Anesth Analg 2001;93:1453-1459
© 2001 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
The In Vitro Reversal of Histamine-Induced Vasodilation in the Human Internal Mammary Artery
Atsushi Tsuda, MD,
Kenichi A. Tanaka, MD,
Catherine Huraux, MD,
Fania Szlam, MMS,
Nobukazu Sato, MD,
Koji Yamaguchi, MD, and
Jerrold H. Levy, MD
Department of Anesthesiology, Emory University School of Medicine, Division of Cardiothoracic Anesthesiology and Critical Care, Emory Healthcare, Atlanta, Georgia
Address correspondence and reprint requests to Jerrold H. Levy, MD, Department of Anesthesiology, Emory University Hospital, 1364 Clifton Rd. NE, Atlanta, GA 30322.
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Abstract
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Anaphylactic shock therapy includes the use of catecholamines but they may not always be effective. Because vasodilation during anaphylaxis is a result of the endothelial release of multiple mediators, we investigated the effects of epinephrine, vasopressin, and inhibitors of nitric oxide and prostanoid pathways on histamine-induced relaxation in human internal mammary artery. The vessel segments were obtained intraoperatively and were suspended in organ chambers to record isometric tension. Norepinephrine (10-6 M) was used to precontract the rings followed by histamine (10-6.5 M) to relax the vessels and mimic vascular collapse. Epinephrine, vasopressin, methylene blue, NG-monomethyl-L-arginine (L-NMA) and indomethacin were added in a cumulative fashion to reverse the histamine-induced vasodilation. The internal mammary artery segments exhibited greater contraction in the presence of the epinephrine (4.9 ± 0.7g) compared with vasopressin (2.6 ± 0.7g). Vasopressin (10-11 to 10-7 M), methylene blue (10-7 to 10-5 M), L-NMA (10-6 to 10-4 M), and indomethacin (10-7 to 10-5 M) were only partially effective. These findings suggest that vasopressin and methylene blue may offer a potential therapeutic option in the treatment of histamine-induced vasodilatory shock.
IMPLICATIONS: Epinephrine only partially reverses histamine-induced vasodilation in human internal mammary arteries, whereas vasopressin, methylene blue, and drugs involved in the inhibition of nitric oxide and prostaglandin generation lead to a complete reversal of the vascular relaxation.
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Introduction
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The cardiovascular system is a major target organ during anaphylactic shock. Hypotension is the most common acute manifestation associated with anaphylactic/anaphylactoid reaction and is produced by the effects of multiple mediators on the heart and peripheral vasculature (1). An important mechanism of vascular collapse during anaphylactic/anaphylactoid reaction is a profound reduction in systemic vascular resistance (1). Standard therapy to reverse the vascular collapse is epinephrine, a catecholamine with both 
- and ß-adrenergic effects. In human anaphylactic or anaphylactoid reactions, studies on the utility of epinephrine in improving hemodynamic recovery have not been totally supportive (2,3). Furthermore, prospective studies to determine the best possible therapy to reverse the vascular collapse are impossible because the occurrence of anaphylactic reactions is rare and unpredictable. Therefore, therapy with epinephrine remains empirical and may not always effectively reverse the vasodilation (2).
Although multiple mediators such as prostanoids, leukotrienes and kinins are responsible for vasodilation, histamine appears to play a major role in the acute cardiovascular collapse (2). Stimulation of endothelial H1 receptors releases nitric oxide (NO) and prostacyclin (4). Blockade of the target enzyme of NO pathway, guanylate cyclase, with methylene blue, or use of vasopressin may represent additional therapeutic options in the treatment of anaphylactic shock (4,5). Vasopressin plasma levels can be increased in hemorrhage, septic shock, cardiopulmonary bypass (5), or cardiac arrest (6), where it plays an important role in cardiovascular homeostasis through both its vasoactive and antidiuretic actions. Two studies suggest that septic shock and vasodilatory shock after cardiac surgery are associated with inappropriately small vasopressin concentrations, and vasopressin administration can reverse the hypotension and need for large-dose catecholamines (7,8). There is little information available regarding the effects of vasopressin and methylene blue on mediator-induced vasodilation in human arteries. Therefore, we investigated novel approaches using these drugs to reverse mediator-induced vasodilation.
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Materials and Methods
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Drugs
The following drugs were used: histamine, norepinephrine, epinephrine, NG-monomethyl-L-arginine (L-NMA), indomethacin, acetylcholine (Sigma Chemical, St. Louis, MO), vasopressin (American Regent Laboratories, Inc., Shirley, NY), and methylene blue (Prometic Pharma, Inc., Joliette, Canada). Indomethacin was dissolved in 50 mM Na2CO3. All other drugs were serially diluted in distilled water before each experiment. The addition of diluted drugs to organ chambers filled with 25 mL Krebs-Henseleit buffer resulted in <1% dilution of the buffer solution. The concentration of the drugs is expressed as final molar concentration in the bath. The final concentrations of all the drugs used in the present investigation were chosen to reflect clinically relevant ranges.
Vessel Preparation
After receiving institutional approval, discarded segments of right and left internal mammary artery (IMA) were obtained from 35 patients undergoing coronary artery bypass surgery. Segments were collected into a container filled with a chilled modified Krebs-HEPES solution of the following composition (in mM): NaCl 118, KCl 4.69, CaCl2 3.35, MgSO4 1.175, KH2PO4 1.04, NaHCO3 25, D-Glucose 11.1, and HEPES 21.8, pH 7.40 and immediately transferred to the laboratory. The vessels were cleaned of adherent connective tissue and cut into 3-mm ring segments. Two to four rings were obtained from each vessel. One-hundred-twenty-eight rings were investigated in the present study.
Organ-Chamber Experiments
The rings were suspended between two wire hooks in organ chambers filled with 25 mL of Krebs-Henseleit solution (37°C, pH 7.40) aerated with O295%/CO25%. The upper hook was connected to a force transducer (Kent-Scientific Corporation, Litchfield, CT), and changes in isometric force were recorded (MacLab system, Milford MA). After a resting tension (4 g) defined by preliminary studies was progressively applied, the rings were allowed to equilibrate for 45 min and were then precontracted with 60 mM potassium chloride. The IMA contraction was allowed to plateau for 15 min and then acetylcholine (10-6 M) was added to assess the endothelial function. Only rings that exhibited >30% relaxation responses to acetylcholine were used in subsequent experiments (9). The rings were washed twice with a fresh buffer solution and then precontracted with norepinephrine (10-6 M) to reach an optimal constriction (50%–80% maximum). After 15 min equilibration time, histamine (10-6.5 M) was added to induce relaxation. The relaxation response was allowed to develop for 10–15 min, until stable baseline was obtained. IMA segments were then randomly assigned to one of the five groups (Epinephrine, Vasopressin, Methylene Blue, L-NMA, Indomethacin) and exposed to increasing concentrations (0.5 log unit steps) of only one drug, which was added in the cumulative fashion every 5 min. No more than 60–75 min was required from the time histamine was added to the bath until the end of the experiment. The concentration of histamine chosen (10-6.5 M) was based on concentration-response data obtained in the pilot study. Direct effects of methylene blue on vessels segments equilibrated at resting tension from three patients were also studied.
Vascular Responses of Histamine, Epinephrine and Vasopressin
Cumulative concentration-response curves were obtained with epinephrine (10-9 to 10-4.5 M) and vasopressin (10-11 to 10-7 M). To study histamine effects, vessel segments were precontracted with norepinephrine (10-6 M) and cumulative concentration-response curves were obtained with histamine concentrations ranging from 10-10 to 10-4 M. Epinephrine and histamine were added to the organ baths in 0.5 log unit steps and vasopressin in 1 log unit steps.
Reversal of Histamine-Induced Vasodilation
After norepinephrine-induced contraction, rings were relaxed with 10-6.5 M histamine, an optimal concentration based on our results obtained from histamine response curves. After an equilibration period of 15 min, the following therapeutic drugs were tested in different IMA segments: epinephrine (10-7 to 10-5 M), vasopressin (10-11 to 10-7 M), methylene blue (10-7 to 10-4 M), L-NMA (10-6 to 10-4 M) and indomethacin, and indomethacin (10-7 to 10-5 M) and L-NMA. Each drug was added in a cumulative fashion to reverse histamine-induced relaxation. L-NMA and indomethacin were tested simultaneously when histamine reversal was incomplete with either indomethacin or L-NMA alone. The amplitude of histamine-induced vasodilation was stable for at least 60–75 min.
Responses to each drug were obtained in 2 to 4 vascular rings and averaged for each patient. For the vascular responses to histamine, the results are expressed as percentage of norepinephrine induced-constriction. The contraction response to the reversal drug is expressed as the percentage of the difference between responses to norepinephrine and histamine and is calculated according to the following formula:
equation
where A is the response to norepinephrine, B is the response to histamine, and X is the response to the vasoconstrictor drug. Data are expressed as mean ± SD. One-way analysis of variance followed by Scheffé’s test was used to assess the differences (if any) in histamine-induced relaxation between the groups. To compare the maximal contraction values between the groups, one-way analysis of variance followed by Scheffé’s test was used. A paired Student’s t-test was performed to compare the vascular responses when L-NMA and indomethacin were tested simultaneously. Linear regression analysis was used to correlate the relaxation responses of acetylcholine to histamine. A value of P < 0.05 was considered significant. The number provided refers to the number of patients.
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Results
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Response to Histamine and Acetylcholine
Histamine produced relaxation at concentrations from 10-9 to 10-6 M and constriction occurred in the 10-5 to 10-4 M range in norepinephrine-constricted IMA rings (Fig. 1). Maximal relaxation occurred at 10-6.5 M, the concentration subsequently used in our experiments. Histamine-induced relaxation correlated well with acetylcholine-induced relaxation (r = 0.76, P < 0.0001) (Fig. 2). This result was expected, as both drugs require intact endothelium to produce relaxation. Epinephrine and vasopressin-induced constriction of the IMA segments was concentration dependent (Fig. 3). The IMA segments exhibited greater maximal contraction in the presence of the epinephrine (4.9 ± 0.7 g) compared with vasopressin (2.6 ± 0.7 g) (Fig. 3, Table 1).
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Figure 1. Concentration-response curve to histamine in the human internal mammary artery. Histamine induces relaxation at small concentrations (10-9 to 10-6.5 M) and constriction at larger concentrations (10-5 and 10-4 M) (n = 6). Maximal relaxation occurs at a concentration of 10-6.5 M.
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Figure 3. Concentration-response curves for epinephrine (n = 9) and vasopressin (n = 9) in human internal mammary artery. Data are expressed in gain of tension (g) (mean ± SD).
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Reversal of Histamine-Induced Relaxation (Epinephrine and Vasopressin)
For all experiments, vascular rings producing <30% of relaxation to histamine were excluded. There were no differences in histamine-induced relaxation at a concentration of 10-6.5 M for the different groups: Epinephrine (51% ± 10%, n = 7), Vasopressin (52% ± 15%, n = 7), Methylene Blue (45% ± 13%, n = 7), L-NMA (52% ± 12%, n = 7), and Indomethacin (50% ± 11%, n = 7). As shown in Figures 4A and 4B, vasopressin completely reversed histamine-induced relaxation, whereas epinephrine (10-7 to 10-5 M) was only partially effective. The maximum vasoconstrictive effect was 199% ± 64% for Vasopressin (10-7 M) and 47% ± 24% for Epinephrine (10-5.5 M) (Table 1). The difference was significant between the two groups (P < 0.05).
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Figure 4. Effects of epinephrine and vasopressin on histamine-induced relaxation in human internal mammary artery. Norepinephrine (10-6 M) is used to precontract the vascular rings (100% contraction). Histamine (10-6.5 M) leads to the relaxation of the vascular rings (0%). Epinephrine does not completely reverse the histamine-induced relaxation (n = 7) (A). However, vasopressin reverses the relaxation to a level more than 100% (n = 7) (B). Data are expressed as mean ± SD.
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Reversal of Histamine-Induced Relaxation (L-NMA, Indomethacin, and Methylene Blue)
L-NMA (10-6 to 10-4 M) or Indomethacin (10-7 to 10-5 M) only partially reversed histamine-induced relaxation (Fig. 5A and 5B) in contrast to Methylene Blue, which completely reversed histamine-induced relaxation (Fig. 5C). The maximum responses were 48% ± 14% for L-NMA (10-4 M), 62% ± 23% for Indomethacin (10-5.5 M), and 132% ± 20% for Methylene Blue (10-4 M) (Table 1). The maximal response was increased to over 100% in the presence of both drugs: 150% ± 37% for the combination L-NMA (10-4 M) and Indomethacin (10-5 M), and 125% ± 26% for the combination Indomethacin (10-5 M) and L-NMA (10-4 M) (Table 2). Methylene Blue had a small, concentration-dependent direct constriction effect on IMA rings; it did not exceed 30% at the largest concentration used (10-4 M) as compared with the baseline (Fig. 6). Additionally, norepinephrine-induced contraction was stable at least for 60 min (Fig. 7, left) and histamine-induced relaxation was stable for at least 75 min (Fig. 7, right). There were no significant differences among the five groups after norepinephrine and after addition of histamine (Table 2).
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Figure 5. Effects of NG-monomethyl-L-arginine (L-NMA), indomethacin and methylene blue on histamine-induced relaxation in human internal mammary artery. Indomethacin (10-5 M) (A) and L-NMA (10-4 M) (B) were added simultaneously when histamine reversal was incomplete with either L-NMA or indomethacin alone. The combination of both L-NMA and indomethacin, and methylene blue reversed the relaxation to a level more than 100% (n = 7 each) (A, B, and C). Data are expressed as mean ± SD. *P < 0.05 compared with 10-4 M L-NMA; #P < 0.05 compared with 10-5 M indomethacin.
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Figure 7. Left, stability of norepinephrine-induced vasoconstriction with time in human IMA. Right, stability of histamine-induced relaxation with time in human IMA.
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Discussion
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The present study compared the effects of vasopressin, methylene blue, L-NMA, indomethacin, and epinephrine in human IMA relaxed with histamine. We found that epinephrine, a mainstay therapeutic drug for anaphylaxis, was only partially effective in reversing histamine-induced vascular relaxation. Because the normal physiologic compensatory response to shock is to increase endogenous catecholamines (10), catecholamines with -adrenergic effects have been recommended for treatment of anaphylactic shock. Further, both vasopressin and methylene blue were able to completely reverse histamine-induced vasodilation, but L-NMA or indomethacin were effective only when used in combination and not as single drugs.
Although multiple mediators such as prostanoids, leukotrienes and kinins are responsible for vasodilation, histamine appears to play a major role in the acute cardiovascular collapse associated with anaphylaxis (2). Histamine has both direct and indirect effects on the vasculature. On vascular smooth muscle, stimulation of H1 receptors produces constriction, and stimulation of H2 receptors produces relaxation. On the endothelium, stimulation of H1 receptors causes vasorelaxation via the release of NO and prostacyclin (3). Histamine, like other mediators, produces vasodilation by stimulating vascular endothelium to release both NO and prostacyclin (11). As our study shows, inhibition of either NO with L-NMA or prostacyclin formation with indomethacin alone was not as effective as a combination of both drugs in reversing the histamine-induced vasodilation. Methylene blue, a strong inhibitor of guanylate cyclase, also effectively reversed histamine-induced vasodilation. These findings suggest that attempts to completely reverse vasodilation with catecholamines in anaphylactic/anaphylactoid shock may be ineffective because of the multitude of vasodilatory mechanisms involved.
A number of factors influence vascular responses during vasodilatory shock. Increased vasopressin levels have been reported in various situations, such as hemorrhage (12), cardiopulmonary arrest (6), endotoxic shock (13), vasodilatory shock after cardiac bypass (7), and anesthetic regimens and surgical procedures (14). However, no information about plasma vasopressin levels during anaphylactic/anaphylactoid reactions has been reported. In these situations, the increased vasopressin levels may be part of a compensatory response serving to maintain hemodynamic stability. In the present study, the maximal contraction of human IMA induced by vasopressin (2.6 ± 0.7 g) was smaller than that of epinephrine (4.9 ± 0.7 g) (Fig. 3), however, vasopressin was a much better drug than epinephrine in reversing histamine-induced vasodilation of IMA (Fig. 4A).
It has been suggested that vasopressin enhances the effects of 1-adrenergic stimulation in animals and human both in vivo and in vitro (15–17). In this study, norepinephrine, used to precontract the vascular rings may have been responsible for the initial stimulation of the -adrenergic receptors. Vasopressin has been included in the recent update of the advanced cardiovascular life support (18). Endogenous vasopressin levels during cardiopulmonary resuscitation are significantly higher in patients who survive (18). This finding suggests that augmenting the levels of vasopressin may be beneficial during cardiac arrest, and based on the results of our study, in vitrovasopressin concentrations of 
10-9 M (150 pg/mL) induce concentration-dependent vasoconstriction. Thus, vasopressin may be a useful pharmacological drug reversing mediator-induced hypotension, especially when catecholamines fail to restore vascular tone.
Endothelial H1 receptor stimulation by histamine causes release of NO and prostacyclin, which induce vasorelaxation. The interaction between NO and cyclooxygenase pathway has been studied (19). Inhibiting NO formation with L-NMA or cyclooxygenase pathway with indomethacin did not completely reverse the vascular relaxation. As shown in Figure 5A and 5B, a combination of L-NMA and indomethacin leads to a vasoconstrictor effect more than 100% in the human IMA, thus suggesting that inhibition of both NO and cyclooxygenase pathways is needed for complete reversal of histamine relaxation. We also found that another drug used in our study, methylene blue, causes a vasoconstrictor effect more than 100% in the human IMA (Fig. 5C). In the study by Yang et al. (11) pretreatment of the IMA rings (segments were initially relaxed with acetylcholine to confirm intact endothelium) with methylene blue abolished the relaxation induced by histamine. Our study confirms their findings in that histamine-induced, endothelium-dependent relaxations of IMA segments can be reversed with methylene blue. This response is likely related to not only the complete inhibition of guanylate cyclase, but other pathways may be involved. The fact that methylene blue appears to inhibit endothelial production of vasodilating prostacyclin, independently from soluble guanylate cyclase, may explain the observed effects (20). Methylene blue has been used in patients with septic shock without any major side effects (21–22) and based on results of this study, it may be another option for treating patients with epinephrine-resistant hypotension associated with an anaphylactic shock. It can, however, produce monitoring interference resulting from a reduction of the calculated SpO2 (23), but PaO2 can be confirmed by arterial blood gas measurement.
Histamine is an important mediator that produces vascular collapse in anaphylactic shock by stimulating the endothelial H1 receptors (24). In our study, the concentration of 10-6.5 M seems to be consistent with the findings of Smith et al. (2) showing a range of histamine plasma levels between 2.5 x 10-7 M and 7.9 x 10-7 M, during anaphylactic reactions. However, histamine concentrations larger than 10-6.5 M caused vasoconstriction in human IMA, demonstrating the bimodal vascular response and depending on the regional vascular bed, on the distribution of the H1 and H2 receptors, and on the concentration of histamine (3,25). Moreover, histamine-induced vasodilation only in rings able to relax to acetylcholine, thus confirming the endothelium-dependent process related to the stimulation of H1 receptor (11).
There are some limitations to our study, including the use of only one mediator to induce vasodilation. We used histamine because it is a prototypic inflammatory mediator with direct and indirect vascular effects, and it is perhaps the only mediator for which plasma levels have been determined during anaphylactic shock. Although the administration of the H1 histamine receptor blocker reversed the vasodilation, in clinical states of anaphylaxis, multiple mediators are released that produce similar vascular effects on the endothelium and vascular smooth muscle (1). Further, the low level of relaxation obtained with histamine (
50%), confirmed by the relaxation level assessed with acetylcholine (47% ± 5%), suggests an impairment of the endothelium-dependent relaxation (26). Our IMA vessels were obtained from patients with coronary artery disease undergoing myocardial revascularization. Thus, these vascular segments have potential atherosclerotic changes, although previous reports assume that IMA is partially preserved from the atherosclerotic process (27). Although the segments of IMA are human tissue samples, the in vitro experiments exclude most of the mechanisms of the vascular tone regulation, such as the sympathetic reflexes. Denervated vessels may not reflect the in vivo vascular tone regulation. Another limitation of this study is the use of norepinephrine for precontracting the vascular rings, which may be responsible for prior stimulation of the -adrenergic receptors and therefore, may lead to a partial saturation of these receptors. However, anaphylaxis causes full sympathetic activation as a defensive reaction. Shellenberg et al. (10) confirmed the release of endogenous catecholamines and particularly norepinephrine from adrenergic nerve terminals occurring during histamine release in humans. Finally, we only studied relaxation responses of internal artery (a less vasospastic artery) to the reversal drugs. Other vessels may behave differently, but our findings still seem pertinent because other systemic arteries and arterioles are more responsive to vasoconstrictive drugs. Additional studies comparing vessels other than IMA are needed to clarify this.
Because patients undergoing cardiac surgery are at significant risk to develop anaphylaxis to a host of antigens, studying human blood vessels may provide additional information needed for a better understanding of drugs and mechanisms important in reversing potential vascular collapse. Animal models may not reliably predict the therapeutic response to a particular pharmacological intervention. Our results suggest that vasopressin and methylene blue should be considered as a potential therapeutic approach for mediator-induced vasodilatory shock, such as in anaphylactic/anaphylactoid reactions, especially when catecholamines fail to restore the vascular tone. Additional in vitroand clinical studies using these drugs individually and in combination warrant future investigations.
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Footnotes
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Presented in part at the Society of Cardiovascular Anesthesiologists 22nd Annual Meeting, Orlando, FL, May 8, 2000.
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Accepted for publication July 25, 2001.
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Abstract
Introduction
