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Ann Thorac Surg 1998;65:101-106
© 1998 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Thromboxane Production in Human Lung During Cardiopulmonary Bypass: Beneficial Effect of Aspirin?

Eldad Erez, MD, Arie Erman, PhD, Eitan Snir, MD, Ehud Raanani, MD, Dan Abramov, MD, Jacqueline Sulkes, PhD, Geoffrey Boner, MD, Bernardo A. Vidne, MD

Department of Cardiothoracic Surgery, Rabin Medical Center, Beilinson Campus, affiliated to the Sackler School of Medicine, Tel Aviv University, Petach Tikva, Israel
Institute of Nephrology and Hypertension, Rabin Medical Center, Beilinson Campus, affiliated to the Sackler School of Medicine, Tel Aviv University, Petach Tikva, Israel
Epidemiology Unit, Rabin Medical Center, Beilinson Campus, affiliated to the Sackler School of Medicine, Tel Aviv University, Petach Tikva, Israel

Accepted for publication July 11, 1997.

Dr Vidne, Department of Cardiothoracic Surgery, Rabin Medical Center (Beilinson Campus), Petach Tikva 41900, Israel.


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Increased systemic levels of thromboxane (Tx) during cardiopulmonary bypass (CPB) in humans have been reported. It is not known whether this reflects a general systemic response to the surgical procedure or an increased pulmonary production of Tx in response to ischemia and reperfusion.

Methods. Thromboxane B2 levels were measured in the right atrium and left atrium of 14 patients undergoing coronary artery bypass grafting for angina. Eight patients (group 1) were without aspirin for at least 15 days before operation, and 6 patients (group 2) were treated with aspirin (100 mg/day) for at least 1 month before operation. Levels of TxB2 were determined by enzyme immunoassay after lipid extraction and separation.

Results. Thromboxane B2 levels were elevated throughout CPB. In group 1, left atrial TxB2 levels were significantly higher (p < 0.05) than right atrial levels at all study points during CPB. After pulmonary reperfusion, TxB2 levels in both atria increased significantly (p < 0.02) compared with the levels before cross-clamping of the aorta, and there was an increasing gradient between the two atria (p < 0.05). Mean plasma TxB2 levels during CPB in group 2 were significantly reduced (p < 0.0001) in the right atrium (by 73%) and in the left atrium (by 69%) compared with levels in group 1.

Conclusions. The rise in TxB2 levels in the left atrium after CPB in humans reflects production of Tx mainly in the lungs, most probably by ischemic pulmonary tissue and intravascular hematologic components. Aspirin markedly reduces Tx production during CPB, and it might play a major role in preventing pulmonary injury after operations with CPB in humans.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Thromboxane (Tx)A2, a derivative of arachidonic acid [1], is known as a potent vasoconstrictor [2][3] and as a powerful inducer of platelet aggregation [1][4]. Aspirin and related antiinflammatory drugs inhibit the synthesis of Tx and other prostaglandins from its precursor, arachidonic acid, through binding to the cyclooxygenase catalytic site of the prostaglandin endoperoxide synthase enzyme [5].

Thromboxane is produced mainly by platelets. It has been shown that the lungs are a rich source of Tx [6][7][8]. Increased Tx production was reported to be associated with ischemic injury to skeletal muscle [9][10][11] and heart [12]. Thromboxane receptor antagonists [13] or inhibitors of Tx synthesis [14][15] have been found to reduce heart ischemic reperfusion injury associated with Tx formation in animals.

Increased systemic plasma levels of Tx during cardiopulmonary bypass (CPB) have been reported [16][17][18][19][20]. Shafique and associates [21] demonstrated that Tx generation in the sheep lung is stimulated during total CPB and is abolished by reperfusion. This elevation of pulmonary Tx levels was associated with pulmonary hypertension, increased pulmonary capillary permeability, and pulmonary cellular sequestration [22]. The lung injury has been eliminated by the inhibition of Tx synthesis [23].

The present study was undertaken to characterize the kinetics of circulatory Tx levels during CPB for coronary artery bypass grafting (CABG) in humans, to determine the contribution of the lungs to changes in circulating Tx levels during CABG, to assess the influence of treatment with aspirin on circulating Tx levels during CPB, and to assess pulmonary function variables after CPB with respect to treatment with and without aspirin and TxB2 levels.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
Patients
The study population consisted of 14 patients with angina pectoris who underwent CABG at the Rabin Medical Center (Beilinson Campus) on an elective basis. Patients with recent myocardial infarction or severe congestive heart failure (ejection fraction less than 0.35 or New York Heart Association functional class III–IV) were excluded, as these conditions in themselves have been found to be associated with elevated plasma levels of Tx [11][12][13][14].

The patients were divided into two groups: group 1 (n = 8) included patients who had not received drugs known to interfere with the synthesis of prostaglandins for at least 15 days preceding the operation, and group 2 (n = 6) had received aspirin (100 mg/d) for at least 1 month prior to CABG. All patients provided written informed consent.

Surgical Protocol
Each patient was anesthetized with an intravenous injection of midazolam hydrochloride (0.05 mg/kg) and fentanyl (30 to 35 µg/kg). Muscular relaxation was obtained using pancuronium bromide (0.2 mg/kg). Patients were mechanically ventilated (Narkomed 2C; North American Drager) with adjustments in variables to maintain normocapnia as determined by frequent arterial blood gas measurements. The radial artery and internal jugular vein were cannulated for blood pressure and central venous pressure monitoring, respectively. Heart rate was monitored by surface electrocardiography.

The mediastinum was exposed by a median sternotomy. Intravenous heparin sodium (3 mg/kg) was administered before cannulas were inserted for CPB, with repeated injections as necessary to maintain activated clotting time higher than 400 seconds. Hypothermic (28°C) nonpulsatile CPB was established through a cannula in the ascending aorta and a cannula in the right atrium (two-stage cannula) for venous return. A disposable membrane oxygenator (Safe II; Polystan, Denmark) with polyvinyl chloride tubing and a roller pump were used. The circuit was primed with Hartman’s solution, and the hematocrit value was maintained at 25% ± 1% during bypass. A small amount of pulmonary perfusion persisted and was returned to the heart-lung machine through left atrial (LA) venting.

Grafting was performed during a single period of aortic occlusion with cold (4°C) crystalloid cardioplegic solution injected into the coronary arteries through the aortic root. The cardioplegic solution consisted of Plasma-Lyte A (Baxter Healthcare Corp) and lidocaine hydrochloride (100 mg), papaverine hydrochloride (40 mg), potassium (12 mEq), and methylprednisolone (500 mg). After induction, cardioplegia was given every 20 to 30 minutes through the aortic root. The cardioplegic solution partially perfused the lungs and was collected outside the CPB circuit.

Bleeding time and blood counts in the two groups were similar at all comparable stages. Perioperative blood loss and transfusion volumes were also similar.

Blood Samples
Thromboxane B2 Levels
Blood samples were drawn from the left atrium (LA) (by direct aspiration or the venting tube) and the right atrium (RA) (through the internal jugular vein). The seven stages at which time blood samples were drawn for each group are shown in Fig 1. The blood sample at stage 7 was taken prior to protamine sulfate administration. Ten milliliters of blood was placed in a precooled tube containing EDTA (ethylenediamine tetraacetic acid) (10 mg/mL) and indomethacin (100 µg/mL). All tubes were immersed in ice and later centrifuged at 3,000 g for 15 minutes at 4°C. The plasma samples were stored in polypropylene vials at -20°C until TxB2 determination.



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  		Seven periods of blood sampling during operation. (CPB = cardiopulmonary bypass.)

 
Pulmonary Function Variables
Ventilatory time (hours) and arterial blood sampling every hour from admission to the intensive care unit and up to 4 hours later were recorded. Differences in alveolar-arterial oxygen pressure gradients with respect to each group were calculated, corrected by inspired-oxygen fraction.

Thromboxane B2 Assay
Plasma samples (3.5 mL) were acidified to pH 3.0 with citric acid (2 mol/L) and loaded on octadecylsilyl silica cartridges, and prostaglandins were eluted with ethyl acetate. The ethyl acetate was evaporated under nitrogen, and the residue was reconstituted in phosphate buffer (0.01 mol/L, pH 7.0) containing 0.1% bovine albumin, 0.15 mol/L sodium chloride, 0.01 mol/L magnesium chloride, and 0.1% sodium azide.

Thromboxane B2 was determined with an enzyme immunoassay kit (Perceptive Diagnostics, Cambridge, MA). Cross reactivity of TxB2 antibodies at 50% binding with 2,3 dinor-TxB2 was 55.8% and less than 0.1% with the prostaglandins E2, F2{alpha}, and 6-keto-prostaglandin F1{alpha}. Thromboxane B2 levels were expressed as picograms per milliliter of plasma.

Because of the wide variation in the degree of hemodilution before and during CPB, the plasma TxB2 levels of sample 1 were corrected by taking into consideration the relationship of plasma to total blood volume (hematocrit) before and during CPB. During all other stages of sampling, hematocrit was maintained at 25% ± 1%.

Statistical Analysis
Results are presented as the mean ± the standard deviation. To analyze significant differences in mean right atrial (RA) and LA Tx levels between the seven time points and Tx levels between the two groups, analysis of variance was performed using the Duncan multiple-comparison option. To compare differences between mean RA and LA Tx levels for each group, the paired Student’s t test was applied. To compare differences in alveolar-arterial oxygen pressure gradient, CPB time, and cross-clamp time between the two groups, the unpaired Student’s t test was applied. A p value of 0.05 or less was considered significant.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
The study population comprised 9 men and 5 women ranging in age from 57 to 80 years (mean age, 66.7 ± 6.5 years). Demographic and clinical data on each patient and data concerning the surgical procedure are presented in Table 1. Aortic cross-clamp time and CPB time were analyzed by group and were as follows: cross-clamp time, 47.9 ± 15.1 minutes and 52.2 ± 6.8 minutes (p = 0.52), and CPB time, 81.5 ± 25.8 minutes and 90.5 ± 7.3 minutes (p = 0.4), group 1 and group 2, respectively.


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  		Demographic, Clinical, and Surgical Data

 
Group 1 Thromboxane B2 Levels
Fig 2AFig 3 indicate the plasma TxB2 levels during CPB in group 1, patients without aspirin treatment. The LA TxB2 levels were significantly higher (p < 0.05) than the RA levels at all study points during CPB. With the onset of CPB, there was an increase in TxB2 levels in samples obtained from the LA (p = 0.02). The RA TxB2 levels also tended to be higher, although not significantly so. After cross-clamping of the aorta and arrest of the heart, TxB2 levels in both atria decreased, with a significant decrease in LA levels (p = 0.003).



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  		Thromboxane B2 (Tx B2) concentration in paired samples simultaneously drawn from right atrium (RA) and left atrium (LA) (A) in patients receiving no aspirin treatment and (B) aspirin-treated patients. The seven sampling times are as shown in Fig 1. (* = p < 0.05, LA > RA; # = p < 0.02, LA 2 > LA 1, LA 3 < LA 2, LA 4 > LA 3; & = p = 0.02, RA 4 > RA 3; {wedge} = p < 0.05, RA 6 > RA 1, RA 7 > RA 1; ** = p = 0.05, LA 5 > LA 3.)

 


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  		Thromboxane B2 (Tx B2) gradient levels between left atrium (LA) and right atrium (RA) during blood sampling times in patients receiving no aspirin (group 1). In group 2, there was no difference in these levels between the LA and RA during the various stages. (* = p < 0.05, LA-RA 4 > LA-RA 3.)

 
Immediately after the heart had recovered its own mechanical activity and the onset of pulmonary reperfusion, TxB2 levels in the LA and RA increased significantly compared with levels prior to aortic cross-clamping (RA, 172 ± 59 pg/mL versus 96 ± 35 pg/mL; p = 0.02; LA, 251.5 ± 61 pg/mL versus 154.6 ± 62.5 pg/mL; p = 0.005). A significantly increasing gradient in TxB2 levels between the LA and RA was documented at this stage (p < 0.05) (see Fig 3). Subsequent samples taken immediately at the end of CPB and 30 minutes later showed a rapid decrease in TxB2 levels on both sides and abolition of the gradient between the atria. Thirty minutes after the end of CPB, the RA TxB2 level remained significantly elevated compared with the value seen before bypass.

The increase in LA TxB2 concentrations compared with RA concentrations demonstrates an increase in plasma TxB2 levels across the pulmonary circuit after rewarming and pulmonary reperfusion.

Group 2 Thromboxane B2 Levels
Fig 2B indicates the plasma TxB2 levels during CPB in group 2, patients treated with aspirin. Mean plasma TxB2 levels during CPB were significantly reduced (p < 0.0001) in the RA by 73% and in the LA by 69% compared with group 1. There was no significant difference between LA and RA TxB2 levels at any time. Only LA TxB2 levels immediately after the heart had recovered its own mechanical activity showed a significant increase compared with values before aortic cross-clamping (90 ± 40 pg/mL versus 44 ± 32 pg/mL; p = 0.05). There were no significant changes in the gradient between the atria during the various stages of CPB. At the end of CPB and 30 minutes later, the TxB2 levels in both atria tended to return to levels seen before bypass.

Pulmonary Function Variables
There was no difference in ventilatory time between groups (11.9 ± 1.3 hours in group 2 13.2 ± 1.5 hours in group 1). The alveolar-arterial oxygen pressure gradient was significantly higher in patients without aspirin treatment immediately on admission to the intensive care unit compared with that in patients treated with aspirin before operation. Differences in alveolar-arterial oxygen pressure gradients were noted for all five blood samples measured (Table 2).


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  		Differences in Alveolar-Arterial Oxygen Pressure Gradient Between Group 1 and Group 2

 

   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
Increased systemic plasma TxB2 levels during CPB in humans have been reported [16][17][18][19][20]. Addonizio and co-workers [16] proposed that elevated plasma TxB2 levels during CPB reflect a direct role of the heart-lung machine, but Faymonville and colleagues [19] failed to demonstrate Tx production in fresh human blood recirculated in circuits containing a membrane oxygenator. Moreover, that study and another [18] reported increased plasma Tx levels at the end of CPB in systemic blood. It has been proposed that elevation of plasma TxB2 concentrations at the end of CPB is due to rewarming and pulmonary reperfusion and is probably the consequence of Tx release from sequestered pulmonary platelets and pulmonary microemboli [19].

The pulmonary contribution of Tx to the elevation in circulating plasma Tx levels during CPB in humans was not examined. A study [21] in a sheep model showed that total CPB (pulmonary artery clamped) stimulated Tx generation in the lung. This effect was progressive and was abolished by reperfusion.

We measured LA and RA levels of TxB2, the stable metabolite of TxA2, during CABG in patients treated with and without aspirin. Our results show that LA TxB2 levels were significantly elevated compared with RA TxB2 levels at all study points during CPB in patients without aspirin treatment (group 1). Moreover, after the aortic cross-clamp was removed and lung reperfusion initiated, there was a significant increase in the TxB2 gradient between the LA and RA. These results suggest TxB2 synthesis in the lungs during CPB. This increased TxB2 production probably does not represent a general effect of CPB on prostanoids. Faymonville and co-workers [19] reported that prostacyclin concentration was reduced during CPB, and Friedman and associates [22] found that leukotriene B4 was unchanged during CPB.

The significant reduction after cross-clamping of the aorta and arrest of the heart represents an acute reduction in pulmonary blood flow, hypothermia, or both [24][25]. At this stage, the source of pulmonary perfusion is mainly through bronchial arterial blood flow and a small amount of pulmonary artery perfusion. As the heart regained mechanical activity and the lungs were reperfused, we observed a significant increase of TxB2 concentration in the effluent (LA). This increase in LA thromboxane levels probably represents washout of TxB2 that has accumulated, increased production in the lungs, or both. These findings combined with those of previous studies suggest that the mechanism of this generation is probably related to blood flow through the lungs.

Patients treated with aspirin before operation have significantly lower production levels of Tx during CPB than untreated patients. The LA TxB2 levels tended to be elevated compared with those of the RA, although the difference did not reach significance.

It is apparent from our data that there are marked fluctuations in Tx levels during CPB. Indeed, the disparity between different studies reported to date regarding the effect of myocardial ischemia and reperfusion on circulating Tx levels [18][19] may be partially explained by temporal differences in drawing the blood samples as well as differences in the source of sampling (arterial, venous, LA, or RA). We chose to obtain baseline Tx levels in all patients immediately prior to CPB (rather than before operation) to preclude possible effects of anesthesia, mechanical ventilation, and vascular injury during venous and arterial manipulation on circulating Tx levels.

Thromboxane has been implicated as an important mediator of ischemic pathophysiologic processes in various tissues [9][10][11][12]. The production of Tx by the lungs as suggested in our study may result from the ischemic conditions present during CPB, when the lungs are mostly dependent on nonpulsatile bronchial arterial flow for their oxygen supply. Thromboxane can be synthesized by the sequestered thrombocytes and polymorphonuclear cells.

The complete clinical significance of elevated pulmonary Tx levels during CABG with CPB has yet to be determined. We did not observe any difference in ventilatory time between the two groups. On the other hand, there was a significant difference in alveolar-arterial oxygen pressure gradient during the first hours after CPB between the two groups, probably indicating ventilation-perfusion mismatch and increased lung water content, both known to be related to lung injury.

Elevated Tx levels were suggested as a cause of the pulmonary pathology in sporadic cases of inexplicable noncardiogenic pulmonary edema occurring after operations requiring CPB [21].

Increased pulmonary vascular resistance, lymph flow, and lung water content have been shown to be factors in lung injury after total CPB in a sheep model [22][23]. Mullose and Fornabaio [14] established previously that TxA2 synthetase inhibitor can reduce experimental cardiac reperfusion injury. Moreover, it has been demonstrated clinically that TxA2 synthetase inhibition reduces pulmonary vascular resistance after mitral valve replacement [26] and augments the effect of nifedipine on reduction of pulmonary vascular resistance in patients with primary pulmonary hypertension [27].

Aspirin is used widely to reduce platelet aggregation and the risk of thromboembolic events in patients with ischemic heart disease. Thus, an increasing number of patients scheduled for elective CABG are treated with aspirin preoperatively. Preoperative aspirin treatment could play a major role in reducing Tx formation and thereby reduce pulmonary injury during and after the use of CPB in CABG.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
We thank Batia Chen-Gal and the heart-lung perfusionists for their technical assistance.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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