Hydration and electrolyte balance in horses during an endurance season.

REASONS FOR PERFORMING STUDY: Limited information exists about the physiological training-induced changes in electrolyte balance of horses competing in long distance endurance races. OBJECTIVES: To determine the effects of endurance training and racing on hydration and electrolyte balance in horses. METHODS: Blood and urine were sampled at rest in 8 endurance horses before training and after two 11 week training periods (T1 and T2). Each training was followed by a 120 km endurance ride and horses were sampled before, during and 2 h after the rides. Blood was analysed for packed cell volume (PCV), total protein (TP), urea, creatinine and electrolyte concentrations. Urine was analysed for pH, specific gravity, creatinine and electrolyte concentrations, which allowed calculation of fractional excretion of electrolytes (FE). Changes associated with training and with the rides were assessed using a Student paired t test (P ≤ 0.05). RESULTS: Plasma TP, urea, creatinine and sodium concentrations increased during T1 and PCV decreased significantly during T2. FE(Cl) increased during T1 then decreased. FE(K) increased significantly during both training periods. Other blood and urine parameters did not show remarkable changes with training. PCV, plasma TP, urea, creatinine and total Ca concentrations increased and plasma Na(+) and Cl(-) concentrations decreased during both rides. Urine concentrations of Na(+), K(+) and Cl(-), FE(Na) and FE(Cl) decreased during the rides while urinary creatinine increased. FE(K) increased during the first part of the rides then decreased. CONCLUSIONS: These data contribute to the understanding of changes associated with training and prolonged endurance exercise.

Effect of a 120 km endurance race on plasma and muscular neutrophil elastase and myeloperoxidase concentrations in horses.

REASONS FOR PERFORMING STUDY: Intense physical exercise can induce the degranulation of neutrophils leading to an increase in plasma concentration of the neutrophil marker enzymes myeloperoxidase (MPO) and elastase (ELT). These enzymes have pro-oxidative and pro-inflammatory properties and may play a role in the exercised-induced muscular damage. OBJECTIVES: To measure MPO and ELT concentrations in plasma and muscles of endurance horses and to correlate them to the extent of exercise-induced muscular damage. METHODS: Seven endurance horses qualified on 120 km races were tested in this study. Neutrophil count, serum creatine kinase (CK), plasmatic and muscular MPO and ELT concentrations were measured before and 2 h after a 120 km endurance race. RESULTS: The race produced a significant increase of neutrophils, CK, and plasma MPO and ELT levels. A significant correlation was observed between the MPO and ELT values in plasma (r(2) = 0.92, P < 0.01) and in muscles (r(2) = 0.89, P < 0.01) while plasmatic concentrations of MPO and ELT were not significantly correlated to muscular ones. An increase of mean concentrations (± s.e.) of MPO (T0: 9.85 ± 3.9, T1: 228.9 ± 95.9 ng/mg proteins) and ELT (T0: 8.4 ± 2.4, T1: 74.5 ± 39.7 ng/mg proteins) in the muscles were observed after the race. Interestingly, the individual data showed large differences between the horses. Muscular MPO and ELT concentrations were significantly correlated to plasma CK levels. The coefficient of correlation (r(2)) was 0.69 (P < 0.01) for MPO and 0.66 (P < 0.01) for ELT, respectively. CONCLUSIONS: Results underline the possible role of MPO and ELT in exercise-induced muscular damage. POTENTIAL RELEVANCE: Further studies should investigate the effect of exercise type and intensity, as well as the role of the training state on MPO and ELT involvement in muscular damage. The assessment of the intensity of exercise-induced neutrophilic degranulation may have a potential role in the monitoring of the athletic career.

Use of the recovery check in long-distance endurance rides.

In an attempt to reduce morbidity, an additional veterinary examination is performed at the end of the hold time--the Recovery Check (RC)--of the last vet gate of all long distance endurance rides held in France. At the RC, a normal FEI-type inspection is performed combined with a cardiac recovery index (CRI): the heart rate is taken before (HR0) and 1 min after (HR1) the horse trotted for 30 m out and back. Results from 12 (130 and 160 km long) rides and based on 489 horses were analysed. Of all RC performed, 10.4% lead to elimination of the horses and lameness was the most frequent reason (45%). Among horses allowed to continue in the ride, elimination rate was significantly higher in horses with HR0 > or = 60/min compared to horses with HR0 < 60. High CRI (HR1-HR0 > or = 4) lead to greater disqualification rates only when HR0 was more than 60/min. RC appears to be useful in the assessment of a horse's fitness. However, standardisation of the examination is necessary in order to optimise its use.

Haemodynamic response to dynamic exercise after heart-lung transplantation.

The purpose of this study was to investigate the haemodynamic response to dynamic exercise after heart-lung transplantation (HLT). Nine stable HLT recipients (6 males) were studied 12-55 months after transplantation. While sitting on a cycle ergometer, they first underwent a maximal symptom-limited exercise test (power increment was 10 W x min(-1)) to determine the maximal tolerable workload. On the next day, they performed a second exercise test at 0, 40, 60 and 80% of their predetermined maximal workload (mean+/-sD: 108+/-20 W). Stage duration was 6 min. Respiratory, gas exchange, and haemodynamic measurements were performed at rest, during the last minute of each stage, and after recovery. Haemodynamic variables at rest were within normal limits except heart rate (HR) which was greater and stroke volume index (SVI) which was lower than normal. Peak oxygen consumption was 61+/-8% of predicted. HR showed an initial slow increase followed by a steeper rise, and a delayed return to baseline during the recovery period. SVI and cardiac index (CI) increased at the onset of exercise but did not change significantly at 40-80% of the maximal workload. Pulmonary capillary wedge pressure increased from 4+/-2 mmHg at rest to 14+/-3 mmHg at maximal exercise. It is concluded that during dynamic exercise, heart-lung transplantation recipients demonstrate a chronotropic incompetence, a reduced increase in cardiac index and stroke volume index, and an excessive rise in left ventricular filling pressures. These alterations may contribute to the persistent exercise limitation.

Absence of L-arginine effect on coronary hypersensitivity to serotonin in cardiac transplant recipients.

Coronary hypersensitivity to serotonin promotes platelet aggregation and, therefore, the progression of the atherosclerotic process. This abnormality occurs in the early stages of coronary atherosclerosis when the responses to bradykinin are still preserved. To determine whether such changes also occur early after cardiac transplantation, intracoronary injections of bradykinin and serotonin were performed in 7 control patients, in 19 patients with dyslipidemia, and in 15 cardiac transplant recipients (1 year after operation). Coronary angiography was normal in the 3 groups. In the segments where serotonin effects were the most pronounced, the diameter changes were measured by quantitative angiography. Bradykinin (60, 200, and 600 ng) increased in the same way as the coronary diameters in the 3 groups; in contrast, serotonin elicited vasodilation only in the control group (7+/-3%, percentage of baseline) and vasoconstriction in the hyperlipidemic group (-9+/-2%) and in transplant recipients (-15+/-3%). After intracoronary infusion of L-arginine (40 mg/min for 14 minutes), serotonin-induced constriction was attenuated in the hyperlipidemic group but not in transplant recipients. Thus, the response to bradykinin is preserved in the early stages of graft vasculopathy. However, in contrast to patients with hyperlipidemia, the absence of an L-arginine effect on the responses to serotonin suggests the involvement of mechanisms other than a decrease in endothelium-derived nitric oxide availability. Immune processes promoting the release of endothelium-derived contracting factors such as endothelin and/or superoxide anion may play a role.

Heparin-coated circuits reduce myocardial injury in heart or heart-lung transplantation: a prospective, randomized study.

BACKGROUND: The effects of heparin-coated (HC) circuits have been primarily investigated in routine cardiac operations with limited duration of cardiopulmonary bypass (CPB) and ischemia. Their benefits have not been conclusively proven but could be more significant when CPB and ischemic times are longer, such as during heart transplantation (HTx) or heart-lung transplantation (HLTx). METHODS: In a 22-month period, 29 patients undergoing HTx and HLTx were randomly divided into two groups using HC (Duraflo II, n = 14, 10 HTx and 4 HLTx) or uncoated but identical circuits (NHC group, n = 15, 10 HTx and 5 HLTx). All patients received full systemic heparinization (3 mg/kg) during CPB. Plasma endotoxin, interleukin (IL)-6, IL-8, IL-10, IL-12, and cardiac troponin-I were measured before heparin administration, immediately after aortic cross-clamping, 5, 30, 60, 90, 120 minutes, and 12 and 24 hours after aortic declamping. The intensive care unit (ICU) staff and the laboratory technologists were blinded as to the use of HC circuits. RESULTS: No statistically significant differences between groups were found with respect to all baseline values, duration of CPB and aortic cross-clamping, graft ischemic time, doses of heparin, postoperative blood loss and transfusion, peak lactate and creatine kinase-MB isoenzyme values, duration of mechanical ventilation, or length of ICU stay. One patient in each group died during the hospital stay. Patients in the HC group needed more protamine sulfate after CPB. Although endotoxin levels were similar in the two groups, significantly lower IL-6, IL-8, and IL-10 levels were observed 1 hour after aortic declamping in the HC group. The release of cardiac troponin-I was also significantly reduced in the HC group 12 and 24 hours after reperfusion. CONCLUSIONS: The use of HC circuit limits both pro- and anti-inflammatory responses to CPB. It may also reduce myocardial injury after prolonged duration of CPB and ischemia.

Can cardioplegia management influence cytokine responses during clinical cardiopulmonary bypass?

BACKGROUND: Cytokines play an important role in the inflammatory response associated with cardiopulmonary bypass (CPB) and may contribute to postoperative complications. Although it has been shown that the production of tumor necrosis factor a (TNF-a) and interleukin (IL)-6 were higher following normothermic CPB than hypothermic CPB, whether different cardioplegic management could influence the release of cytokines remains unknown. METHODS: We compared the blood concentrations of four cytokines (TNF-a, IL-6, IL-8, and IL-10) in two groups of patients undergoing complete revascularization with CPB in the same study period. Seventeen patients received cold crystalloid cardioplegia at a Belgian center (group-CC), while 21 patients received warm blood cardioplegia at a center in Hong Kong (group-WB). Blood samples were collected before and after surgery in each patient. RESULTS: There were no differences between the 2 groups in terms of age, sex ratio, number of grafts, duration of CPB and aortic crossclamping. All patients survived their hospital stay. The levels of TNF-a, IL-6 and IL-8 after surgery were higher in group-CC than in group-WB. However, IL-10 levels were significantly lower at the end of surgery in group-CC than in group-WB. CONCLUSIONS: Our data suggest that the use of warm blood cardioplegia, rather than cold crystalloid cardioplegia, may reduce the inflammatory response to CPB. This observation warrants future randomized investigation to determine its clinical relevance.

Does steroid pretreatment increase endotoxin release during clinical cardiopulmonary bypass?

OBJECTIVE: The mechanism involved in the endotoxemia frequently recognized during cardiopulmonary bypass remains unclear. It has also been suggested that endotoxin levels were higher in steroid-pretreated patients undergoing cardiopulmonary bypass. METHODS: Twenty patients undergoing cardiopulmonary bypass were randomly pretreated with steroids (methylprednisolone, 30 mg/kg) or placebo. Blood samples for endotoxin measurement were drawn simultaneously from the superior and inferior venae cavae before heparin administration, 5 and 50 minutes after the onset of bypass, 5 minutes after aortic declamping, at the end of bypass, and 1, 2, and 20 hours after the end of cardiopulmonary bypass. RESULTS: The perioperative variables in the two groups were similar. Blood endotoxin levels were higher in the inferior vena cava than in the superior vena cava immediately after the onset of bypass. Endotoxin levels in inferior vena cava blood were significantly lower in steroid-pretreated patients than those in patients not receiving steroids. CONCLUSIONS: Endotoxin is released during cardiopulmonary bypass from the region drained by the inferior vena cava. Steroid pretreatment may actually reduce endotoxin release during bypass.

Endothelial function of internal mammary artery in patients with coronary artery disease and in cardiac transplant recipients.

The objective of this study was to examine the endothelial function of internal mammary artery in patients with coronary artery disease and in heart transplant recipients. Therefore the response of this artery to increasing concentrations of acetylcholine (1, 10, 20 microg/min for 2.5 minutes each) was assessed in 6 patients in a control group, 16 patients with coronary artery disease (CAD group) matched for risk factors with 16 heart graft recipients (who underwent transplantation for nonischemic heart failure), and 12 patients with coronary artery disease and peripheral vascular disease (PVD group). Diameters of proximal and middle segments of internal mammary artery were measured by quantitative angiography. The responses to the first concentration of acetylcholine were attenuated in these three groups compared with the control group. At the highest concentration of acetylcholine the diameter increase was similar in the control and CAD groups, whereas the responses remained significantly impaired in the transplant and PVD groups. However, after selective infusion of L-arginine (30 mg/min for 11 minutes), the precursor of endothelium-derived nitric oxide, was performed, the responses to acetylcholine were restored in these two latter groups. Endothelin plasma levels were significantly enhanced in the PVD group, which exhibited the most severe impairment in acetylcholine-induced vasodilation. Thus some patients with CAD, mainly those with advanced atherosclerosis, and cardiac transplant recipients exhibit internal mammary artery endothelial dysfunction, and this abnormality seems reversible.

Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies.

BACKGROUND: Recent study of the inflammatory reactions occurring during and after cardiopulmonary bypass (CPB) has improved our understanding of the involvement of the inflammatory cascade in perioperative injury. However, the exact mechanisms of this complex response remain to be fully determined. METHODS: Literature on the inflammatory response to CPB was reviewed to define current knowledge on the possible pathways and mediators involved, and to discuss recent developments of therapeutic interventions aimed at attenuating the inflammatory response to CPB. RESULTS: CPB has been shown to induce complement activation, endotoxin release, leukocyte activation, the expression of adhesion molecules, and the release of many inflammatory mediators including oxygen-free radicals, arachidonic acid metabolites, cytokines, platelet-activating factor, nitric oxide, and endothelins. Therapies aimed at interfering with the inflammatory response include the administration of pharmacologic agents such as corticosteroids, aprotinin, and antioxidants, as well as modification of techniques and equipment by the use of heparin-coated CPB circuits, intraoperative leukocyte depletion, and ultrafiltration. CONCLUSIONS: Improved understanding of the inflammatory reactions to CPB can lead to improved patient outcome by enabling the development of novel therapies aimed at limiting this response.

Thrombus formation on a calcific and severely stenotic bicuspid aortic valve.

We report on a case of thrombus formation on a native bicuspid aortic valve, which was found during an elective operation for aortic valve replacement. Although no apparent predisposing cause of thrombosis could be ascertained, severe calcific stenosis of the bicuspid valve and cardiac catheterization may have played a role. The patient is in excellent condition 9 months after the operation.

Hepatic release of interleukin-10 during cardiopulmonary bypass in steroid-pretreated patients.

With its antiinflammatory properties, interleukin (IL)-10 may play an important role in limiting complications associated with cardiopulmonary bypass (CPB). We previously demonstrated that pretreatment with steroids can significantly increase IL-10 production during CPB, but neither the heart nor the lung was found to be its main source. To define whether the liver is the source of IL-10, hepatic venous cannulation was performed in 12 patients undergoing CPB. Each patient received 30 mg/kg of methylprednisolone before operation. Plasma levels of IL-10 were simultaneously measured in peripheral arterial blood and hepatic venous blood before heparin administration, before aortic cross-clamping, and 5, 30, 60, 90, and 120 minutes after aortic declamping. The duration of CPB and aortic cross-clamping was 113 +/- 7 minutes and 75 +/- 6 minutes (mean +/- SEM), respectively. IL-10 levels 30 minutes after declamping were significantly higher in hepatic venous blood than in arterial blood (1187 +/- 573 pg/ml vs 911 +/- 405 pg/ml, p < 0.01 by Wilcoxon's signed-rank test). To determine whether steroids can also induce the release of another antiinflammatory cytokine, IL-4, plasma IL-4 levels were measured simultaneously. IL-4 was detected in the arterial blood of only 4 of the 12 patients, transiently after aortic declamping. IL-4 was not detected in hepatic venous blood. In conclusion, the liver is a major source of IL-10 during CPB. However, steroid-treated patients do not show an increase in IL-4, and the liver is not the source of IL-4 during and after CPB.

Cytokine responses to cardiopulmonary bypass: lessons learned from cardiac transplantation.

BACKGROUND: A growing body of evidence relates the release during cardiopulmonary bypass (CPB) of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, to the postoperative systemic inflammatory response syndrome. Antiinflammatory cytokines, such as IL-10, however, may also play an important role in limiting these complications. METHODS: The English-language literature was reviewed. Emphasis was placed on cytokine responses during clinical CPB for cardiac operations and, in particular, for heart and heart-lung transplantation. RESULTS: The recent data indicate that (1) although cytokine release can be triggered by many factors during CPB, ischemia-reperfusion may play the most important role; (2) the levels of tumor necrosis factor-alpha, IL-6, and IL-8 are correlated with the duration of cardiac ischemia and the myocardium is a major source of these three cytokines during CPB; (3) IL-10 levels are correlated with the duration of CPB and the liver is a major source of IL-10 during CPB; and (4) steroid pretreatment is an effective intervention to inhibit the release of proinflammatory cytokines and enhance IL-10 production. CONCLUSIONS: The improved knowledge of cytokine responses to CPB may help to develop interventions aimed at reducing postoperative morbidity and mortality.

Oxygenation improvement with nitric oxide in right-to-left shunt without significant effects on pulmonary arterial pressure.

Following surgical closure of an interventricular communication complicating an anterior myocardial infarction, a 74-year-old woman developed severe right ventricular failure and hypoxemia due to the opening of a patent foramen ovale (PFO). Mean pulmonary artery pressure was 24 mm Hg. Treatment with inhaled nitric oxide (5 ppm) increased PaO2 from 47 to 90 mm Hg (FIo(2)1). The present observation points out that nitric oxide inhalation could be useful in the management of severe hypoxemia from a right-to-left shunt due to a PFO even when there is no significant pulmonary hypertension present.

Myocardium is a major source of proinflammatory cytokines in patients undergoing cardiopulmonary bypass.

Proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-6, and interleukin-8, and anti unflammatory cytokines, such as interleukin-10, may play an important role in patient responses to cardiopulmonary bypass. We sought to define whether the myocardium and the lungs serve as important sources of these cytokines under conditions of cardiopulmonary bypass. Ten patients (age 64 +/- 3 years, mean +/- standard error of the mean) undergoing elective coronary artery bypass grafting were monitored with an arterial catheter, a coronary sinus catheter, and pulmonary artery catheter. Plasma levels of tumor necrosis factor-alpha, interleukin-6, interleukin-8, and interleukin-10 were measured simultaneously in peripheral arterial blood, coronary sinus blood, and mixed venous blood before heparin administration, 1 minute before aortic crossclamping, 5 minutes after aortic declamping, and at 0.5, 1, 1.5 and 2 hours after aortic declamping. The durations of cardiopulmonary bypass and aortic crossclamping were 114 +/- 9 and 64 +/- 5 minutes, respectively. Levels of tumor necrosis factor-alpha and interleukin-6 were significantly higher in coronary sinus blood than in arterial blood after aortic declamping. Tumor necrosis factor-alpha and interleukin-6 levels were also higher in mixed venous blood than in arterial blood within 1 hour after declamping. There were no significant differences among the three sampling sites with respect to interleukin-8 and interleukin-10 levels. In one patient who had postoperative myocardial infarction, however, interleukin-8 levels were three times as high as in coronary sinus blood than in arterial blood. These data indicate that the myocardium is a major source of tumor necrosis factor-alpha and interleukin-6 in patients undergoing cardiopulmonary bypass. The lungs may consume rather than release proinflammatory cytokines in the early phase of reperfusion. The source under these conditions of the antünflammatory cytokine interleukin-10 remains to be determined.

Cardiac tamponade due to spontaneous rupture of right coronary artery aneurysm.

A case of acute cardiac tamponade caused by spontaneous rupture of a right coronary artery aneurysm is reported. The aneurysm, which was present distally, was ligated during operation. Postoperative angiography suggested the aneurysm was congenital. The patient is doing well 5 months after operation.

Human cytokine responses to cardiac transplantation and coronary artery bypass grafting.

Cardiac surgery with cardiopulmonary bypass triggers an inflammatory response involving proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin-6, and interleukin-8. To elucidate the pathophysiology of this cytokine response, we explored the possible differences in cytokine responses between patients undergoing heart transplantation and those undergoing coronary artery bypass grafting. Plasma levels of tumor necrosis factor-alpha, interleukin-6, interleukin-8, and interleukin-10 were measured in eight patients undergoing heart transplantation (mean age 44 years) and eight patients undergoing coronary artery bypass grafting (mean age 61 years). Duration of cardiopulmonary bypass and ischemic time were both longer in the heart transplantation group than in the coronary artery bypass grafting group (133 +/- 26 min vs 100 +/- 31 min, p < 0.05, and 130 +/- 47 min vs 58 +/- 21 min, p < 0.005, respectively). Samples were collected before heparin administration, at aortic crossclamping and declamping, and at 0.5, 1, 1.5, 2, 4, 12, and 24 hours after declamping. Tumor necrosis factor-alpha levels were significantly higher 30 minutes after aortic declamping in the heart transplantation group than in the coronary artery bypass grafting group (68 +/- 30 vs 18 +/- 5 pg/ml, p < 0.05). Interleukin-6 and interleukin-8 levels were also significantly higher 90 minutes after declamping in patients undergoing heart transplantation than in those undergoing coronary artery bypass grafting (310 +/- 63 vs 169 +/- 24 pg/ml, p < 0.05, and 73 +/- 17 vs 24 +/- 5 pg/ml, p < 0.01, respectively). Furthermore, interleukin-6 and interleukin-8 values 90 minutes after declamping were significantly correlated with the ischemic time (r = 0.72 and r = 0.82, respectively, both p < 0.05). Interleukin-10 levels in both groups rose to reach a peak value of around 115 pg/ml 1 hour after declamping. Patients undergoing heart transplantation exhibited a second peak of tumor necrosis factor-alpha, interleukin-8, and interleukin-10 levels 12 hours after declamping, probably related to the administration of rabbit antihuman thymocyte immunoglobulin (Thymoglobuline) 3 hours after declamping. Interleukin-6 levels decreased more significantly 12 and 24 hours after declamping in patients undergoing heart transplantation, probably related to methylprednisolone therapy. In conclusion, cardiopulmonary bypass is associated with the production of both proinflammatory and antiinflammatory cytokines. The production of proinflammatory cytokines in patients undergoing heart transplantation is higher than that in patients undergoing coronary artery bypass grafting, and this increase could be related to the longer duration of ischemia in the former group. The later course of cytokine levels after heart transplantation may be further influenced by immunosuppressive therapy.

Steroid administration in heart and heart-lung transplantation: is the timing adequate?

BACKGROUND: The release of cytokines after cardiopulmonary bypass may play an important role in postoperative morbidity. The release of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin (IL)-6 and IL-8, is even greater in patients undergoing heart transplantation (HTx) than coronary artery grafting. We tested the hypothesis that in HTx patients the earlier administration of steroids, before rather than after cardiopulmonary bypass as usual, can reduce the inflammatory response. METHODS: In 20 consecutive patients who underwent HTx or heart-lung transplantation (HLTx), plasma levels of tumor necrosis factor alpha, IL-6, IL-8, and anti-inflammatory cytokine IL-10 were measured before heparin administration, at aortic cross-clamping and declamping, and 0.5, 1, 1.5, 2, 4, 12, and 24 hours after aortic declamping. In 10 patients (group I, 6 HTx and 4 HLTx), 500 mg of methylprednisolone was first given as usual at 1.5 hours after aortic declamping (at the end of cardiopulmonary bypass). In the next 10 patients (group II, 6 HTx and 4 HLTx), the first doses of methylprednisolone were given 1 hour before operation. In both groups, 125 mg of methylprednisolone were given every 8 hours thereafter during the first postoperative day. RESULTS: The ischemic time and cardiopulmonary bypass time were similar in the two groups (166 +/- 16 minutes versus 157 +/- 13 minutes, and 192 +/- 21 minutes versus 186 +/- 20 minutes, respectively, mean +/- standard error of the mean). At 30 minutes after aortic declamping and throughout the next 4 hours, tumor necrosis factor alpha levels were significantly lower in group II than in group I (all p < 0.03). Interleukin-8 values 1 hour after declamping were also lower in group II than in group I (49 +/- 15 pg/mL versus 130 +/- 38 pg/mL, p < 0.02). Interleukin-10 levels were significantly higher in group II than in group I from 30 minutes after declamping through 2 hours after (all p < 0.03). Interleukin-6 levels were similar in the two groups. CONCLUSIONS: Earlier steroid administration in the immunosuppressive protocol for HTx or HLTx may be preferable to reduce the inflammatory response to cardiopulmonary bypass, as reflected by a lower production of tumor necrosis factor alpha and IL-8, and a greater release of IL-10.

Determinants of right ventricular failure after heart transplantation.

Predictive factors of right ventricular failure after heart transplantation are not well identified. Clinical and hemodynamic data from 20 patients who developed right heart failure were compared to those of 20 matched patients who did not experience this complication after cardiac transplantation. Preoperative systemic and pulmonary hemodynamics were comparable in the two groups. Patients with posttransplant right ventricular failure had longer waiting time (27 +/- 6 vs 16 +/- 3 weeks, mean +/- SE, P < 0.05), no regression of pulmonary hypertension (0 +/- 0.1 vs 2.3 +/- 0.3 Wood units reduction in pulmonary vascular resistance after transplantation, P < 0.01), and had been ventilated with higher levels of positive end-expiratory pressure (5 +/- 1 vs 1.5 +/- 0.5 cm H2O, P < 0.05). One-month postoperative evolution (mortality, hospital stay, radionuclide ejection fractions) was similar in the two groups. These results suggest that a lesser reversibility of pulmonary hypertension (possibly due to a longer evolution of the cardiac disease, as indicated by the longer waiting time) is the main determinant of right ventricular failure after heart transplantation.

Corticosteroids increase blood interleukin-10 levels during cardiopulmonary bypass in men.

BACKGROUND: Interleukin (IL)-10 is a potent antiinflammatory cytokine inhibiting the release of tumor necrosis factor--alpha (TNF-alpha) and IL-8 by activated macrophages and polymorphonuclear leukocytes. Cardiopulmonary bypass (CPB) represents a unique situation where an inflammatory reaction is predictably induced. The present study examined the influence of CPB on the release of TNF-alpha, IL-1 beta, IL-8, and IL-10 and also defined the effects of pretreatment with corticosteroids on the release of these cytokines. METHODS: The study included 22 patients undergoing coronary artery bypass graft operations, including eight control patients and seven patients who received dexamethasone, and seven patients who received methylprednisolone 4 hours before the operation. Cytokines were measured with the enzyme-linked immunosorbent assay technique before treatment, before anesthesia induction, immediately before heparin administration, before aorta declamping, 10 minutes and 90 minutes after aorta declamping, and 4 hours after the end of CPB. RESULTS: In the control patients the TNF-alpha levels and especially the IL-8 levels increased during CPB and reached their maximal levels 4 hours after CPB. IL-10 levels rose moderately and transiently, reaching peak values 90 minutes after aorta declamping. Notably, administration of corticosteroids prevented IL-8 release but increased IL-10 levels, which were tenfold higher than in the control group 90 minutes after aorta declamping (dexamethasone, 271 +/- 128 pg/ml; methylprednisolone, 312 +/- 213 pg/ml; control, 17 +/- 12 pg/ml, p < 0.05). IL-1 beta was not detected in any group of patients. CONCLUSIONS: The present data indicate that IL-10 is released together with proinflammatory cytokines during and after CPB and that pretreatment with corticosteroids markedly enhances this release. The release of IL-10 may play an important role in the antiinflammatory effects of corticosteroids.