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Ann Thorac Surg 2000;69:1035-1040
© 2000 The Society of Thoracic Surgeons

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ORIGINAL ARTICLES: CARDIOVASCULAR

Differential effects of calcium channel antagonists in the amelioration of radial artery vasospasm

^a Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, South Carolina, USA
^b Division of Anesthesiology, Medical University of South Carolina, Charleston, South Carolina, USA

Address reprint requests to Dr Spinale, Strom Thurmond Research Building, Medical University of South Carolina, 114 Doughty St, Suite 625, Charleston, SC 29403

Presented at the Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, Nov 4–6, 1999.

	Abstract

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Background. Radial artery (RA) is being used for coronary artery bypass grafting (CABG) with greater frequency. However, RA is prone to post-CABG vasospasm, which may be neurohormonally mediated. Use of the calcium channel antagonist diltiazem has been advocated as a strategy to reduce post-CABG RA vasospasm. However, whether and to what degree different calcium channel antagonists influence neurohormonally induced RA vasoconstriction remains unknown.

Methods. RA segments were collected from patients undergoing elective CABG (n = 13), and isometric tension was examined in the presence of endothelin (10 nM) or norepinephrine (1 µM). In matched RA, endothelin- or norepinephrine-induced contractions were measured in the presence of diltiazem (277 nM), amlodipine (73 nM), or nifedipine (145 nM). These concentrations of calcium channel antagonists were based upon clinical plasma profiles.

Results. Endothelin and norepinephrine caused a significant increase in RA-developed tension (0.54 ± 0.1 and 0.68 ± 0.1 g/mg, respectively; p < 0.05). Amlodipine or nifedipine significantly reduced RA vasoconstriction in the presence of endothelin (30 ± 6% and 41 ± 9%, respectively; p < 0.05) or norepinephrine (27 ± 8% and 53 ± 9%, respectively; p < 0.05), whereas diltiazem did not significantly reduce RA vasoconstriction.

Conclusions. These results demonstrate that neurohormonal factors released post-CABG can cause RA vasoconstriction, and that calcium channel antagonists are not equally effective in abrogating that response. Both amlodipine and nifedipine, which have a higher degree of vascular selectivity, appear to be the most effective in reducing RA vasoconstriction.

	Introduction

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The radial artery (RA) is being used as a conduit for coronary artery bypass grafting (CABG) with increased frequency due to reports of long-term patency, accessibility, and the need for additional conduits [1–3]. However, early use of RA for CABG was associated with a high incidence of vasospasm during the immediate postoperative period [4, 5]. Neurohormonal activation occurs perioperatively with CABG, which includes elevated plasma levels of endothelin and norepinephrine [6–9]. These potent neurohormones cause vascular smooth muscle vasoconstriction, which may contribute to RA vasospasm [10, 11]. Therefore, pharmacologic intervention that prevents vascular smooth muscle vasoconstriction, such as the use of the calcium channel antagonist diltiazem, has been advocated [1–3, 12, 13]. The underlying rationale for use of diltiazem is the prevention of RA vasospasm in the perioperative period.

However, the use of diltiazem can produce negative chronotropic and inotropic effects that may not be desirable in the post-CABG setting [14]. Whether and to what degree other calcium antagonists prevent neurohormonally mediated RA vasoconstriction remains to be defined. Amlodipine and nifedipine are two dihydropyridine calcium channel antagonists that are more vascular selective than diltiazem and thus have less effect on myocardial performance [15–17]. Therefore, the overall goal of this study was to perform a comparative study of the effectiveness of diltiazem, amlodipine, and nifedipine on the prevention of endothelin- or norepinephrine-induced RA vasospasm. The first objective of this study was to quantify the contributory role of endothelin and norepinephrine in RA vasospasm in vitro. The second objective was to determine the degree to which each of these calcium channel antagonists prevents RA vasospasm induced by these vasoactive substances.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Overview
RA samples were collected from patients undergoing elective CABG and used for vascular contractility studies. Contractile function of matched RA segments was examined using well-described vascular ring in vitro methods [10, 11]. Endothelin- or norepinephrine-induced RA vasoconstriction was examined alone and also in the presence of different calcium channel antagonists.

Patients and vessel collection
After approval by the Institutional Review Board of the Medical University of South Carolina (IRB #7147), patients (n = 13) undergoing elective CABG and providing informed consent were enrolled in this study. The mean age of patients was 58 ± 4 years (male-to-female ratio of 12:1). The technique for RA dissection has been described previously [1–4]. Briefly, after careful dissection from the arm, the RA was flushed with dilute papaverine (1 mg/mL) and placed in iced saline. Immediately before anastomosis, the RA conduit was flushed with saline. No marking dyes or bulldog clamps were used. This institution and others have successfully performed this harvesting technique to collect RA for use as a coronary conduit [1–3]. After anastomosis, the remaining RA was placed into iced oxygenated Krebs-Hanseleit buffer (4.6 mM KCl, 2.5 mM CaCl₂, 1.2 mM KH₂PO₄, 118 mM NaCl, 2.5 mM NaHCO₃, and 11 mM glucose) and immediately transported to the laboratory.

Experimental protocol
While remaining in iced Krebs-Hanseleit buffer, fat and connective tissue were removed and the RA was divided into four 4-mm segments, with careful attention paid to avoid damaging the endothelium. These rings were then mounted at optimal diastolic tension (3 g) in a 10-mL organ bath chamber containing oxygenated Krebs-Hanseleit solution maintained at pH 7.4 and 37°C [10, 11]. The rings were then flushed eight times over 2 hours with fresh Krebs-Hanseleit buffer. Developed tension from each RA ring was measured by digital force transducers (Radnoti, Monrovia, CA), and the digital signal was acquired for analysis by an acquisition system (BioBench; National Instruments, Austin, TX). Final tension values were reported as tension generated (g) per milligram of tissue. The rings were allowed to equilibrate at resting tension for 1 hour and then randomly assigned to four treatment protocols: 1) diltiazem (277 nM; Bedford Laboratories, Bedford, OH; n = 13); 2) amlodipine (73 nM; Pfizer, Groton, CT; n = 13); 3) nifedipine (145 nM; Sigma, St. Louis, MO; n = 10); and 4) vehicle (n = 13). These concentrations of calcium channel antagonists were predicated upon previously published, clinically relevant, steady-state plasma levels [14–18].

The rings were preincubated for 1 hour in the presence of calcium channel antagonists or vehicle. All calcium channel antagonists were prepared fresh daily to maintain activity. These treatment interventions did not significantly change the ambient resting tension. Endothelin (10 nM; Sigma) was then added to each chamber for 30 minutes, during which time steady-state vasoconstriction was achieved, and the maximum developed tension was recorded. This concentration of endothelin was based upon a preliminary RA dose-response study using endothelin (0.1 to 100 nM) (Fig 1). These initial studies were performed on a set of four radial arteries that were not used in the subsequent protocol. Generation of these dose-response curves allowed for the computation of the endothelin concentration necessary to induce 50% of maximal vasoconstriction (8.5 ± 1.2 nM), which closely approximates the concentration of 10 nM used in later studies.

View larger version (13K): [in this window] [in a new window]   Fig 1. Endothelin tension response curves were generated from RA samples (n = 4) exposed to increasing concentrations of endothelin (0.1 to 100 nM). These curves allowed for the computation of the concentration of endothelin necessary to induce 50% of maximal vasoconstriction (EC50 = 8.5 ± 1.2 nM). The concentration of endothelin used in subsequent RA experiments (10 nM) was based upon this EC50 value.

View larger version (12K): [in this window] [in a new window]   Fig 2. Norepinephrine tension response curves were generated from RA samples (n = 13). Norepinephrine (1 µM) induced a time-dependent increase in RA developed tension that reached a plateau value after 5 minutes.

	Results

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Endothelin-mediated RA vasoconstriction: effect of calcium channel antagonists
A robust increase in RA tension was observed in the presence of endothelin (absolute tension development, 0.54 ± 0.1 g/mg) over basal resting tension (p < 0.05). In order to examine the effects of the calcium channel antagonists, the endothelin response was computed as percent change from matched vehicle RA samples (Fig 3). While treatment with diltiazem reduced endothelin-mediated vasoconstriction, this effect did not reach statistical significance (p = 0.32). In contrast, both amlodipine and nifedipine treatment significantly reduced endothelin-mediated developed tension. Moreover, the reduction in endothelin-induced developed tension was significantly greater with both nifedipine and amlodipine treatment when compared with diltiazem.

View larger version (15K): [in this window] [in a new window]   Fig 3. The percent reduction in endothelin-induced RA developed tension with calcium channel antagonist treatment with diltiazem (125 ng/mL; n = 13), amlodipine (30 ng/mL; n = 13), and nifedipine (50 ng/mL; n = 10). Diltiazem did not significantly alter endothelin-induced vasoconstriction (p = 0.32 vs baseline). However, amlodipine or nifedipine significantly reduced endothelin-mediated vasoconstriction (*p < 0.05 vs baseline). In addition, both amlodipine and nifedipine significantly reduced endothelin-mediated RA vasoconstriction when compared with diltiazem (#p < 0.05 vs diltiazem).

View larger version (15K): [in this window] [in a new window]   Fig 4. The percent reduction in norepinephrine-induced RA developed tension with calcium channel antagonist treatment with diltiazem (125 ng/mL; n = 13), amlodipine (30 ng/mL; n = 13), and nifedipine (50 ng/mL; n = 10). Diltiazem did not significantly alter norepinephrine-induced vasoconstriction (p = 0.86 vs baseline). However, amlodipine and nifedipine significantly reduced norepinephrine-mediated vasoconstriction (*p < 0.05 vs baseline). In addition, both amlodipine and nifedipine significantly reduced norepinephrine-mediated RA vasoconstriction when compared with diltiazem (#p < 0.05 vs diltiazem).

	Comment

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To our knowledge, there have been no comparative studies assessing the effects of different calcium channel antagonists on neurohormonally mediated RA vasoconstriction. However, past reports have examined the vasoconstrictive response of RA after exposure to vasoactive peptides in vitro [3, 10, 11]. For example, Chardigny and associates described norepinephrine-mediated vasoconstriction in the RA, internal mammary artery, and gastroepiploic artery [10], and demonstrated increased RA sensitivity to norepinephrine. It has also been demonstrated that a potent RA vasoconstrictive response occurs with endothelin concentrations similar to those used in the present study [11]. A potential reason for the heightened vasospasm observed in RA is its unique structural morphology, including a greater amount of vascular smooth muscle and less elastin than other vessels commonly used as CABG conduits [3]. The present study builds upon these previous reports by demonstrating that vascular selective calcium channel antagonists attenuated the potent vasoconstrictive response of RA segments exposed to endothelin or norepinephrine.

Neurohormonal activation during and after CABG stimulates the release of bioactive peptides and catecholamines such as endothelin and norepinephrine, particularly in the setting of cardiopulmonary bypass [6–9]. Endothelin activates two distinct receptor subtypes expressed in the RA. Activation of the endothelin A receptor, primarily located on smooth muscle cells, results in the opening of calcium channels, thereby allowing calcium entry and vasoconstriction [19, 20]. Conversely, activation of the endothelin B receptor localized on endothelial cells induces the production of nitric oxide, which mediates vasorelaxation [19, 20]. The balance between endothelin A and endothelin B receptor activation determines whether and to what degree vasoconstriction occurs. The endothelin A receptor subtype predominates in the arterial vasculature. Thus, in muscular arteries such as the RA, exposure to endothelin induces potent vasoconstriction [19, 20]. Norepinephrine preferentially activates the ₁ subtype of adrenergic receptors located on vascular smooth muscle cells. The stimulation of ₁-adrenergic receptors results in the opening of calcium channels, allowing an influx of calcium [21]. Thus, the contributory mechanism by which both endothelin and norepinephrine cause vascular smooth muscle contraction is through activation of calcium channels. The increase in calcium flux into the vascular smooth muscle cell will engage the contractile apparatus, resulting in vasoconstriction. Thus, calcium channel antagonists attenuate endothelin- or norepinephrine-mediated RA vasoconstriction by reducing calcium flux through calcium channels.

It must be recognized that the present study employed only one concentration of each calcium channel antagonist. For diltiazem, the concentration used was based upon previously measured plasma levels in patients [14, 18]. Specifically, an intravenous delivery of 10 mg/h achieved a plasma concentration of approximately 333 nM [18]. In other studies reporting the use of diltiazem for the prevention of RA vasospasm with CABG, a dose of 4 to 5 mg/h has been described [1–3, 13]. Thus, the concentration of diltiazem used in the present study exceeds that of the predicted diltiazem concentration that would be employed clinically for RA vasospasm. Nevertheless, this increased concentration of diltiazem did not attenuate endothelin- or norepinephrine-induced RA vasoconstriction. A study by Cable and associates reported that a twofold higher concentration of diltiazem failed to attenuate potassium chloride- or norepinephrine-mediated RA vasospasm [22]. Moreover, Shapira and associates reported that a fourfold higher concentration of diltiazem failed to inhibit thromboxane-mediated RA spasm [12]. Thus, these past studies suggest that diltiazem may be ineffective for the prevention of RA vasoconstriction. The concentrations of amlodipine and nifedipine used in the present study were predicated upon past pharmacologic doses used in humans [15–17]. Specifically, the amlodipine and nifedipine concentrations employed in this study are derived from clinically effective concentrations utilized for the treatment of mild hypertension [16, 17]. Moreover, these concentrations of calcium channel antagonists were used in the absence of in vivo influences such as binding and clearance. Thus, the concentrations used in the present in vitro study likely exceed clinically effective plasma concentrations. Another consideration of the present study is that the vessels were harvested using the vasodilator papaverine. While the experimental protocol included vigorous washing of these vessel preparations, whether and to what degree there was any residual effect of the vasodilator papaverine could not be addressed.

The three classes of calcium channel antagonists, dihydropyridines, benzothiazepines, and phenylalkylamines, have been demonstrated to interact at distinct sites within the voltage-sensitive calcium channel [23]. Both nifedipine and amlodipine possess a 1,4-dihydropyridine ring that may be responsible for their increased vascular selective properties [23, 24]. Moreover, amlodipine, due to its ionic charge, is more vascular selective and achieves a more prolonged therapeutic effect [23, 24]. Furthermore, this class of calcium channel antagonist produces less severe effects on myocardial conduction and activation [15–17]. In contrast, diltiazem is a 1,5-benzothiazepine that can produce significant effects on myocardial conduction [14]. Therefore, the differential effects observed among diltiazem, amlodipine, and nifedipine with respect to the reduction in endothelin- and norepinephrine-mediated RA vasoconstriction are likely based upon differences in structural class and mechanism of action among these different types of calcium channel antagonists. Moreover, amlodipine has high vascular selectivity, a long half-life, and can be safely used in the setting of compromised ventricular performance [16]. Thus, the new dihydropyridines, such as amlodipine, may have a more desirable pharmokinetic profile for use in the setting of CABG. Future directions include performing a complete dose-response curve for endothelin and norepinephrine in the presence of these calcium channel antagonists.

In summary, the present study examined select calcium channel antagonists for differential effects upon endothelin- or norepinephrine-induced RA vasoconstriction in vitro. Both endothelin and norepinephrine levels have been demonstrated to be elevated after CABG [6–9]. This activation of the neurohormonal system may contribute to postoperative RA vasospasm and lead to early graft failure. Thus, early vasospasm and stenosis must be prevented if RA is to be successfully used as a CABG conduit [1–3]. The prototypical calcium channel antagonist diltiazem has been traditionally used in the prevention of early post-CABG RA vasospasm [1–3, 12, 13]. However, the present study provides evidence to suggest that amlodipine and nifedipine provide a greater attenuation in RA vasoconstriction in vitro when compared with diltiazem. These disparate effects among calcium channel antagonists are likely due to differences in vascular selectivity and inhibitory profiles. Thus, calcium channel antagonists with greater vascular selectivity may be better indicated for preemptive treatment for RA vasospasm in CABG patients. Future studies determining the efficacy of these calcium channel antagonists for the inhibition of preexisting RA vasospasm would be valuable to further define the optimal dose and treatment period for the prevention of RA vasospasm.

	Acknowledgments

 
This work was supported in part by National Institutes of Health grant HL-59165 (FGS), and a Basic Research Grant from Pfizer (FGS). We thank Dr Adviye Ergul for her critical reading of this manuscript, as well as John Tzaferis and Emily Keeling for their technical assistance.

	References

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This Article Abstract Full Text (PDF) 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): James L. Zellner John M. Kratz Arthur J. Crumbley, III Fred A. Crawford, Jr Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bond, B. R. Articles by Spinale, F. G. Search for Related Content PubMed PubMed Citation Articles by Bond, B. R. Articles by Spinale, F. G. Related Collections Related Articles