Aortic Unclamping Research Articles

Peroxynitrite formation from human myocardium after ischemia-reperfusion during open heart operation

Background. Current experimental studies have demonstrated that peroxynitrite (ONOO −) has both cytotoxic and cytoprotective effects on myocardial ischemia-reperfusion injury. However, even myocardial ONOO − formation has not yet been investigated in humans undergoing open heart operation. We measured plasma nitrotyrosine as an indicator of ONOO − formation during open heart operation and examined its association with myocardial ischemia-reperfusion injury. Methods. Twenty adult patients undergoing mitral valve replacement under cardiopulmonary bypass between 1997 and 1998 were enrolled in this study (6 men and 14 women). Arterial blood (Ao) and coronary sinus effluent (CS) were obtained: (1) before the initiation of cardiopulmonary bypass, (2) just after aortic unclamping, (3) at 5 minutes, (4) at 10 minutes, (5) at 15 minutes, and (6) at 20 minutes after aortic unclamping. Results. At every sampling point after reperfusion, plasma nitrate and nitrite was significantly lower in CS than in Ao, and the percentage ratio of nitrotyrosine to tyrosine (%NO 2-Tyr; an index of ONOO − formation) was significantly higher in CS than in Ao. The CS-Ao difference in %NO 2-Tyr, myocardium-derived ONOO −, reached its peak at 5 minutes after reperfusion (2.17 ± 0.74%), which was significantly correlated with the peak CS-Ao difference in plasma malondialdehyde, and with postoperative maximum creatine kinase-MB. Conclusions. These results first demonstrate that ONOO − is produced from human myocardium after ischemia-reperfusion during open heart operation, and myocardium-derived ONOO − can be determined by the CS-Ao difference in %NO 2-Tyr.

Effects of L-Arginine Cardioplegia on Myocardium

Infusion of L-arginine (a precursor of nitric oxide, NO) in cardioplegia was examined to test its effect on metabolism of myocardium after myocardial ischemia and reperfusion (IR). Twenty-eight patients undergoing valve replacement were involved and randomly divided into two groups: the control group (crystalloid cardioplegia) and the experimental group (crystalloid cardioplegia + L-arginine). Blood samples were taken both before aortic clamping and after aortic unclamping from right radial artery to measure the concentrations of NO2−/NO3−, lactic acid (LA), malondialdehyde (MDA), superoxide dismutase (SOD), and xanthine oxidase (XOD). In the control group, the NO2−/NO3− level decreased at aortic unclamping, and 30 min later, it decreased significantly as compared with that before aortic clamping (p < .05). In the experimental group, it increased at aortic unclamping (p < .05), and 60 min later, increased to the peak. Five, fifteen, and thirty min after aortic unclamping, the concentrations of LA and MDA in the experimental group were lower than those in the control group (p < .05). Thirty and sixty min after aortic unclamping, the concentrations of SOD remained higher in the experimental group than those in the control group (p < .05). There was no difference between groups in the concentrations of XOD. The addition of L-arginine to the cardioplegia can protect the myocardium from injury by releasing nitric oxide.

Postischemic Reperfusion Injury Can Be Attenuated by Oxygen Tension Control

Oxygen-derived free radicals cause cytotoxic damage during reperfusion after a period of ischemia and the production of these free radicals may be proportionate to oxygen tension (PO2). The present study tested the hypothesis that oxidative damage may be limited by maintaining a more physiologic PO2 following ischemia. An experimental study in Wistar rats were mounted on a Langendorff apparatus was conducted to estimate baseline aortic flow (AF), coronary flow (CF), cardiac output (CO), systolic pressure (SP), heart rate (HR), and the rate-pressure product (RPP: HRxSP). The hearts were divided into 3 groups (n=7, hearts/group): group 1, hypoxic (PO2=300+/-50 mmHg) reperfusion; group 2, middleoxic (PO2=500+/-50 mmHg) reperfusion; and group 3, hyperoxic (PO2=700+/-50 mmHg) reperfusion. Following 30 min of warm ischemia, hearts in all groups were reperfused at each oxygen pressure. The recovery of cardiac function of each heart was measured at the end of reperfusion. Concentrations of lactate (LAC), lactate dehydrogenase (LDH), and creatine kinase (CK) in the coronary perfusate during reperfusion were measured. The recovery rate of CO, SP, and RPP in group 2 were all significantly better than in the other 2 groups. CK leakage in group 2 was significantly lower than in group 3. A clinical study was also conducted during elective coronary artery bypass grafts in 16 consecutive patients who underwent either hyperoxic (n=8, PO2=450-550 mmHg) or more physiologic (n=8, PO2=200-250 mmHg) cardiopulmonary bypass after aortic unclamping. The clinical study assessed CK-MB, LDH, LAC, and malondialdehyde (MDA) in patient blood prior to starting the surgical procedure and at 30 min and 3, 9, and 21 h after unclamping. Cardiac index (CI), central venous pressure, pulmonary capillary wedge pressure, systolic arterial pressure, and the dose of cathecholamines were also measured. Although no significant differences were present in the dose of cathecholamines, the CI in the more physiologic oxygen tension group was significantly higher than in the hyperoxic group at 3 and 6 h after unclamping. The levels of MDA in the more physiologic PO2 group was significantly lower at 30 min after aortic unclamping than in the hyperoxic group. The present results suggest that in the experimental as well as in the clinical study, high PO2 leads to myocardial reperfusion damage; however, maintaining a more physiologic PO2 during reperfusion following ischemia may attenuate reperfusion injury.

Cardiac troponin I release after open heart surgery: a marker of myocardial protection?

Background. Unlike creatine kinase MB isoenzyme, cardiac troponin I (cTnI) is a highly specific marker of myocardial injury. Its release has recently been studied after coronary artery bypass grafting operation. However, its significance after open heart surgery (OHS) remains to be determined. This protein release could be a marker of myocardial protection. We sought to study cTnI release after OHS in patients with normal coronary arteries and to compare it with cTnI release in patients after coronary artery bypass graft (CABG) surgery. Methods. Eighty-five patients undergoing OHS and 86 patients undergoing CABG were enrolled in the study. CTnI concentrations were measured in serial venous blood samples drawn before surgery and immediately, 12 hours, 24 hours, 48 hours, and 5 days after aortic unclamping. Results. In the OHS group and in the CABG group without acute myocardial infarction (AMI), cTnI peaked at 12 hours postoperatively (6.35 ± 6.5 and 5.38 ± 8.55 ng/mL, respectively) and normalized on day 5 postoperatively (0.57 ± 2 and 0.72 ± 1.62 ng/mL, respectively). CTnI concentration did not differ significantly between the OHS group and the CABG group in the absence of AMI for any samples considered. In the CABG group, 2 patients had AMI. In the OHS group, cTnI levels at 12 hours postoperatively were found to correlate closely with CPB and aortic cross-clamping (ACC) times, contrary to the CABG group, which correlated only with occurrence of AMI. CTnI release was independent of age and ejection fraction in either group. Conclusions. cTnI release in patients after OHS with normal coronary arteries has the same profile as cTnI release in patients after CABG in the absence of AMI. However, its peak at 12 hours postoperatively is only correlated to ACC and CPB times, which is contrary to cTnI release after CABG surgery. This observation suggests that cTnI could be a marker of myocardial ischemia after OHS.

The effect of leukocyte-depleted blood cardioplegia in patients with severe left ventricular dysfunction: A randomized, double-blind study

Background: The propensity for leukocytes to cause reperfusion injury in patients undergoing heart surgery is widely accepted. Reperfusion injury may result in myocardial damage and unfavorable operative outcome, especially in patients with severely reduced ejection fractions. This study was performed to evaluate the impact of leukocyte filtration on the postoperative course of patients undergoing coronary bypass surgery. Methods: Thirty-two patients with coronary artery disease and left ventricular ejection fraction less than 35% were included in this double-blind, randomized study. Two serial leukocyte removal filters (Pall BC1B filter [Pall Biomedical, Portsmouth, England], group F, 15 patients) or two dummy filters (group C, 17 patients) were connected to the blood cardioplegia line. Leukocyte count, hemodynamic measurement, and transesophageal echocardiography were performed before and after cardiopulmonary bypass. Cardiac-specific enzymes were analyzed from arterial blood during the first 72 hours and from coronary sinus blood 30 and 60 minutes after aortic unclamping. Results: Patient characteristics were similar in the two groups (ejection fraction 20.9% ± 4.3% in group C and 21.1% ± 4.8% in group F; P = .773). No early death or perioperative myocardial infarction occurred. Leukocyte count, hemodynamic parameters, cardiac troponin T, cardiac troponin I, and creatine kinase MB mass levels in arterial blood were similar in the two groups. Group F showed lower release of cardiac troponin T from the coronary sinus 30 minutes after unclamping of the aorta (group F, 0.263 ± 0.12 ng/mL; group C, 0.6 ± 0.32 ng/mL; P = .005). Lower doses of dopamine were necessary after cardiopulmonary bypass (group F, 0.36 ± 0.11 mg · kg–1 · min–1; group C, 0.49 ± 0.14 mg · kg–1 · min–1; P = .003). A moderate increase in ejection fraction was observed at 30 minutes in both groups (group F, 30.3% ± 6.2%; group C, 28.0% ± 6.3%; P = .239) and a significant increase at 60 minutes in group F (group F, 32.5% ± 6.0%; group C, 27.4% ± 7.5%; P = .012). Conclusions: These results indicate that serial leukocyte filters connected to the blood cardioplegia line decrease myocardial cell injury and may therefore help to improve outcome of patients with severely depressed ejection fractions undergoing coronary artery bypass grafting. (J Thorac Cardiovasc Surg 2000;120:642-50)

Short-Chain Fatty Acid Enemas Stimulate Plasminogen Activator Inhibitor-1 after Abdominal Aortic Graft Surgery: A Double-Blinded, Placebo-Controlled Study

Colonic ischaemia may complicate aortic graft surgery with high mortality from associated colonic necrosis. Loss of the mucosal barrier function due to ischaemia may promote translocation of endotoxins with secondary systemic disseminated coagulation leading to multiple organ failure. Short-chain fatty acids (SCFAs) stimulate the microcirculation in the human rectum. The aim of this study was to investigate whether SCFA enemas influence systemic endotoxinaemia and fibrinolytic activity during and after elective aortic graft surgery for arteriosclerosis. Thirty-two patients were randomized to SCFA or placebo enemas twice daily from the day before surgery to 7 days after. Blood samples for endotoxin, plasminogen activator inhibitor-1 (PAI-1) activity, tissue-type plasminogen activator (t-PA) antigen, and cross-linked fibrin degradation products (XL-FDP) were drawn before, during, and 7 days after surgery. Four patients, two in each treatment group, developed postoperative endotoxinaemia. PAI-1 was significantly higher on days 2 and 4 in SCFA-treated patients, whereas t-PA was comparable between the groups. During the postoperative course, a progressive and near-identical XL-FDP increase was found in the two groups. In elective aortic graft surgery for arteriosclerosis, SCFA enemas likely stimulate systemic PAI-1 activity by promoting colonic tissue reperfusion following aortic unclamping. Endotoxinaemia and fibrinolytic shutdown are uncommon findings.

Laparoscopic aortorenal bypass.

Open surgical renovascular repair, although producing excellent results, confers significant operative morbidity. As a result, less morbid procedures such as percutaneous balloon angioplasty and stenting have gained increasing acceptance. Laparoscopic techniques have not previously been applied to renal revascularization. The aim of this study was to demonstrate the technical feasibility and the long-term clinical and pathologic outcomes of laparoscopic aorto-left renal artery bypass in a chronic porcine model. Eight animals were used in the study. All laparoscopic suturing and knot-tying were performed intracorporeally using free-hand techniques. The following operative steps were employed: (1) aortic dissection and cross-clamping; (2) transection and refashioning of the left renal artery ostium; (3) in-situ renal hypothermia; (4) end-to-side aorto-left renal artery anastomosis; and (5) aortic unclamping. In situ renal hypothermia was achieved laparoscopically by infusion of ice-cold heparinized saline into the renal artery through a balloon catheter. All eight pigs underwent laparoscopic aortorenal bypass successfully. The median surgical time was 110 minutes, and the aortic cross-clamping time was 45.5 minutes. The median anastomotic time was 40 minutes, and the renal warm ischemia time was 9 minutes. The median estimated blood loss was 30 mL. An intraoperative complication of suture breakage leading to anastomotic hemorrhage occurred in one animal; the problem was corrected laparoscopically. Postoperatively, one animal died from pneumonia. The remaining seven animals experienced no postoperative complications and were euthanized, one each at postoperative day 0 and 1 and week 1, 2, 3, 4, and 6. The median preoperative and postoperative (at euthanasia) serum creatinine values (1.15 mg/dL v 1.2 mg/dL; P = 0.39) were similar. However, compared with preoperative peripheral renin activity (0.25 microg/L per hour), the postoperative peripheral renin activity was elevated (0.9 microg/L per hour; P = 0.047). Autopsy revealed a grossly normal left kidney, with Doppler confirmation of flow in the repaired renal artery in all seven animals. Ex vivo angiography confirmed a patent anastomosis. On histopathology examination, the early left renal parenchymal specimens revealed transient, mild acute tubular necrosis that resolved over sequential specimens without significant long-term sequelae. Histologic analysis of the aorto-left renal artery anastomotic site revealed gradual endothelialization with time. Laparoscopic aortorenal artery revascularization is technically feasible. Our chronic animal model has demonstrated durable success over a 6-week follow-up. This study represents the initial report in the literature.

Continuous pulmonary perfusion during cardiopulmonary bypass prevents lung injury in infants

Background. Lung injury after cardiopulmonary bypass is a serious complication for infants with congenital heart disease and pulmonary hypertension. Excessive neutrophil sequestration in the lung occurring after reestablishment of pulmonary circulation implies that interaction between neutrophils and pulmonary endothelium is the major cause of lung injury.Methods. Thirty infants with either ventricular septal defect or atrioventricular septal defect and with pulmonary hypertension were enrolled in this study. We performed continuous pulmonary perfusion during total cardiopulmonary bypass on 16 patients (perfused group) and conventional cardiopulmonary bypass on 14 patients (control group). PaO2/FiO2 and neutrophil counts were assessed from immediately before surgery to 24 hours after termination of cardiopulmonary bypass.Results. PaO2/FiO2 was higher in the perfused group than in the control group, and the difference was significant throughout the study period. Neutrophil counts decreased below prebypass values in both groups at 30 minutes after aortic unclamping, and the difference was significant in the control group but was not in the perfused group. Duration of postoperative ventilatory support was significantly less in the perfused group.Conclusions. Our study demonstrates that arrested pulmonary circulation during cardiopulmonary bypass is the major risk factor of lung injury and that continuous pulmonary perfusion is effective in preventing lung injury.

Impact of Blood Transfusions on Inflammatory Mediator Release in Patients Undergoing Cardiac Surgery

This study was conducted to investigate whether intraoperative blood transfusions affect the release of proinflammatory mediators in patients undergoing cardiac surgery. Therefore, we measured plasma levels of bactericidal permeability increasing protein (BPI) as a marker of neutrophil activation, interleukin-6 (IL-6), lipopolysaccharide binding protein (LBP), and C-reactive protein (CRP). In addition, these mediators, except CRP, were also measured in packed red cell units (PCs) administered to these patients. Prospective study. Cardiopulmonary surgery department in a university hospital. One hundred fourteen consecutive patients undergoing cardiac surgery. Blood samples were taken at induction of anesthesia, at the start of aortic cross-clamping, at aortic unclamping, and at 0.5, 4, 8, and 18 h thereafter. Thirty-six patients received PC intraoperatively. BPI levels in patients who received transfusions were significantly higher at 0.5 and 4 h after aortic unclamping than in patients without transfusions (p < 0.05), and increased with the number of PC administered. IL-6 levels at 0.5, 4, and 18 h after aortic unclamping were also significantly higher in patients who received transfusions (p < 0.01). BPI was found in all units of packed red cells tested at concentrations up to 15 times preoperative plasma levels in patients. However, PC IL-6 could be detected in none of the samples. Plasma levels of LBP and CRP were similar in both patient groups. LBP was found in very low concentrations in all PC. Patients who received intraoperative transfusions had a worse postoperative performance. Intraoperative PC transfusions do contribute to the inflammatory response after cardiac surgery both by enhancing part of the response and by directly changing plasma concentrations of inflammatory mediators. Furthermore, these data show that intraoperative PC transfusion is associated with a worse postoperative performance.

Respiratory mechanics during and after anaesthesia for major vascular surgery.

To evaluate the effects of major vascular surgery on respiratory mechanics, 11 patients undergoing general anaesthesia for abdominal aortic surgery were studied. Before aortic cross-clamping, chest wall elastance and resistance both increased (by 126% and 58%, respectively) when surgical retractors were placed. After aortic cross-clamping, lung elastance increased by 29%, accompanied by a decrease in cardiac index (22%) and an increase in pulmonary (17%) and systemic (15%) vascular resistance. After aortic unclamping, lung elastance decreased, although it remained higher than baseline values (by 12%). All cardiovascular variables returned to the values obtained before aortic cross-clamping.

Cardiopulmonary bypass and activation of antithrombotic plasma protein C

Objective: We hypothesized that antithrombotic plasma-activated protein C plays a defensive antithrombotic role during coronary ischemia and postischemic reperfusion. Methods and results: We evaluated protein C activation during cardiopulmonary bypass and coronary reperfusion in 20 patients undergoing coronary bypass surgery. During cardiopulmonary bypass and during the 10 minutes after aortic unclamping, the plasma levels of protein C (mean ± standard error of the mean) decreased from 123% ± 7% to 74% ± 5% of normal mean. In contrast, the levels of activated protein C in plasma increased from 122% ± 8% to 159% ± 21%, and the activated protein C/protein C ratio increased from 1.04 ± 0.08 to 2.29 ± 0.31 ( P = .006, 2-tailed Wilcoxon signed rank test). Patients were stratified on the basis of the increase in activated protein C in the coronary sinus plasma at 10 minutes after reperfusion by means of the arbitrary value of 1.5 for the activated protein C/protein C ratio. Within 24 hours, the patients with low increases in activated protein C (ratio < 1.5, n = 8) had a significantly ( P < .05) lower cardiac output and mean pulmonary artery pressure, as well as a higher systemic vascular resistance, than patients (n = 11) with high increases in activated protein C (ratio > 1.5). The rapid increase in activated protein C during the first 10 minutes after aortic unclamping indicated protein C activation in the reperfused vascular beds. Conclusions: The antithrombotic protein C pathway was significantly activated during cardiopulmonary bypass mainly during the minutes after aortic unclamping in the ischemic vascular beds. Suboptimal protein C activation during ischemia may impair the postischemic recovery of human heart and circulation. (J Thorac Cardiovasc Surg 1999;118:422-31)

Release of cardiac troponin I in antegrade crystalloid versus cold blood cardioplegia

Objective: The purpose of this study was to assess the efficacy of myocardial protection, comparing antegrade crystalloid cardioplegia with cold blood cardioplegia, in patients with preserved left ventricular function who were undergoing elective first coronary artery bypass grafting. Release of cardiac troponin I was used as a marker for the effectiveness of myocardial protection. Methods: A consecutive series of 62 patients were randomly assigned to receive crystalloid or blood cardioplegia. Cardiac troponin I concentrations were determined in venous blood samples before the operation, immediately after unclamping, at 6, 9, 12, and 24 hours, and daily thereafter for 5 days. Results: Rising levels of troponin I were found in all patients. The time course and peak release were similar in the crystalloid cardioplegia and the blood cardioplegia groups. No patients in either group had electrocardiographic evidence of perioperative myocardial infarction. Cardiac troponin I was able to detect small areas of myocardial damage, not revealed by electrocardiography or creatine kinase MB release. Aprotinin administration was associated with lower cardiac troponin I release in both groups. Cardiac troponin I was lower in patients whose conditions did not require electrical defibrillation after aortic unclamping, irrespective of cardioplegia type. The presence of a main stem lesion was associated with higher cardiac troponin I release only in the crystalloid cardioplegia group. Conclusions: Antegrade cold blood cardioplegia is equally effective as antegrade crystalloid cardioplegia in a randomized group of patients with preserved left ventricular function who were undergoing elective first coronary artery bypass grafting. Aprotinin administration resulted in lower cardiac troponin I release, whereas electrical defibrillation was related to a higher release irrespective of cardioplegia type. The presence of a main stem lesion resulted in higher cardiac troponin I release in the crystalloid cardioplegia group. (J Thorac Cardiovasc Surg 1999; 118:452-9)

Pulmonary Arterial and Right Ventricular Responses to Prophylactic Albumin Administration Before Aortic Unclamping During Abdominal Aortic Aneurysmectomy

Pulmonary Arterial and Right Ventricular Responses to Prophylactic Albumin Administration Before Aortic Unclamping During Abdominal Aortic Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

Right Ventricular Response to Aortic Unclamping During Aneurysmectomy

IS CARDIAC TROPONIN I A RELIABLE MARKER TO ASSESS MYOCARDIAL INJURY AFTER PEDIATRIC CARDIAC SURGERY?

Introduction: Cardiac troponin I (CTnI) as been used as a specific marker to assess the postoperative myocardial injury in congenital heart diseases [1]. The aim of our study was to evaluate in a large cohort of pediatric patients how CTnI (in association with other techniques) could assess the postoperative myocardial injury and the severity of the early postoperative outcome. Methods: A group of 263 consecutive patients (mean 8.2 years), undergoing cardiac surgery with cardiopulmonary bypass and aortic cross clamping for congenital heart diseases was studied. All patients received the same protocol of anesthesia, management of CPB and myocardial protection. CTnI was measured routinely by the Stratus fluorometric enzyme immunoassay technique (Dade). Blood samples were collected after induction of anesthesia, 15 minutes and 3 hours after aortic unclamping and then every 6 hours during 45 hours. After the procedure and during 45 hours, the patients were enrolled in three groups after meeting criteria of severity of myocardial dysfunction. Group 1: unchanged EKG, unchanged ventricular kinesia on TTE and dobutamine or dopamine requirement < 5 mcg/kg/min. Group 2: modified EKG with Q wave or ST segment changes or arrhythmias or conduction abnormalities, echocardiography with ventricular hypokinesia and dobutamine or dopamine requirement > 5 mcg/kg/min. Group 3: modified EKG (same than Gr. 2), echocardiography with ventricular akinesia, and dobutamine or dopamine requirement > 5 mcg/kg/min associated with epinephrine associated or not with delayed sternal closure. For the comparison of the mean value between two groups, two-tailed Student t-test and Z-test were used. A probability of less than 0.05 was considered significant. Results: 185 patients (70%) were assigned group 1, 38 (14.4%) patients group 2 and 40 (15.2%) patients group 3. Mean CTnI plasma levels of groups 1, 2 and 3 were not statistically different in the preoperative period (first sample) and 15 minutes after aortic unclamping. From H 3 to H 45, mean CTnI plasma levels of group 1 were statistically different from groups 2 and 3 (p<0.01). Mean CTnI plasma levels were not statistically different between groups 2 and 3. The profiles of the perioperative CTnI plasma level time course are similar in the three groups and peaked between H 15 and H 21. In group 3, the peak of CTnI plasma level is 2.1 times as elevated as in group 1 at H 3 and 2.48 times at H 21. There was no mortality in group 1 and 2, and 26 deaths (9.8%) occured in group 3. Discussion: Any procedure for correction of congenital heart disease may result in postoperative myocardial dysfunction related to the surgical technique, the cardiopulmonary bypass and/or the myocardial protection. In this study, the CTnI plasma level time course during the first 45 hours compared with the severity score is related with the severity of the myocardial dysfunction. The predictive value of a high concentration of CTnI during the nine first hours suggested by Taggart [1], is demonstrated with the occurence of the whole mortality in the group 3 where the CTnI plasma levels are the more elevated during the first 45 hours. Conclusion: An early post-operative increase of CTnI plasma level, associated with an echocardiographic myocardial dysfunction allow to apply the adequate therapy before any clinical sign of hemodynamic failure appear. Figure 1Figure 1

Ethane: a marker of lipid peroxidation during cardiopulmonary bypass in humans

The goals of this study were to (1) determine the utility of quantification of ethane as a marker of ischemia-reperfusion during human cardiopulmonary bypass (CPB); and (2) determine, using an animal model for this surgical procedure, whether the mode of surgical approach produced increases the quantity of exhaled ethane. Human CPB was initiated following standard anesthetic and monitoring regimens. Samples of gas were collected at baseline and at multiple defined time points throughout the studies. Ethane was determined using cryogenic concentration and gas chromatography. Sternotomy increased exhaled ethane compared to baseline ( p < .007; 5.8 ± 1.7 vs. 3.0 ± 0.7 nmol/m 2 · min); ethane returned to baseline levels prior to the initiation of CPB. Aortic unclamping produced ethane elevation ( p < .05; 2.3 ± 0.8 vs. 1.5 ± 0.4 nmol/m 2 · min) with the levels being related to a lower cardiac index and a higher systemic vascular resistance post aortic unclamping. Termination of CPB significantly increased ethane levels compared to baseline ( p < .002; 4.8 ± 1.7 vs. 3.0 ± 0.7 nmol/m 2 · min). Independent variables that correlated with increased ethane measurements included a higher arterial blood pH on bypass and the change in hemoglobin pre- and post-CPB. Electrocautery, but not scalpel, incision of the porcine abdominal wall increased ethane levels significantly ( p < .02). These results indicate that exhaled ethane may be a valuable marker of lipid peroxidation during and following CPB.

Changes in ionized calcium concentrations and acid-base status during abdominal aortic vascular surgery

Abdominal aortic surgery may produce significant haemodynamic instability (from a combination of factors: hypovolaemia, acid-base disturbances, vasoactive metabolite release from ischaemic tissues and hypocalcaemia). Calcium is often given after aortic unclamping to attenuate this instability. We studied 20 patients undergoing elective abdominal aortic surgery and observed a triphasic change in ionized calcium concentrations and acid-base status. Initially, during the cross-clamp period (when patients were cardiovascularly stable), ionized calcium concentrations decreased significantly (mean 1.06 (SD 0.08) to 0.91 (0.13) mmol litre-1; P < 0.01), while a significant metabolic acidosis developed (pH 7.38 (0.05) to 7.30 (0.05); P < 0.05). Second, release of the aortic cross-clamp resulted in further acidosis (pH 7.27 (0.05) (P < 0.05) mixed respiratory and metabolic) with a decrease in mean arterial pressure, with no change in ionized calcium concentrations. The third phase was associated with spontaneous restoration of acid-base status and ionized calcium concentrations to normal over 2 h. There was no correlation between units of blood given, volume of blood lost, fluid volume given or duration of aortic cross-clamping and degree of ionized hypocalcaemia. We conclude that ionized hypocalcaemia occurred during the cross-clamp period of aortic surgery, was unrelated to the volume of blood given and did not appear to be responsible for the changes in arterial pressure during surgery.

Pulmonary Arterial and Right Ventricular Responses to Prophylactic Albumin Administration Before Aortic Unclamping During Abdominal Aortic Aneurysmectomy

Pulmonary Arterial and Right Ventricular Responses to Prophylactic Albumin Administration Before Aortic Unclamping During Abdominal Aortic Aneurysmectomy