EJCTS Click here for details of sales representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Hikaru Matsuda
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ohata, T.
Right arrow Articles by Matsuda, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohata, T.
Right arrow Articles by Matsuda, H.

Eur J Cardiothorac Surg 2000;18:342-347
© 2000 Elsevier Science NL

Role of nitric oxide in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass

Toshihiro Ohataa, Yoshiki Sawab, Keishi Kadobab, Koji Kagisakib, Ken Suzukib, Hikaru Matsudab

a First Department of Surgery, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
b Division of Cardiovascular Surgery, Osaka Police Hospital, 10-31 Kitayama-cho, Tennoji-ku, Osaka 543-0035, Japan

Received 4 February 2000; received in revised form 7 April 2000; accepted 12 April 2000.

Corresponding author. Tel.: +81-6-6771-6051; fax: +81-6-6775-2889
e-mail: tohata{at}aol.com


   Abstract
Top
 Abstract
1. Introduction
 2. Patients and methods
 3. Results
 4. Comment
 References
 
Objectives: Nitric oxide is the most potent vasodilator among inflammation-mediated vasoactive substances. Tepid cardiopulmonary bypass has been known to maintain low vascular resistance and nitric oxide may also be involved. There has been no previous clinical study elucidating a role of nitric oxide in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass. Methods: Thirty-one patients who underwent valvular surgery were randomly divided into two comparable groups; consisting of the hypothermic cardiopulmonary bypass (28°C:14 patients) and the tepid cardiopulmonary bypass group (34°C:17 patients). The serum levels of nitric oxide (NO2-+NO3-), prostaglandin E2, bradykinin, 6-keto PGF1{alpha}, thromboxane B2, endothelin-1, systemic vascular resistance index were measured before, 0, 12 and 24 h after cardiopulmonary bypass. Results: The pattern of change in systemic vascular resistance index and nitric oxide during and after cardiopulmonary bypass were significantly different between the two groups (P=0.0008, P=0.02). The tepid group showed significantly lower levels of systemic vascular resistance index after cardiopulmonary bypass than the hypothermic group (0 h: 2278±735 vs. 4387±1289, 12 h: 1827±817 vs. 2817±1146 and 24 h: 1690±548 vs. 2761±641 dyne s cm-5 m2, P=0.0001, P=0.03, P=0.0006). The nitric oxide levels were significantly higher at 0, 12 and 24 h after cardiopulmonary bypass in the tepid group than those in the hypothermic group (84.7±33.3 vs. 46.3±18.1, 69.8±31.1 vs. 40.1±17.5 and 80.1±38.5 vs. 39.1±15.6 µmol/l, P=0.008, P=0.03, P=0.01). The prostaglandin E2 levels in the tepid group was significantly higher just after cardiopulmonary bypass than that in the hypothermic group (37.3±20.0 vs. 15.8±8.6 pg/ml, P=0.02). The bradykinin level in the hypothermic group was significantly higher just after cardiopulmonary bypass than that in the tepid group (2.40±0.32 vs. 1.85±0.21 log10 (pg/ml), P=0.005). Only nitric oxide showed a significant negative correlation with the systemic vascular resistance index both during and after cardiopulmonary bypass (r=-0.60, P<0.0001) as compared with prostaglandin E2 and bradykinin. Conclusions: These findings demonstrated that serum nitric oxide levels in tepid cardiopulmonary bypass were significantly higher than those in hypothermic cardiopulmonary bypass. Nitric oxide correlated with systemic vascular resistance. Thus, nitric oxide may play a pivotal role in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass.

Key Words: Endothelium-derived relaxation factors • Cardiopulmonary bypass • Vasoconstriction


   1. Introduction
Top
 Abstract
 1. Introduction
2. Patients and methods
 3. Results
 4. Comment
 References
 
Cardiopulmonary bypass (CPB) has been reported to cause temperature-dependent changes of systemic vascular resistance (SVR) since it causes systemic vasoconstriction under hypothermic conditions. On the other hand, a relatively low SVR followed by a hyperdynamic state is known to occur frequently in normothermic CPB [1–3]. Systemic vascular resistance in CPB has been attributed to hemodilution, decreased blood viscosity, hyperkalemia, baroreceptor reflexes and, especially, changes in vasoactive substances [2,4]. However, a key factor of these vasoactive substances in terms of SVR in CPB remains unknown. Nitric oxide (NO) is one of the most potent vasodilators among the known vasoactive substances [5]. A few studies have reported only the changes in serum NO levels in CPB, however little study has elucidated its role in regulating vascular resistance during and after CPB [6–9]. NO may thus regulate vascular resistance during and after CPB. This study was undertaken to investigate whether NO may play a pivotal role in a temperature dependent regulation of systemic vascular resistance in CPB.


   2. Patients and methods
Top
 Abstract
 1. Introduction
 2. Patients and methods
3. Results
 4. Comment
 References
 
2.1. Patients
Thirty-one patients who underwent valvular surgery at our institution in 1995 and 1996 were included in this study. All the patients in this study had normal coronary arteries in their coronary angiograms. Nitroglycerin affected the NO2-/NO3- levels caused by CPB, which are the metabolites of nitroglycerin and nitric oxide. Therefore, none of the patients throughout the study received nitroglycerin during and after CPB in this study period. Informed consent was obtained either from all patients after the procedural approval by our internal review board. Anesthesia was induced with fentanyl citrate (10 µg/kg) and midazolam (50 µg/kg), and neuromuscular blockade was produced by vecuronium (0.1 mg/kg). All patients were blindly randomized as to which blood temperature was chosen during CPB, and then divided into two groups: the tepid CPB group (TEP; lowest blood temperature: 34°C; n=17) and the moderate hypothermic CPB group (HYP; lowest blood temperature: 28°C; n=14). We measured the blood temperature in the arterial line just after going through the heat exchanger. The CPB circuits consisted of a centrifugal pump, a membrane oxygenator and an arterial filter primed without blood. CPB was controlled by µ-stat management with blood-flow rates of 2.2–2.6 l/min per m2 for TEP and 2.0–2.4 l/min per m2 for HYP to keep the mean arterial pressure at between 60 and 90 mmHg with norepinephrine. We did not use nitro-dilators such as nitroglycerin and sodium nitroprusside. There was no significant difference in catecholamine and vasodilators usage in either group. Intermittent cold blood cardioplegia was employed antegradely and retrogradely. The myocardial temperature at the ventricular septum was monitored and maintained below 20°C by additional infusions of retrograde cardioplegia. There were no significant differences between the two groups regarding age at operation, CPB time, aortic cross clamping time, the CPB hemodilution ratio or the dose of norepinephrine (Table 1).


View this table:
[in this window]
[in a new window]
  		Table 1. Comparison of the basic data of cardiopulmonary bypass in TEP and in HYPa

 
2.2. Measurements
The arterial blood was sampled from the radial arterial catheter before 0, 12 and 24 h after CPB. NO degrades very rapidly into nitrate (NO3-) and nitrite (NO2-) in the blood and the level of these metabolites also reflects the NO production. Nitrate was converted into nitrite using the cadmium column. The amount of total nitrite was measured as the absorbency at 546 nM using Griess reagent [10]. The serum levels of bradykinin (BK), prostaglandin (PG) E2, 6-keto prostaglandin F1µ (PGI2), thromboxane (TX) B2 and endothelin (ET)-1 were measured by a radioimmunoassay (RIA) [11]. All postbypass data are expressed in the corrected correlation for hemodilution occurring after CPB to express the effect of hemodilution. The systemic vascular resistance index (SVRI) was also analyzed. The SVRI was calculated as follows:

(1)

SVRI before CPB was analyzed during cardiac catheterization. The temperature after CPB was similar in both groups because the patients in both groups had been rewarmed using the same technique with the same heat exchanger.

2.3. Statistics
Comparisons between the groups over time were performed by a two-way analysis of variance with repeated measurements. The data were further compared by Bonferroni's test if significance was indicated (P<0.05). And a non-paired test was added in all points between the two groups. P values of less than 0.05 were regarded as statistically significant. The bradykinin data was analyzed after the transformation for logarithm because that was extensively distributed. Correlation between the groups was indicated by Pearson's correlation efficient. All values are expressed as the mean ± standard deviation of the mean.


   3. Results
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
4. Comment
 References
 
None of the patients in this study suffered any neurological incidents, myocardial infarction, or other complications due to the blood temperature in CPB.

3.1. SVRI
The pattern of change in SVRI during and after CPB was significantly different between the two groups (P=0.0008). TEP showed significantly lower levels of SVRI after CPB compared with HYP (0 h: 2278±735 vs. 4387±1289, 12 h: 1827±817 vs. 2817±1146 and 24 h: 1690±548 vs. 2761±641 dyne s cm-5 m2, P=0.0001, P=0.03, P=0.0006; Fig. 1) .



View larger version (17K):
[in this window]
[in a new window]
  		Fig. 1. The comparison of systemic vascular resistance index between the tepid and the hypothermic group. The tepid group showed significantly lower levels of systemic vascular resistance index after cardiopulmonary bypass compared to the hypothermic group. Values are mean ± SD. {dagger} P<0.01, TEP vs. HYP.

 
3.2. Nitric oxide
NO levels showed an increase in TEP during and after CPB whereas those in HYP stayed low. The pattern of change in NO during and after CPB was significantly different between the two groups (P=0.02). The TEP NO levels were significantly higher just after, 12 and 24 h after CPB than those for HYP (84.7±33.3 vs. 46.3±18.1, 69.8±31.3 vs. 40.1±17.5 and 80.1±38.5 vs. 39.1±15.6 µmol/l, P=0.008, P=0.03, P=0.01) (Fig. 2) .



View larger version (17K):
[in this window]
[in a new window]
  		Fig. 2. The change in nitric oxide levels before and after cardiopulmonary bypass between the tepid and the hypothermic group; The increase in nitric oxide levels just, 12 and 24 h after cardiopulmonary bypass were significantly higher in the tepid group than those in the hypothermic group. Values are mean ± SD. {dagger} P<0.01, TEP vs. HYP, * P<0.05, TEP vs. HYP.

 
3.3. PGE2
Both groups showed an increase in the serum PGE2 levels just after CPB, which then gradually decreased 12 and 24 h after CPB. There was no significant difference in the pattern of change in PGE2 during and after CPB (P=0.16). Just after CPB, TEP showed a significantly higher serum level of PGE2 than did HYP (37.3±20.0 vs. 15.8±8.6 pg/ml, P=0.02). However, there was no significant difference in PGE2 at 12 and 24 h after CPB (Fig. 3) .



View larger version (15K):
[in this window]
[in a new window]
  		Fig. 3. The change in prostaglandin E2 levels before and after cardiopulmonary bypass between the tepid and the hypothermic group; The increase in prostaglandin E2 levels just after cardiopulmonary bypass was significantly higher in the tepid group than that in hypothermic group. Values are mean ± SD. * P=0.02, TEP vs. HYP.

 
3.4. BK
The TEP serum BK levels remained low both during and after CPB, while the HYP levels increased. There was no significant difference in the pattern of change in BK transformed for logarithm during and after CPB (P=0.78). These levels in TEP were significantly lower just after CPB than those in HYP (2.40±0.32 vs. 1.85±0.21 log10 (pg/ml), P=0.005) (Fig. 4) .



View larger version (14K):
[in this window]
[in a new window]
  		Fig. 4. The change in bradykinin levels before and after cardiopulmonary bypass between the tepid and the hypothermic group; The bradykinin level after cardiopulmonary bypass were significantly higher in the hypothermic group than that in the tepid group. The data was transformed for logarithm. Values are mean ± SD. {dagger} P=0.005, TEP vs. HYP.

 
3.5. PGI2 and TXB2
Both groups showed a significant increase in the serum PGI2 and TXB2 levels just after CPB, which then decreased 12 and 24 h after CPB. There were no significant differences in the patterns of change, and PGI2 and TXB2 levels at any time between the two groups.

3.6. ET-1
The pattern of change in the ET-1 levels was different from that of other vasoactive substances. The ET-1 levels for both groups did not increase just after CPB, but did increase 12 h after CPB and then remained at the same level until 24 h after CPB. There were no significant differences in the pattern of change, and the levels between the two groups.

3.7. Relationship between SVRI and vasoactive substances
There was a significant negative correlation between SVRI and NO during and after CPB (r=-0.60, P<0.0001) (Fig. 5) . This relation was also confirmed in these groups of TEP and HYP, respectively, (TEP; r=-0.71, P<0.0001, HYP; r=-0.67, P=0.0002). In addition, no significant correlation was observed between SVRI and other vasoactive substances.



View larger version (20K):
[in this window]
[in a new window]
  		Fig. 5. The correlation between systemic vascular resistance index and serum nitric oxide levels during and after cardiopulmonary bypass. There was a significant negative correlation between systemic vascular resistance index and serum nitric oxide levels during and after cardiopulmonary bypass (r=-0.674, P<0.001).

 

   4. Comment
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Comment
References
 
In the present study, the serum levels in nitrate and nitrite were significantly higher in the tepid group than in the moderate hypothermic group. Regarding the relationship between the vasodilative factors and vasomotor tones, only nitrate and nitrite showed a significant negative correlation. These results demonstrated that nitrate and nitrite increased both during and after CPB and correlated with the systemic vascular resistance in both tepid and hypothermic CPB. Especially, the production of NO was enhanced by tepid blood temperature resulting in higher blood level and the decrease of systemic vascular resistance. Therefore, these results indicate that NO plays a role in the regulation of temperature dependent systemic vasodilatation in CPB.

It is still controversial as to whether or not a lower systemic vascular resistance is beneficial for whole organs and tissues after the weaning from CPB. The inflammatory reactions induced by CPB are related to the post-CPB organ impairment such as respiratory dysfunction, which has been reported in post perfusion syndrome [12,13]. These reactions cause interstitial edema, insufficiency in organ microcirculation due to an increase in protease activity and free radical production derived partly from granulocytes, [14] and decreased endogenous NO production [15,16]. The results of the present study showed that tepid temperature showed higher levels of the NO production resulting in lower vascular resistance. These results coincide with our previous study comparing tepid and hypothermic CPB which showed lower levels in serum interleukin-8 and neutrophil elastase suggesting the attenuation of the post perfusion syndrome to be more advantageous in tepid CPB [17]. Thus, it is speculated that the increase in serum NO production may be advantageous for the hemodynamic state to decrease afterload of the heart. On the other hand, there were some reports concerning no increase in NO production during and after CPB [8], and no association between low SVR and NO production [9]. Blood temperature of CPB was moderate hypothermia in their study. Therefore, these results almost coincided with our data. Namely, NO production doesn't increase under hypothermic perfusion. The blood temperature of CPB is considered to be an important factor which determine of NO production.

Nitric oxide is one of the most potent vasodilators which relaxes smooth muscle cells in the medial layer in the arterial wall [5] to maintain the homeostasis of the vasculature. Nitric oxide synthesized from endothelial constitutive NO synthase (ecNOS) is known to play a role in the regulation of both cell function and cell to cell communication, including the inhibition of platelet aggregation and adhesion to the subendothelial extracellular matrix, as well as neutrophil adhesion to endothelial cells [18]. In this study, the serum nitrate and nitrite levels after CPB in the tepid group were elevated about two times above the pre-CPB levels. Such level of NO appears to be too low to be induced by iNOS [19], because NO from iNOS is tremendous higher levels compared to our data. Regarding the higher level of NO from the beginning of CPB, ecNOS appears to be a major source during the early phase of CPB because of the prompt increase of NO. However, several inflammatory factors induced by CPB might stimulate the expression of iNOS [19]. Moreover, several blood cells and or macrophages might also be a candidate as an origin of NO production. On the other hand, little injury of endothelial cells under tepid-thermic perfusion may result an increase of NO production, and several vasoconstrictors may also affect this phenomenon. Therefore, a complicated mechanism may be included in the pathogenesis of NO synthesis and regulation of vasomotor tone in CPB. Further investigation is thus required to clarify the regulating mechanism in vascular resistance, the relationship between arterial, and venous NO levels and the cNOS and/or iNOS activities in the serum and tissues.

Nitric oxide, Prostaglandin E2, prostacyclin and bradykinin are the major intrinsic vasodilators introduced during CPB [20] and these mediators might be candidates as factors causing low systemic vascular resistance. In this study, lower systemic vascular resistance under tepid temperature was associated with the difference in NO but not with those in bradykinin, prostaglandin E2 or prostacyclin. Bradykinin is released from bradykininogen by kallikrein, and disappears for the most part in a single passage through pulmonary circulation [21]. In addition, the change in bradykinin did not coincide with SVRI either during or after CPB in the present study. The higher bradykinin level after CPB in the hypothermic group is likely to be caused by the elevation of bradykinin as a reaction against vasoconstrictor elevation and/or as a self-protective process, which has been reported as an intrinsic ischemic-preconditioning factor [22]. Bradykinin is also reported to stimulate the release of NO by endothelium [23]. The serum bradykinin levels in the hypothermic group were higher than those in the tepid group. These data may suggest that serum bradykinin may be related to the decrease of the serum NO levels under hypothermic conditions. On the other hand, PGE2 is synthesized and released by neutrophils trapped in the lung or damaged by CPB circuits, and metabolized in the pulmonary vasculature [24,25]. PGE2 may contribute to systemic vascular resistance during CPB. However, there was no significant correlation between PGE2 and SVRI in the present study, and this finding suggests that the effectiveness of PGE2 for SVR may be relatively lower than that of NO. On the other hand, the pattern of change in the ET-1 was different from that of other vasoactive substance. ET-1 is thought not to be under temperature dependent regulation, and there is no significant correlation between ET-1 and NO levels. Further investigation is required to clarify the role of endothlin-1 in CPB.

In conclusion, the above findings demonstrated that serum nitric oxide levels in tepid cardiopulmonary bypass were significantly higher than those in moderate hypothermic cardiopulmonary bypass, and nitric oxide correlated with systemic vascular resistance. Thus, nitric oxide may play a pivotal role in a temperature dependent regulation of systemic vascular resistance in cardiopulmonary bypass.


   References
Top
 Abstract
 1. Introduction
 2. Patients and methods
 3. Results
 4. Comment
 References
 

  1. Tonz M., Mihaljevic T., von Segesser L.K., Schmid-E R., Joller-Jemelka H.I., Pei P., Turina M.I. Normothermia versus hypothermia during cardiopulmonary bypass: a randomized, controlled trial. Ann Thorac Surg 1995;9:137-143.
  2. Christakis G.T., Fremes S.E., Koch J.P., Harwood S., Juhasz S., Sharpe E., Deemar K.A., Hamilton C., Chen C., Rao V. Determinants of low systemic vascular resistance during cardiopulmonary bypass. Ann Thorac Surg 1994;58:1040-1049.[Abstract]
  3. Menasche P., Haydar S., Peynet J., Du Buit C., Merval R., Bloch G., Piwnica A., Tedgui A. A potential mechanism of vasodilatation after warm heart surgery. The temperature dependent release of cytokines. J Thorac Cardiovasc Surg 1994;07:293-299.
  4. Gordon R.J., Ravin M., Rawitscher R.E., Diacoff G.R. Changes in arterial pressure, viscosity and resistance during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1975;9:552-561.
  5. Moncada S., Radomski M.W., Palmer R.M. Endothelium-derived relaxing factor. Identification as nitric oxide and role in the control of vascular tone and platelet function. Biochem Pharmacol 1988;7:2495-2501.
  6. Ruvolo G., Speziale S., Greco E., Tritapepe L., Mollace V., Nistico G., Marino B. Nitric oxide during hypothermic versus normothermic cardiopulmonary bypass. Eur J Cardio-thorac Surg 1995:651-654.
  7. Mathie R.T., Ohri S.K., Keogh B.E., Williams J., Shiney L., Griffth T.M. Nitric oxide activity in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996;12:1394-1395.
  8. Brett S.J., Quinlan G.J., Mitchell J., Pepper J.R., Evans T.W. Production of nitric oxide suring surgery involving cardiopulmonary bypass. Crit Care Med 1998;6:272-278.
  9. Myles P.S., Leong C.K., Curry J. Endogenous nitric oxide and low systemic vascular resistance after cardiopulmonary bypass. J Cardio-thorac Vasc Anesth 1997;1:571-574.
  10. Green L.C., Wagner D.A., Glogowski J., Skipper P.L., Wishnok J.S., Tannernbaum S.R. Analysis of nitrate, nitrite, and 15 N nitrate in biological fluids. Anal Biochem 1982;26:131-138.
  11. Kohno M., Yasunari K., Murakawa K., Yokokawa K., Horio T., Fukui T., Takeda T. Plasma immunoreactive endothelin in essential hypertension. Am J Med 1990;8:614-618.
  12. Westaby S. Organ dysfunction after cardiopulmonary bypass. A systemic inflammatory reaction initiated by the extracorporeal circuit. Intensive Care Med 1987;3:89-95.
  13. Hashimoto K., Miyamoto H., Suzuki K., Horikoshi S., Matsui M., Arai T., Kurosawa H. Evidence of organ damage after cardiopulmonary bypass. The role of elastase and vasoactive mediators. J Thorac Cardiovasc Surg 1992;04:666-673.
  14. Royston D., Fleming J.S., Desai J.B., Westaby S., Tayler K.M. Increased production of peroxidation products associated with cardiac operations. J Thorac Cardiovasc Surg 1986;1:759-766.
  15. Wehberg K.E., Foster A.H., Wise R.M., McLaughlin J.S., Brunner M.J. Nitric oxide mediates fluid accumulation during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1996;12:168-174.
  16. Fukuda H., Sawa Y., Kadoba K., Taniguchi K., Shimazaki Y., Matsuda H. Supplement of nitric oxide attenuates neutrophil-mediated reperfusion injury. Circulation 1995;2(2):413-416.
  17. Ohata T., Sawa Y., Kadoba K., Masai T., Ichikawa H., Matsuda H. The effect of cardiopulmonary bypass under tepid temperature on inflammatory reactions. Ann Thorac Surg 1997;4:124-128.
  18. Provost P., Lam J.Y., Lacoste L., Merhi Y., Waters D. Endothelium-derived nitric oxide attenuates neutrophil adhesion to endothelium under arterial flow conditions. Atheroscler Thromb 1994;4:331-335.
  19. Pinsky D.J., Cai B., Yang X., Rodriguez C., Sciacca R.R., Cannon P.J. The lethal effects of cytokine-induced nitric oxide on cardiac myocytes are blocked by nitric oxide synthase antagonism or transforming growth factor beta. J Clin Invest 1995;5:677-685.
  20. Downing S.W., Edmonds H., Jr Release of vasoactive substances during cardiopulmonary bypass. Ann Thorac Surg 1992;4:1236-1243.
  21. Pang L.M., Stalcup S.A., Lipset J.S., Hayes C.J., Bowman F.O., Jr, Mellins R.B. Increased circulating bradykinin during hypothermia and cardiopulmonary bypass in children. Circulation 1970:1503-1507.
  22. Goto M., Liu Y., Yang X.M., Ardell J.L., Cohen M.V., Downey J.M. Role of bradykinin in protection of ischemic preconditioning in rabbit hearts. Circ Res 1995;7:611-621.
  23. Palmer R.M., Rees D.D., Ashton D.S., Moncada S.L. Arginine is the physiological precursor for the formation of nitric oxide in the endothelium-dependent relaxation. Biochem Biophys Res Commun 1989;53:1251-1256.
  24. Faymonville M.E., Deby G., Larbisson R., Deby C., Bodson L., Limet R., Lamy M. Prostaglandin E2, prostacyclin and thromboxane changes during nonpulsatile cardiopulmonary bypass in humans. J Thorac Cardiovasc Surg 1986;1:858-866.
  25. Lavee J., Naveh N., Dinber I., Shinfeld A., Goor D.A. Prostacyclin and prostaglandin E2 mediate reduction of increased mean arterial pressure during cardiopulmonary bypass by aspiration of shed pulmonary venous blood. J Thorac Cardiovasc Surg 1990;00:546-551.




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Hikaru Matsuda
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ohata, T.
Right arrow Articles by Matsuda, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohata, T.
Right arrow Articles by Matsuda, H.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS