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From the Department of Anaesthesiology, Oita Medical University, 1-1, Idaigaoka, Hasama-machi, Oita 879-5593, Japan.
Address correspondence to: Hideo Iwasaka MD DMSC, Phone: +81-97-586-5943; Fax: +81-97-586-5949; E-mail: hiwasaka{at}oita-med.ac.jp
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Abstract |
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Methods: We prospectively studied 10 patients undergoing cardiac surgery (coronary artery bypass grafting) using cardiopulmonary bypass (CPB). Plasma G-CSF levels and neutrophil count were measured before induction of anaesthesia, at the end of surgery, and on the first postoperative day. These changes were compared with those in patients undergoing non-cardiac major surgery (control group).
Results: At the end of surgery, G-CSF levels increased (P < 0.01) in both groups, but were higher in the control than in the cardiac group (3,250 ± 690 vs 194 ± 29.5 pg•ml–1, respectively, mean ± SEM, P < 0.01). On the first postoperative day, G-CSF levels were still high in both groups, and were still higher in the control (710 ± 179 vs 122 ± 19.9, respectively, P < 0.01). However, neutrophilia was greater in the cardiac group than in the control. G-CSF response correlated positively with neutrophilia in the control group (r=0.656, P < 0.05) but not in the cardiac group.
Conclusions: Our results indicate that changes in leukocyte count following cardiac surgery are unique to patients undergoing CPB. G-CSF plays an important role as the mediator of neutrophilia after non-cardiac surgery, but not after cardiac surgery with CPB.
NEUTROPHIL activation occurs in patients who have undergone cardiopulmonary bypass (CPB).1 The process and consequences of neutrophil activation are complex and the data available are insufficient to explain the complex processes. Recently, it has become apparent that human granulocyte colony-stimulating factor (G-CSF) is the main regulator of the production as well as functional state of neutrophilic granulocytes. 2,3 The purpose of this study was to determine the relationship between changes in neutrophil counts and G-CSF levels after CPB.
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Methods |
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Blood samples for the measurement of plasma G-CSF, total and differential leukocyte counts, were obtained prior to the induction of anesthesia, at the end of surgery, and on the first postoperative day. Total leukocyte and neutrophil counts were determined by routine laboratory methods. For the determination of serum G-CSF levels, the blood samples were analyzed using enzyme immunoassay.4
Another group of eight patients (two male, six female; mean age, 63.9 yr, range 55-83) who underwent major surgery (esophagectomy and esophageal reconstruction) without CPB were recruited as the control sample. Approval for the study was also obtained from the Human Subjects Committee.
A high-dose fentanyl (50-75 µg•kg–1)-oxygen-vecuronium bromide technique supplemented with diazepam and an inhalation agent, isoflurane (0.5-1.0%), was used in the cardiac surgery group. In the non-cardiac group, anesthesia was induced with thiamylal and maintained with isoflurane (1.5-2.0%) and nitrous oxide, and occasionally supplemented with low-dose fentanyl (0.1-0.2 mg).
All data were expressed as mean ± SEM. Differences between groups were examined for statistical significance using ANOVA, Fisher's Protected Least Significant Difference, Student's t test, and linear regression analysis. A P value less than 0.05 denoted the presence of a statistically significant difference.
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. The amount of transfused blood during surgery was significantly lower (P < 0.01) in the cardiac group than in the non-cardiac group. In addition, the duration of surgery and anesthesia were shorter in the cardiac group.
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). At the end of surgery, G-CSF concentrations increased (P < 0.01) in both groups, and were higher in the non-cardiac than in the cardiac group (3,250 ± 690 vs 194 ± 29.5 pg•ml–1, respectively, P < 0.01). On the first postoperative day, G-CSF levels were still high in both groups, and were still higher in the non-cardiac group.
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). Statistical analysis showed higher increase in leukocyte and neutrophil counts in the cardiac group than in the control group, contrary to the changes in G-CSF levels. There was a positive correlation between the G-CSF response to surgery and postoperative leukocyte counts in the non-cardiac group (r=0.656, P < 0.05, Figure 2). In contrast, no such correlation was identified in the cardiac group.
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Discussion |
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Despite the uncomplicated perioperative courses, leukocytosis and neutrophilia are generally encountered after CPB.6,7 However, the complex mechanisms and mediators are not well understood. One may speculate that increased concentrations of G-CSF contributed to post-CPB leukocytosis. To confirm this, we investigated the relationship between changes in neutrophil counts and G-CSF levels in patients undergoing cardiac and non-cardiac major surgery. Our results demonstrated that plasma G-CSF levels correlated with neutrophil counts after non-cardiac major surgery, but not cardiac surgery. In contrast to leukocyte counts, G-CSF levels were lower in the cardiac surgery than in the non-cardiac surgery group. Patients undergoing cardiac surgery showed a greater increase in neutrophils, but a smaller increase in G-CSF. These results suggest that G-CSF may not play an important role as the mediator of neutrophilia in cardiac surgery. One reason for these results may be related to the two different anesthetics used in the present study. We used a high dose of fentanyl for cardiac surgery and isoflurane inhalation anesthesia for non-cardiac surgery. In vitro studies have shown that opioids, at higher concentrations, reduced hyperactivation of granulocytes and monocytes exposed to the stimulatory effects of plasma obtained from CPB patients.8,9 Therefore, the high-dose fentanyl in cardiac surgery might attenuate the surgical stress response better than inhalation anesthetics. This may well explain the suppressed G-CSF response in cardiac surgery. However, the use of different anesthetics could not explain the marked post-CPB neutrophilia.
In conclusion, our results suggest that G-CSF plays an important role as the mediator of neutrophilia in non-cardiac surgery, but not in cardiac surgery with CPB.
Accepted for publication October 9, 2000.
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2 Asano S. Human granulocyte colony-stimulating factor: its basic aspects and clinical applications. Am J Pediatr Hematol Oncol 1991; 13: 400–13.[Medline]
3 Sieff CA. Hematopoietic growth factors. J Clin Invest 1987; 79: 1549–57.
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Watari K, Asano S, Shirafuji N, et al. Serum granulocyte colony- stimulating factor levels in healthy volunteers and patients with various disorders as estimated by enzyme immunoassay. Blood 1989; 73: 117–22.
5 Pearl RG, Sladen RN, Rosenthal MH. Hematologic effects of cardiac and noncardiac surgery. J Cardiothorac Anesth 1987; 1: 205–9.[Medline]
6 Cullen BF, van Belle G. Lymphocyte transformation and changes in leukocyte count: effects of anesthesia and operation. Anesthesiology 1975; 43: 563–9.[Medline]
7 Ryhänen P, Herva E, Hollmen A, Nuutinen L, Pihlajaniemi R, Saarela E. Changes in peripheral blood leukocyte counts, lymphocyte subpopulations, and in vitro transformation after heart valve replacement. J Thorac Cardiovasc Surg 1979; 77: 259–66.[Medline]
8 Stefano GB, Kushnerik V, Rodriquez M, Bilfinger TV. Inhibitory effect of morphine on granulocyte stimulation by tumor necrosis factor and substance P. Int J Immunopharmacol 1994; 16: 329–34.[Medline]
9 Stefano GB, Leung MK, Bilfinger TV, Scharrer B. Effect of prolonged exposure to morphine on responsiveness of human and invertebrate immunocytes to stimulatory molecules. J Neuroimmunol 1995; 63: 175–81.[Medline]
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P < 0.01 vs the cardiac group.