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Ann Thorac Surg 1998;66:56-59
© 1998 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Inflammatory response after myocardial revascularization with or without cardiopulmonary bypass

^a Discipline of Cardiovascular Surgery, Escola Paulista de Medicina and São Paulo Hospital, Federal University of São Paulo, São Paulo, Brazil
^b Discipline of Infectious Diseases, Escola Paulista de Medicina and São Paulo Hospital, Federal University of São Paulo, São Paulo, Brazil

Accepted for publication December 15, 1997.

Address reprint requests to Dr Brasil, Cardiovascular Surgery Discipline, Escola Paulista de Medicina and São Paulo Hospital, Federal University of São Paulo, Rua Botucatu 740, São Paulo, SP 04023-900, Brazil
e-mail: (ebuffollo.dcir{at}epm.br)

	Abstract

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Background. Tumor necrosis factor- has been implicated in complications seen after cardiac operations with cardiopulmonary bypass. The release of tumor necrosis factor- and its possible effects were studied in patients undergoing coronary artery bypass grafting with and without cardiopulmonary bypass.

Methods. Twenty patients were studied, 10 with (group 1) and 10 without cardiopulmonary bypass (group 2). Serial blood samples were obtained before, during, and up to 48 hours after operation. Circulating tumor necrosis factor- levels, leukocyte counts, and erythrocyte sedimentation rates were measured. Hemodynamic variables (blood pressure and heart rate), temperature, orotracheal intubation time, postoperative bleeding, and inotropic drug requirements were compared.

Results. Serum levels of tumor necrosis factor- were detected in 6 patients (60%) in group 1 and none in group 2. The patients in group 1 had more hypotension than those in group 2 (7.4 ± 1.0 mm Hg versus 8.5 ± 0.7 mm Hg), required more inotropic drugs (8 patients versus 1 patient), and had a higher heart rate (114 ± 8 beats per minute versus 98 ± 10 beats per minute), a higher temperature (37.1° ± 0.5°C versus 36.6° ± 0.3°C), increased postoperative bleeding (820 ± 120 mL versus 360 ± 84 mL), a longer orotracheal intubation time (13.6 ± 2.2 hours versus 9.3 ± 1.4 hours), and a more pronounced leukocytosis.

Conclusions. Cardiopulmonary bypass induces the whole-body inflammatory response through the release of tumor necrosis factor , resulting in adverse systemic effects.

	Introduction

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The systemic inflammatory response syndrome induced by cardiopulmonary bypass (CPB) is responsible for organ dysfunction observed in patients after cardiovascular surgical procedures. This is the so-called postperfusion syndrome [1]. Tumor necrosis factor- (TNF-) has been implicated in many complications occurring after cardiac operations with CPB [2, 3]. The aim of this study was to compare the release of TNF- and its possible effects in patients with obstructive atherosclerotic coronary artery disease who underwent coronary artery bypass grafting (CABG) with and without CPB.

	Material and methods

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Twenty patients undergoing elective CABG were studied consecutively, 10 with (group 1) and 10 without CPB (group 2). Whether CPB was used or not was determined by the experience of the surgical group, as already reported [4]. Patients were excluded from the study if they had previously had CPB, if they had insulin-dependent diabetes mellitus or chronic obstructive pulmonary disease, or if corticosteroids or antiinflammatory drugs were being prescribed.

Operation
The same general anesthesia regimen was used in all patients. It comprised intravenous administration of midazolam hydrochloride, fentanyl citrate, sufentanil citrate, alfentanil hydrochloride, and pancuronium bromide.

In group 1, routine operations were performed using a membrane oxygenator (Oxim II; Macchi, São Paulo, Brazil), a 4 mg/kg dose of heparin sodium, 1,200 mL of Ringer’s lactate priming, a roller pump and nonpulsatile flow, an arterial line filter, a body temperature of 28°C, and antegrade hypothermic intermittent blood cardioplegia. In group 2, operative procedures were done as previously described [4, 5]. Briefly, after 2 mg/kg of heparin, with a normothermic beating heart, the distal anastomosis was performed after a temporary interruption in coronary blood flow achieved by snaring sutures with a thin silicone tube. When necessary, the proximal anastomosis of the aorta was performed using tangential clamping.

Sample collection
Seven serial blood samples were obtained from each patient in each group before, during, and up to 48 hours after operation. The samples for TNF- quantification were immediately centrifuged, and the plasma was separated and frozen at -70°C until use. In group 1, the first sample was collected during anesthesia induction; the second, 10 minutes after aortic cross-clamping; the third, after release of the aortic cross-clamp and protamine sulfate infusion; and the fourth, at the end of the operation. In group 2, the first sample was drawn during anesthesia induction; the second, 10 minutes after the first temporary coronary occlusion; the third, after completion of all anastomoses and protamine infusion; and the fourth at the completion of the operation. In both groups, samples were obtained 12, 24, and 48 hours postoperatively.

Laboratory and clinical variables
The presence of circulating TNF- was measured using enzyme-linked immunosorbent assay (Genzyme, Cambridge, MA), following the manufacturer’s instructions. Sensitivity of the test is 10 pg/mL. The leukocyte count and the erythrocyte sedimentation rate were also measured in the samples.

Mean blood pressure, heart rate, temperature, orotracheal intubation time, postoperative bleeding, and inotropic drug requirement during the postoperative period were recorded and compared. Inotropic drugs were given when necessary to obtain hemodynamic stabilization.

Statistical analysis
Statistical analysis was performed with the use of nonparametric tests for data comparison (Mann-Whitney, Friedman, and Fisher). Significance was accepted when the value of p was 0.05 or less.

	Results

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The patients in groups 1 and 2 did not differ significantly in respect to age, sex, body weight, and number of grafts. The operation time was prolonged (p < 0.001) in group 1 (Table 1).

The patients in group 1 experienced more severe hypotension (p < 0.02) than those in group 2. Group 1 patients also required more inotropic drugs (p = 0.0027), had a higher heart rate (p < 0.02), had a higher temperature (p < 0.05), had more prominent postoperative bleeding (p < 0.001), and required a longer orotracheal intubation time (p < 0.001) (Table 2).

View larger version (20K): [in this window] [in a new window]   Fig 1. Circulating levels of tumor necrosis factor- (TNF-) in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass. Samples: 1 = plasma was obtained during anesthesia induction; 2 = plasma was obtained 10 minutes after aortic cross-clamping; 3 = plasma was obtained after aortic cross-clamp release and protamine infusion; 4 = plasma was obtained at the end of operation, and 5, 6, and 7 = plasma was obtained 12, 24, and 48 hours postoperatively, respectively.

	Comment

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After a cardiac surgical procedure, the occurrence of a systemic inflammatory response syndrome induced by the use of CPB is well established. This is called postperfusion syndrome and is caused mainly by the contact of blood with the foreign materials used in the extracorporeal circuit [6, 7]. This systemic inflammatory reaction induces the release of substances that promote diffuse endothelial lesions and can lead to organ injury and postoperative morbidity [8]. Studies [2, 9, 10] have suggested that the activation and the release of cytokines, especially TNF-, play an important role in the pathogenesis of the systemic inflammatory response syndrome induced by CPB. Tumor necrosis factor- may induce endothelial dysfunction with enhanced vascular permeability, decreased systemic vascular resistance, fever, hypotension, and leukopenia followed by leukocytosis, hemoconcentration, metabolic acidosis, and circulatory shock [11, 12].

Cardiovascular effects of cytokines are mediated by nitric oxide and by means of the interaction between leukocytes and endothelium [13]. The trigger for these effects may be the presence of circulating endotoxins, lipopolysaccharides of the cell wall of gram-negative bacteria that, on interaction with the host cells, promote the release of mediators such as cytokines, among them, TNF- [14]. High levels of circulating endotoxins during CPB have been demonstrated and may be due to splanchnic hypoperfusion. Cardiopulmonary bypass may produce ischemic damage in the organs perfused by the splanchnic circulation, thus causing edema, intestinal congestion, and passage of bacteria from the interior of the intestine into the circulation [15, 16]. In vivo studies [17] have shown that endotoxins induce TNF- formation by activation of macrophages and monocytes and that the peak concentration occurs after 60 to 90 minutes.

The presence of TNF- in the blood of 6 of 10 patients having CABG with CPB suggests that the other 4 patients might have had intermittent release into the blood. However, because TNF- is quickly cleared from the blood by the reticuloendothelial system, our sampling frequency was insufficient to capture it.

We observed a significant increase in circulating TNF- levels in patients undergoing CABG with CPB. The higher levels of TNF- were observed during aortic cross-clamping and during reperfusion after the release of the aortic cross-clamp (see Fig 1), as reported in previous studies [2, 18].

Other reports [10, 19] indicate that the CPB–induced release of cytokines such as interleukins and TNF- is related to time of perfusion and clamping of the aorta. In 1 patient in our series, the patient with the longest CPB time (160 minutes) (see Fig 1), TNF- was found in all samples, and this suggests a relation to the intensity of the inflammatory response.

The cytokine release during and after CPB could be related to the degree of tissue injury, as it appears that cytokines function as markers of intensity of the inflammatory reaction [20, 21]. Supporting a role for TNF- in this response, we observed that the patients in group 1 (CABG with CPB) compared with those in group 2 showed the following: more hypotension, a greater requirement of inotropic drugs, a higher heart rate, a higher temperature, increased postoperative bleeding, a longer orotracheal intubation time, and a more pronounced leukocytosis.

Tumor necrosis factor- could also be implicated in the pathophysiology of the vasoplegic syndrome, in which patients who have had cardiac surgical intervention with the use of CPB exhibit severe and persistent low systemic vascular resistance, hypotension, decreased filling pressures, normal or elevated cardiac output, and tachycardia in the postoperative period [22, 23]. These patients need a high dose of vasoconstrictor drugs (eg, norepinephrine) for hemodynamic control.

One study [24] has reported the presence of TNF- in human atherosclerotic tissues and its absence in tissues classified as normal. In our study, we compared the release of TNF- in patients who had a similar disease, ie, coronary atherosclerosis, and underwent a similar procedure (CABG) but differed in the use of CPB.

We conclude that CPB induces the whole-body inflammatory response through the release of TNF- among other possible mediators, resulting in adverse systemic effects. It is possible that TNF- plays a role in the pathophysiology of the alterations observed in this study and that its inhibition could contribute to minimizing these effects.

	References

Top Abstract Introduction Material and methods Results Comment References

 

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