardioplegic and organ preservation solutions in animal vessels is also valid in the human heart.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Due to the wide use of hyperkalemic cardioplegia and organ preservation solutions in cardiac and transplantation operations, the effect of such solutions on endothelial function has been the focus of several recent studies [1–5]. In perfused rat hearts, previous studies have suggested that infusion of hyperkalemic cardioplegic solution damages coronary endothelium [1]. In contrast, studies by others [2] suggested that crystalloid cardioplegia does not impair the endothelium-dependent relaxation. My colleagues and I [3, 4] further demonstrated that the noncyclooxygenase pathway-mediated endothelium-dependent relaxation in porcine coronary arteries [3] or neonatal rabbit aortas [4] is not altered by exposure to hyperkalemia or cardioplegia. However, most recently, we have discovered that the endothelium-dependent relaxation mediated by the noncyclooxygenase and non–nitric oxide pathway (ie, the endothelium-derived hyperpolarizing factor [EDHF] pathway) in porcine coronary arteries is altered by exposure to hyperkalemia [6, 7], and we have suggested that the discrepancy between the studies in beating heart experiments and in the isolated coronary arteries may be due to the altered, EDHF-related endothelial function.

Endothelium-dependent relaxation is known to be the effect of a variety of different endothelium-derived relaxing factors. These are endothelium-derived nitric oxide (EDNO), prostacyclin, and EDHF. Endothelium-derived nitric oxide and prostacyclin have been well studied. In contrast, the nature of EDHF has not been conclusively identified, although most recently the cytochrome P450-monooxygenase metabolite of arachidonic acid has been suggested to be EDHF [8]. Endothelium-derived hyperpolarizing factor induces vascular smooth muscle relaxation via hyperpolarization of the smooth muscle cells [9–14], which may involve potassium channels [12–14]. In contrast, EDNO relaxes blood vessels through the cyclic guanosine monophosphate pathway [9, 15]. However, all of these endothelium-derived relaxing factors are released in response to the increase in intracellular (cytosolic free) calcium concentration in the endothelial cell [7].

The present study was designed to examine whether the previously observed effect of hyperkalemia on EDHF-related endothelial function in animal vessels [6, 7] exists in the human coronary artery. The study was focused on the effect of hyperkalemia without ischemia.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Isometric Tension Studies
Human coronary arteries were taken from explanted hearts of patients undergoing heart transplantation without coronary artery disease. The explanted heart was immediately placed in a container filled with Krebs' solution at 4°C and transferred to the laboratory. Epicardial coronary arteries were dissected free from the surrounding connective tissue, cut into 3-mm-long rings, and mounted on a pair of stainless steel wires in organ chambers [16] filled with Krebs' solution at 37°C. The Krebs' solution had the following composition (in mmol/L): Na⁺, 144; K⁺, 5.9; Ca²⁺, 2.5; Mg²⁺, 1.2; Cl^-, 128.7; HCO₃^-, 25; SO₄^2-, 1.2; H₂PO₄^-, 1.2; and glucose, 11. The solution was aerated with a gas mixture of 95% O₂ and 5% CO₂ at 37°C.

A previously described organ-chamber technique [16] was used to normalize vascular rings under a pressure simulating the conditions encountered by the artery at its normal transmural pressure, according to their own length-tension curves. The normalization procedure was performed with a computerized program (VESTAND 2.1 by Yang-Hui He, Princeton University, Princeton, NJ).

The endothelium was intentionally preserved by cautiously dissecting and mounting the rings [6, 7, 17, 18].

Protocol
All rings were equilibrated for 30 minutes before and after normalization. U46619 (30 nmol/L) was then added into the organ chamber to contract the rings. When the contraction reached a stable plateau (usually 10 minutes), cumulative concentration-response curves were established for calcium ionophore A23187 (calcimycin) at concentrations of -10 to -6.5 log mol/L. The relaxation induced by A23187 has been well demonstrated as endothelium-dependent in the coronary artery [7] and human vessels [19].

CONTROL.
The concentration-relaxation curves were established with the presence of indomethacin (7 µmol/L), a cyclooxygenase inhibitor, and N^G-nitro-L-arginine (L-NNA, 300 µmol/L), a nitric oxide biosynthesis/release inhibitor.

HYPERKALEMIA TREATMENT.
In separate experiments, rings were exposed to hyperkalemic solutions containing 20 mmol/L K⁺ replacing Na⁺ in the Krebs' solution. After exposure for 1 hour, the chamber solutions was changed back to normal Krebs' solution again and the rings were frequently washed with Krebs' solution to restore the baseline. The above protocol was applied to establish the concentration-relaxation curves to A23187.

Indomethacin and L-NNA were added 30 minutes before the concentration-relaxation curves for A23187 were started. Only one concentration-relaxation curve was obtained from each coronary ring. Nitroglycerin (-4.5 log mol/L) was added at the end of the experiments to test whether the rings were still able to be relaxed with this endothelium-independent vasorelaxant agent [3, 16]. From a number of rings in each group of experiments, a mean concentration-relaxation curve was constructed. During the experiments, the solutions in the organ chamber were continuously aerated with a mixture of 95% O₂ and 5% CO₂ to exclude the effect of ischemia.

Data Analysis
The effective concentration of the relaxation agent that caused 50% of maximal contraction (or relaxation) was defined as EC₅₀. The EC₅₀ was determined from each concentration-relaxation curve by a logistic, curve-fitting equation: E = MA^P/(A^P + K^P), where E is response, M is maximal contraction (or relaxation), A is concentration, K⁺ is EC₅₀ concentration, and P is the slope parameter [16]. From this fitted equation, the mean EC₅₀ value ± standard error of the mean was calculated for each group.

Data were analyzed by unpaired t test. Values of p less than 0.05 were considered significant.

Drugs
Drugs used and their sources were as follows: A23187 (calcimycin), L-NNA, and indomethacin were from Sigma, St. Louis, MO. U46619 was from Cayman Chemical, Ann Arbor, MI. The L-NNA (dissolved in distilled water) and indomethacin (dissolved in ethanol) were stored at 4°C. The solution of U46619 was held frozen until required.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Hyperkalemia Exposure and Coronary Tone
Hyperkalemia-exposure increased the coronary tone by 4.2 ± 0.9 g (n = 6; p < 0.001). After 1 hour of incubation, even with frequent washout by the normal Krebs' solution, the tone slowly returned to the previous basal level, and this took about 1 hour.

Comparison of Precontraction
Precontraction by U46619 (30 nmol/L) was little affected by the hyperkalemia exposure. In control rings, after treatment with indomethacin and L-NNA (n = 6) without exposure to K⁺, the contraction force to U46619 was 4.0 ± 0.6 g, whereas it was 2.9 ± 0.4 g (n = 6) after incubation with 20 mmol/L K⁺ for 1 hour (p = 0.1).

A23187-Induced Relaxation
In control rings, with the presence of indomethacin and L-NNA, A23187 induced 50.7% ± 3.2% relaxation of the precontraction. Exposure to hyperkalemia (20 mmol/L K⁺) for 1 hour significantly reduced the maximal relaxation resistant to indomethacin and L-NNA. In the rings exposed to 20 mmol/L K⁺, the relaxation was reduced to 30.4% ± 4.6% (n = 6; p = 0.005) (Fig 1). The difference existed at the concentrations of -8.5 to -6.5 log mol/L (Fig 1). At the end of the experiment, nitroglycerin fully (>90%) relaxed all vessels (data not shown). With regard to the EC₅₀, it was 8.1-fold higher in rings treated with 20 mmol/L K⁺ than in the control rings (-7.37 ± 0.17 versus -8.28 ± 0.27 log mol/L; p = 0.019).

View larger version (22K): [in this window] [in a new window]   Fig 1. . Mean concentration (-log mol/L)-relaxation (percentage of contraction by U46619, 30 nmol/L) curves for calcium ionophore A23187 in the human coronary artery. Symbols represent data averaged from a group of rings. Vertical bars are 1 standard error of the mean of the response at each concentration. The control group (n = 6; black circles) was studied in the presence of indomethacin (7 µmol/L) and NG-nitro-L-arginine (300 µmol/L); In the hyperkalemia exposure group (n = 6; white circles), coronary rings were incubated with Krebs' solution containing 20 mmol/L K+ replacing Na+ for 1 hour. The rings were washed to restore the baseline. The A23187 relaxation curve was then established with the presence of indomethacin (7 µmol/L) and L-NNA (300 µmol/L). (EDHF = endothelium-derived hyperpolarizing factor; *p < 0.05; **p < 0.01.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

Indomethacin- and L-NNA–Resistant, Endothelium-Dependent Relaxation
As described above, endothelium-dependent relaxation is composed of three major components. To demonstrate the EDHF-related relaxation, the other two components-EDNO and prostacyclin-must be inhibited by specific inhibitors. In the present study, L-NNA and indomethacin were used for this purpose. My study shows that with the presence of these two inhibitors, A23187 evoked 50.7% relaxation. This is obviously related to EDHF. In our previous studies, my colleagues and I [7] demonstrated that in the porcine coronary artery A23187 induced 93% relaxation when L-NNA and indomethacin were present. In a previous study it was suggested that basal release of EDHF may exist in the human coronary artery [20]. The present study demonstrates that the L-NNA and indomethacin-resistant, EDHF-related relaxation contributes to the endothelium-dependent relaxation in the human coronary artery. This finding has a physiologic meaning: EDHF may play a role in the human coronary circulation in regulating the tone and resistance, as was suggested in animal blood vessels [6–9].

Effect of Hyperkalemia on EDHF-Related Relaxation in the Human Coronary Artery
The effect of hyperkalemia on the coronary circulation has a strong clinical implication. If the coronary tone is altered by the exposure, the coronary resistance must be changed under some circumstances. In particular, during the reperfusion period, the perfusion of myocardium or other organs is critical. The vascular tone is determined by the balance between endothelium-dependent relaxation and smooth muscle contraction [21]. If EDHF plays a role in regulating vascular tone, as suggested [6–11], the impairment of EDHF-mediated relaxation facilitates vasoconstriction and, therefore, may reduce the perfusion flow. Based on this hypothesis, my colleagues and I designed studies to investigate the effect of hyperkalemia exposure. We have recently discovered that hyperkalemia exposure reduces EDHF-mediated relaxation [6, 7] and proposed that the mechanism of such alteration is through Ca²⁺-activated K⁺ channels and prolonged membrane depolarization in the porcine coronary artery [7]. The present study was designed to see whether such effects also exist in the human coronary artery.

The present study demonstrates that hyperkalemia exposure for 1 hour, similar to that observed in the porcine coronary artery, also significantly reduces EDHF-related, (indomethacin- and L-NNA–resistant) endothelium-dependent relaxation in the human coronary artery. One hour of exposure to 20 mmol/L K⁺, the usual concentration in cardioplegia, reduces the relaxation from 50.7% to 30.4% (p = 0.005).

The results of the present study show that the effect of hyperkalemia exposure on the EDHF-related endothelial function lasts for at least 1 hour after the exposure. The arteries were frequently washed with normal Krebs' solution for half an hour to restore the baseline and incubated with inhibitors for another half an hour. My results demonstrate that even after this 1-hour period, the effect of hyperkalemia exposure on EDHF-related relaxation still existed. It is therefore logical to postulate that during this 1-hour washout period, which simulates the clinical reperfusion period, the EDHF-related endothelial function may be more significantly impaired.

It has been demonstrated that ischemia impairs the release of EDNO [22]. The present study demonstrates that the effect of EDHF is altered by hyperkalemia even without ischemia. Therefore, both EDNO and EDHF are altered after ischemia-reperfusion, although through different mechanisms. The alteration may increase the coronary tone that is unfavorable to the coronary flow and myocardial perfusion during this critical period.

The results from the present study also have an implication in organ preservation for transplantation. In commonly used organ preservation solutions such as the University of Wisconsin solution (containing potassium concentrations as high as 125 mmol/L) or Euro-Collins solution (containing 115 mmol/L potassium), the K⁺ concentrations are even higher than that of cardioplegia [22–25]. Hyperkalemic organ preservation solutions may also reduce the vasorelaxant effect of EDHF during and soon after the preservation.

I conclude that exposure to hyperkalemia reduces the indomethacinand L-NNA–resistant, EDHF-related, endothelium-dependent relaxation in the human coronary artery. These findings, in addition to the previous ones, provide useful information about endothelial dysfunction after exposure to hyperkalemic cardioplegia or organ preservation solutions and have strong clinical implications. A perfect method of myocardial and other organ preservation should be able to eliminate such effects and restore the EDHF-related endothelial function.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
This study was supported by Committee of Research and Conference grant 3370480018 and Vice-Chancellor grant 35017209, University of Hong Kong. I gratefully acknowledge the excellent experimental work by Dr Cheng-Qin Yang.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Prof He, Division of Cardiothoracic Surgery, University of Hong Kong, Grantham Hospital, 125 Wong Chuk Hang Rd, Aberdeen, Hong Kong (e-mail: gwhe{at}hkucc.hku.hk).

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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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): Guo-Wei He Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by He, G.-W. Search for Related Content PubMed PubMed Citation Articles by He, G.-W.