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Ann Thorac Surg 1997;64:124-128
© 1997 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Effect of Cardiopulmonary Bypass Under Tepid Temperature on Inflammatory Reactions

Toshihiro Ohata, MD, Yoshiki Sawa, MD, Keishi Kadoba, MD, Takafumi Masai, MD, Hajime Ichikawa, MD, Hikaru Matsuda, MD

First Department of Surgery, Osaka University Medical School, Osaka, Japan

Accepted for publication January 17, 1997.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background. Cardiopulmonary bypass (CPB) causes inflammatory reactions and abnormal responses of vascular resistance. Theoretically, the difference in the blood temperature during CPB may influence the degree of CPB-induced inflammatory reactions.

Methods. To elucidate the effect of the perfusate temperature during CPB, serum levels of inflammatory cytokines, neutrophil elastase, complements, and vasoactive substances were measured in 18 patients undergoing elective coronary artery bypass grafting under tepid temperature (34°C) and moderate hypothermia (28°C). Respiratory index and systemic vascular resistance index during and after CPB and intubation time after postoperative course were also analyzed.

Results. The patterns of the change in interleukin-8 and neutrophil elastase were significantly different between the two groups. The tepid group showed an earlier decrease in interleukin-8 and neutrophil elastase levels as compared with the hypothermic group. The prostaglandin E2 level just after CPB was significantly higher in the tepid group than in the hypothermic group. Systemic vascular resistance index and respiratory index and intubation time were significantly lower in the tepid group than in the hypothermic group.

Conclusions. These results demonstrated that tepid CPB affected the inflammatory cytokine release and neutrophil activation compared with hypothermic CPB, resulting in the attenuation of respiratory dysfunction. This may suggest a beneficial effect of tepid temperature in CPB with possible attenuation of the postperfusion syndrome.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Inflammatory reactions are induced by cardiopulmonary bypass (CPB) from the activation of complements, macrophages, neutrophils, and inflammatory cytokines such as interleukin-6 and interleukin-8 (IL-8) [1–6]. Abnormality in vasomotor tones is also evoked by CPB. These reactions are known as "postperfusion syndrome," a status of organ dysfunction after CPB, which consists of pulmonary, renal, and coagulatory dysfunctions, neurologic changes, and fever of noninfectious origin [7, 8]. Hypothermic CPB has been widely employed in the clinical situation, taking advantage of reduced oxygen consumption of organs and body. On the other hand, the benefits of normothermic CPB have been reported in terms of better organ and hemostatic functions after CPB [9–14]. A comparative study with different temperatures reported the aggravation of cytokine release and vasomotor tones caused by normothermia [3]. Therefore, it is controversial that normothermic temperature may cause a greater degree of CPB-induced inflammatory reactions. Recently, CPB under "tepid" temperature was proposed to be beneficial in terms of the clinical results as compared with normothermic CPB [15]. It is hypothesized that tepid temperature may affect CPB-induced inflammatory rections and postperfusion syndrome. This study was undertaken to investigate whether tepid temperature affects the degree of CPB-induced inflammatory reactions and the subsequent postperfusion syndrome.


   Patients and Methods
Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Patients
Eighteen patients who underwent elective coronary artery bypass grafting at Osaka University Hospital in 1994 were included in this study. Informed consent was given by all patients after approval by our internal review board. Patients were blindly randomized as to which blood temperature was chosen during CPB. Patients were divided into two groups: tepid CPB group (lowest blood temperature, 34°C; n = 10) and moderate hypothermic CPB group (lowest blood temperature, 28°C; n = 8). The CPB circuits consisted of a centrifugal pump, a membrane oxygenator, and an arterial filter primed without blood. Cardiopulmonary bypass was controlled by {alpha}-stat management, with blood flow rates of 2.2 to 2.6 L • min • m-2 in the tepid group and 2.0 to 2.4 L • min • m-2in the hypothermic group to keep mean arterial pressure between 60 and 90 mm Hg. Intermittent cold blood cardioplegia was employed antegradely and retrogradely to obtain myocardial protection. Myocardial temperature at the ventricular septum was monitored and maintained at less than 20°C by additional infusions of retrograde cardioplegia. There were no significant differences in age at operation, CPB time, aortic cross-clamping time, CPB hemodilution ratio, or the dose of norepinephrine between the two groups (Table 1Go).


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  		Table 1. . Comparison of the Basic Data of Cardiopulmonary Bypass in Tepid and Hypothermic Cardiopulmonary Bypassa
 
Measurements
Arterial blood was sampled from the radial arterial catheter before CPB and 0, 12, and 24 hours after CPB. Serum levels of interleukin-6, IL-8, tumor necrosis factor-{alpha}, interleukin-1ß, neutrophil elastase, C3a, C5a, CH50, bradykinin, prostaglandin E2 (PGE2), and 6-keto prostaglandin F1{alpha} were measured by enzyme-linked immunosorbent assay, enzyme immunoassay, and radioimmunoassay. All postbypass data are expressed corrected for hemodilution occurring during CPB.

Respiratory index and systemic vascular resistance index were also analyzed. Respiratory index is an index of oxygenation and reflects the presence of pulmonary shunting in a variety of circumstances including atelectasis, pulmonary contusion, and pulmonary emboli [16]. Respiratory index and systemic vascular resistance index were calculated as follows:


(1)

(2)

(3)

Statistics
Comparisons between groups over time were performed by two-way analysis of variance with repeated measures. Data were further compared by Bonferroni's test or nonpaired ttest if significance was indicated (p < 0.05). Values of pless than 0.05 were regarded as statistically significant. All values were expressed as mean ± standard error of the mean.


   Results
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 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
No neurologic accident, no myocardial infarction, and no other complications due to the blood temperature in CPB occurred in any patient in this study.

Inflammatory Cytokines and Neutrophil Elastase
Both groups showed a significant increase in IL-8 level just after CPB. Levels of IL-8 decreased 12 hours after CPB in the tepid group, whereas they increased in the hypothermic group. The tepid group showed a significantly lower IL-8 level 12 hours after CPB than the hypothermic group in (15.6 ± 3.5 versus 96.1 ± 34.3 pg/mL; p= 0.0188). Finally, there was no significant difference 24 hours after CPB (Fig 1Go). However, the pattern of change in IL-8 level was significantly different (p = 0.0286). Both groups showed a significant increase in serum interleukin-6 level just after CPB, which then decreased 12 and 24 hours after CPB in both groups. There was no significant difference at any point. Levels of tumor necrosis factor-{alpha} and interleukin-1ß were as low as the minimum detection level throughout the perioperative course in both groups (Table 2Go). Twelve hours after CPB, neutrophil elastase level decreased in the tepid group, whereas it increased in the hypothermic group. The tepid group showed a significantly lower neutrophil elastase level 12 hours after CPB than the hypothermic group (353 ± 105 versus 1,108 ± 311 µg/L; p = 0.0250). Finally, there was no significant difference 24 hours after CPB between the two groups (Fig 2Go). However, the pattern of the change in neutrophil elastase was significantly different (p = 0.0401).



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  		Fig 1. . Change in interleukin-8 (IL-8) levels before (pre) and after cardiopulmonary bypass between the tepid (T) and the hypothermic group (H). The increase in IL-8 levels 12 hours after cardiopulmonary bypass was significantly smaller in T than in H. Values are mean ± standard error. (*p < 0.05 versus pre; **p < 0.01 versus pre; {dagger}{dagger}p < 0.01, T versus H.)

 

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  		Table 2. . Change in Interleukin-6 Level Before and After Tepid and Hypothermic Cardiopulmonary Bypassa
 


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  		Fig 2. . Change in neutrophil elastase (PE) levels before (pre) and after cardiopulmonary bypass between the tepid (T) and the hypothermic group (H). The increase in PE levels 12 hours after cardiopulmonary bypass was significantly smaller in T than in H. Values are mean ± standard error. (*p < 0.05 versus pre; **p < 0.01 versus pre; {dagger}{dagger}p < 0.01, T versus H.)

 
Bradykinin, Prostaglandin E2, and 6-Keto Prostaglandin F1{alpha}
Both groups showed an increase in serum bradykinin levels just after CPB. There was no significant difference as the bradykinin level gradually decreased 12 and 24 hours after CPB. Just after CPB, the tepid group showed a significant higher serum level of PGE2 than did the hypothermic group (16.6 ± 3.9 versus 6.0 ± 1.9 pg/mL; p = 0.0417). However, there was no significant difference in PGE2level 12 and 24 hours after CPB (Fig 3Go). Both groups showed an increase in 6-keto prostaglandin F1{alpha} levels just after CPB, followed by a gradual decrease 12 and 24 hours after CPB. There was no significant difference in 6-keto prostaglandin F1{alpha} level at any point (Table 3Go).



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  		Fig 3. . Change in prostaglandin E2 (PGE) levels before (pre) and after cardiopulmonary bypass between the tepid (T) and the hypothermic group (H). The PGE level just after cardiopulmonary bypass was significantly higher in T than in H. Values are mean ± standard error. ({dagger}p < 0.05, T versus H.)

 

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  		Table 3. . Change in Bradykinin and 6-Keto Prostaglandin F1{alpha} Before and After Tepid and Hypothermic Cardiopulmonary Bypassa
 
C3a, C5a, and CH50
Serum C3a level increased in both the tepid and hypothermic groups just after CPB and decreased 12 and 24 hours after CPB. There was no significant difference at any point. Both groups showed a decrease in CH50 level just after CPB. This increased in both groups 12 and 24 hours after CPB. There was no significant difference at any point (Table 4Go). In spite of the significant change in C3a and CH50 levels after the initiation of CPB in both groups, the C5a level was as low as the minimum detection level throughout the perioperative course.


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  		Table 4. . Change in Complement Levels Before and After Tepid and Hypothermic Cardiopulmonary Bypassa
 
Respiratory and Hemodynamic Data
Immediately after CPB, both groups showed increases in respiratory index compared with before CPB, whereas the tepid group showed a significantly lower respiratory index than did the hypothermic group (0.69 ± 0.14 versus 1.23 ± 0.18; p = 0.0356). There was no significant difference in respiratory index between the two groups 2, 6, and 12 hours after CPB (Fig 4Go). The intubation time was significantly shorter in the tepid group than in the hypothermic group (8.3 ± 1.4 versus 13.3 ± 1.0 hours, respectively; p= 0.0133). The systemic vascular resistance index was significantly lower throughout and just after CPB in the tepid group than in the (30 minutes: 2,318 ± 332 versus 3559 ± 224 dynes•s•cm-5•m2, p = 0.0208; 60 minutes: 2,179 ± 256 versus 3,858 ± 328 dynes•s•cm-5•m2, p= 0.0019; 90 minutes: 2,329 ± 352 versus 3,816 ± 345 dynes•s•cm-5•m2, p= 0.0162; CPB off: 1,602 ± 145 versus 2,147 ± 94 dynes•s•cm-5•m2, p = 0.0281, respectively) (Fig 5Go).



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  		Fig 4. . Comparison of respiratory index (RI) between the tepid (T) and the hypothermic group (H). The RI just after cardiopulmonary bypass was significantly lower in T than in H. Values are mean ± standard error. (pre = before cardiopulmonary bypass; 2h, 6h, and 12h = 2, 6, and 12 hours after cardiopulmonary bypass; {dagger}p < 0.05, T versus H.)

 


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  		Fig 5. . Comparison of systemic vascular resistance index (SVRI) between the tepid (T) and the hypothermic group (H). The SVRI during and just after cardiopulmonary bypass was significantly lower in T than in H. Values are mean ± standard error. (off = just after cardiopulmonary bypass; 30m, 60m, and 90m = 30, 60, and 90 minutes after the initiation of cardiopulmonary bypass; {dagger}p < 0.01, T versus H; {dagger}{dagger}p < 0.05, T versus H.)

 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
In the present study, the serum levels of IL-8 and neutrophil elastase, respiratory functions, and vasomotor tone were affected in the tepid group as compared with those in the moderate hypothermic group. Tepid temperature introduced an earlier decrease in inflammatory cytokine with an improvement in respiratory index and intubation time, and an increase in PGE2level with lower systemic vascular resistance index. The lower systemic vascular resistance may contribute to better organ perfusion after CPB. The better respiratory index in the tepid group may be related to the suppression of neutrophil activation, which may cause leukosequestrations in the pulmonary microvasculature or the generation of free radical species on reperfusion [17]. These results suggest that tepid temperature causes a reduced degree of postperfusion syndrome after CPB.

The degree of inflammation induced by the activation of neutrophils is thought to be related to the serum levels of IL-8, a major neutrophil chemotactic factor [18], and neutrophil elastase, a specific enzyme of neutrophils [19]. These two indices appeared to be related to the respiratory dysfunction after CPB in the present study [20]. The tepid temperature group showed an earlier decrease in IL-8 and neutrophil elastase levels as compared with the moderate hypothermic group. These results suggested that some of the inflammatory mediators may be metabolized earlier in the tepid group than in the moderate hypothermic group, possibly because of the temperature-dependent function of metabolic enzymes [21].

In this study, a difference in the response of IL-8, neutrophil elastase, and PGE2 levels was detected between the two groups. The PGE2 level in the tepid group was significantly higher than that in the moderate hypothermic group just after CPB. On the other hand, tepid CPB caused an earlier decrease in IL-8 and neutrophil elastase levels compared with hypothermic CPB. Therefore, we cannot conclude that tepid CPB attenuated the inflammatory response induced by CPB as compared with the moderate hypothermic CPB. Moreover, it is speculated that the PGE2 level may not correlate with IL-8 and neutrophil elastase levels even under inflammatory reactions. On the other hand, there is no report that PGE2 is a key factor that aggravates the postperfusion syndrome, whereas IL-8 and neutrophil elastase play a pivotal role in postperfusion syndrome [18]. Thus, the earlier decrease in levels of inflammatory mediators such as IL-8 and neutrophil elastase, especially during the post-CPB course, may be advantageous for attenuation of the postperfusion syndrome. The mechanism of difference between the response of IL-8 and PGE2 levels was not elucidated in this study. However, PGE2 is metabolized mainly in pulmonary vascular endothelium, whereas IL-8 is metabolized in the liver. On the other hand, IL-8 is produced from neutrophils, macrophages, and monocytes [22], and PGE2 is released from neutrophils and endothelial cells during CPB [23, 24]. Therefore, the differences of metabolism and production may cause the different results of inflammatory response between the two inflammatory factors.

Systemic vascular resistance is affected mainly by vasoactive substances during and after CPB [25–27]. In this study, the lower systemic vascular resistance in the tepid group was associated with a difference in PGE2 level but not with a difference in levels of bradykinin or 6-keto prostaglandin F1{alpha} (metabolite for prostacyclin). Prostaglandin E2 may contribute to systemic vascular resistance during CPB. However, other vasodilative substances such as nitric oxide may relate to vascular resistance. In this study containing coronary artery bypass grafting cases, nitric oxide was not investigated because nitroglycerin injection affects the serum nitric oxide level. Further investigation of the correlation between nitric oxide and vascular resistance is required.

Arom and associates [15] have recommended the tepid temperature in CPB because of the clinical outcomes. Blood in the heat exchanger for CPB is heated up around 38° to 40°C to maintain the perfusate temperature at 37°C. This hyperthermic blood can be the cause of excessive release of the inflammatory cytokines resulting in organ dysfunction [28]. Globus and associates [29] have reported that brains perfused with blood at 34°C had reduced intracellular acidosis and more rapid return of high-energy phosphate compounds compared with controls perfused at 37°C in the cerebral occlusion-reperfusion animal models. Therefore, we employed 37°C as the physiologic upper limit of the blood temperature in the outflow of the heat exchanger, so that the perfusate temperature in the body was maintained around 34°C, so-called tepid temperature.

In conclusion, cardiopulmonary bypass under tepid temperature (34°C) caused an earlier decrease in IL-8 and neutrophil elastase levels and a subsequent increase in PGE2 level, suggesting a beneficial effect of cardiopulmonary bypass under tepid temperature with possible attenuation of the postperfusion syndrome.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Matsuda, First Department of Surgery, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565, Japan.


   References
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 Footnotes
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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