Successful management of temporary veno-venous extracorporeal membrane oxygenation for a pediatric lung transplant recipient with bronchiolitis obliterans syndrome awaiting lung re-transplantation: a case report.

BACKGROUND: The use of extracorporeal membrane oxygenation (ECMO) as a bridge to lung transplantation is an uncommon strategy in Japan owing to the severe donor shortage and absence of urgent allocation policy. Moreover, the use of veno-venous (VV) ECMO for immunosuppressed patients is controversial; thus, applying ECMO to patients who await lung re-transplantation is challenging. CASE PRESENTATION: A 16-year-old lung transplant recipient with grade 3 bronchiolitis obliterans syndrome was waitlisted for lung re-transplantation. Eleven months later, he fell into severe respiratory acidosis with hypercapnia, which were not resolved with mechanical ventilation. VV ECMO was introduced to minimize lung stress and strain. Tracheostomy was additionally performed on day 5 after the start of ECMO, and respiratory condition swiftly improved; hence, the weaning process from VV ECMO began on day 9. Rehabilitation became implementable, and bilateral re-lung transplantation was successfully performed 6 months after the ECMO treatment. No critical complication related to the precedent use of ECMO was noted. CONCLUSIONS: VV ECMO can be a feasible treatment option even for lung transplant candidates awaiting re-transplantation for a prolonged period. Introduction of ECMO and tracheostomy in the early deterioration stage may be crucial to successful subsequent patient management.

Whole lung lavage decreases physiological dead space in patients with pulmonary alveolar proteinosis: two case reports.

BACKGROUND: Pulmonary alveolar proteinosis (PAP) is a rare disease characterized by progressive accumulation of the alveolar surfactant. Whole lung lavage (WLL) using a high volume of warmed saline remains the standard therapy. However, no established bedside monitoring tool can evaluate the physiological effect of WLL in the perioperative period. Indirect calorimetry, which is generally used to measure resting energy expenditure, can detect carbon dioxide (CO2) production and mixed-expired partial pressure of CO2 breath by breath. In this physiological study, we calculated CO2 elimination per breath (VTCO2,br) and Enghoff's dead space using indirect calorimetry and measured the extravascular lung water index to reveal the effect of WLL. CASE PRESENTATION: We measured VTCO2,br, Enghoff's dead space, and the extravascular lung water and cardiac indices before and after WLL to assess the reduction in shunt by washing out the surfactant. A total of four WLLs were performed in two PAP patients. The first case involved an Asian 62-year-old man who presented with a 3-month history of dyspnea on exertion. The second case involved an Asian 48-year-old woman with no symptoms. VTCO2,br increased, and the Enghoff's dead space decreased at 12 h following WLL. An increase in the extravascular lung water was detected immediately following WLL, leading to a transient increase in Enghoff's dead space. CONCLUSION: WLL can increase efficient alveolar ventilation by washing out the accumulated surfactant. However, the lavage fluid may be absorbed into the lung tissues immediately after WLL and result in an increase in the extravascular lung water.

Long-Term Exposure to Morphine Induces Cross-Tolerance to Acute Antinociceptive Effect of Remifentanil on Somatic and Visceral Stimuli in Rats.

Purpose: Remifentanil is one of the most commonly used opioids intraoperatively. Previous reports indicate that long-term use of opioids may lead to cross-tolerance to remifentanil, which poses a challenge in the control of acute pain intraoperatively. However, there is limited information regarding cross-tolerance to remifentanil, especially in visceral pain. Therefore, this study aimed to examine cross-tolerance to remifentanil in somatic and visceral tolerance using morphine-tolerant rats. Methods: Six male Sprague-Dawley rats were allocated to the morphine and saline groups each. Tolerance to the antinociceptive effect of morphine was induced in rats in the morphine group. Remifentanil was continuously infused intravenously at 10 mcg/kg/min for 120 min to assess cross-tolerance from morphine to remifentanil. The antinociceptive effects on somatic and visceral nociceptive stimuli were measured using the tail-flick (TF) and colorectal distension (CD) tests, respectively. The antinociceptive efficacy was evaluated by converting the response threshold to the percentage maximal possible effect (%MPE). Results: Remifentanil increased the %MPE in the morphine and saline groups in both the tests; however, the increase in %MPE was attenuated significantly in the morphine group compared with that in the saline group at 60, 90, and 120 min (all P < 0.01) in the TF test and at 90 and 120 min in the CD test (all P <0.05). Conclusion: Our results indicate that morphine-tolerant rats exhibit cross-tolerance to remifentanil's acute antinociceptive effects on somatic and visceral stimuli. Cross-tolerance to remifentanil should be considered in the perioperative management of patients using morphine.

Recombinant Human Soluble Thrombomodulin Suppresses Monocyte Adhesion by Reducing Lipopolysaccharide-Induced Endothelial Cellular Stiffening.

Endothelial cellular stiffening has been observed not only in inflamed cultured endothelial cells but also in the endothelium of atherosclerotic regions, which is an underlying cause of monocyte adhesion and accumulation. Although recombinant soluble thrombomodulin (rsTM) has been reported to suppress the inflammatory response of endothelial cells, its role in regulating endothelial cellular stiffness remains unclear. The purpose of this study was to investigate the impact of anticoagulant rsTM on lipopolysaccharide (LPS)-induced endothelial cellular stiffening. We show that LPS increases endothelial cellular stiffness by using atomic force microscopy and that rsTM reduces LPS-induced cellular stiffening not only through the attenuation of actin fiber and focal adhesion formation but also via the improvement of gap junction functionality. Moreover, post-administration of rsTM, after LPS stimulation, attenuated LPS-induced cellular stiffening. We also found that endothelial cells regulate leukocyte adhesion in a substrate- and cellular stiffness-dependent manner. Our result show that LPS-induced cellular stiffening enhances monocytic THP-1 cell line adhesion, whereas rsTM suppresses THP-1 cell adhesion to inflamed endothelial cells by reducing cellular stiffness. Endothelial cells increase cellular stiffness in reaction to inflammation, thereby promoting monocyte adhesion. Treatment of rsTM reduced LPS-induced cellular stiffening and suppressed monocyte adhesion in a cellular stiffness-dependent manner.

Positive End-expiratory Pressure and Distribution of Ventilation in Pneumoperitoneum Combined with Steep Trendelenburg Position.

BACKGROUND: Pneumoperitoneum and a steep Trendelenburg position during robot-assisted laparoscopic prostatectomy have been demonstrated to promote a cranial shift of the diaphragm and the formation of atelectasis in the dorsal parts of the lungs. However, neither an impact of higher positive end-expiratory pressure (PEEP) on preserving the ventilation in the dorsal region nor its physiologic effects have been fully examined. The authors hypothesized that PEEP of 15 cm H2O during robot-assisted laparoscopic prostatectomy might maintain ventilation in the dorsal parts and thus improve lung mechanics. METHODS: In this randomized controlled study, 48 patients undergoing robot-assisted laparoscopic prostatectomy were included in the analysis. Patients were assigned to the conventional PEEP (5 cm H2O) group or the high PEEP (15 cm H2O) group. Regional ventilation was monitored using electrical impedance tomography before and after the establishment of pneumoperitoneum and 20° Trendelenburg position during the surgery. The primary endpoint was the regional ventilation in the dorsal parts of the lungs while the secondary endpoints were lung mechanics and postoperative lung function. RESULTS: Compared to that in the conventional PEEP group, the fraction of regional ventilation in the most dorsal region was significantly higher in the high PEEP group during pneumoperitoneum and Trendelenburg position (mean values at 20 min after taking Trendelenburg position: conventional PEEP, 5.5 ± 3.9%; high PEEP, 9.9 ± 4.7%; difference, -4.5%; 95% CI, -7.4 to -1.6%; P = 0.004). Concurrently, lower driving pressure (conventional PEEP, 14.9 ± 2.5 cm H2O; high PEEP, 11.5 ± 2.8 cm H2O; P < 0.001), higher lung dynamic compliance, and better oxygenation were demonstrated in the high PEEP group. Postoperative lung function did not differ between the groups. CONCLUSIONS: Application of a PEEP of 15 cm H2O resulted in more homogeneous ventilation and favorable physiologic effects during robot-assisted laparoscopic prostatectomy but did not improve postoperative lung function.

Plasma proteomic changes during therapeutic hypothermia in resuscitated patients after cardiac arrest.

Hypothermia is used for several h during cardiac and aortic surgery to protect ischemic organs. Therapeutic hypothermia (TH) is used for ≤24 h as a treatment for comatose patients after the return of spontaneous circulation (ROSC) following cardiac arrest. The proteomic approach may provide unbiased data on alterations in the abundance of proteins during TH. The objective of this study was to assess the effects of cooling/rewarming on the plasma proteome during TH after ROSC and to identify the mechanism underlying its therapeutic effects. A total of nine comatose adult patients, resuscitated shortly after cardiac arrest, were cooled to 34°C for 24 h and slowly rewarmed to 36°C. A quantitative gel-free proteomic analysis was performed using the isobaric tag for relative and absolute quantification labeling tandem mass spectrometry. Plasma samples were obtained prior to cooling and rewarming, and immediately after rewarming, from all patients during TH after ROSC. A total of 92 high-confidence proteins were identified. Statistically significant alterations were observed (>1.2-fold increase or <0.833-fold decrease) in the levels of 15 of those proteins (P=0.003-0.047), mainly proteins belonging to the acute-phase response or platelet degranulation. Unexpectedly, the levels of free hemoglobin (hemoglobin subunits α and ß) were significantly downregulated during TH (P<0.05). The level of the terminal complement complex (SC5b-9) showed significant reduction after cooling (P=0.023). Although the acute-phase response proteins were upregulated, the abundance of complement proteins did not change, and the levels of SC5b-9 and free hemoglobin decreased during TH in patients after ROSC.

Biphasic Cuirass Ventilation During Anesthesia for Tracheobronchial Stent Insertion or Removal by a Rigid Bronchoscope: A Case Report.

Airway management and ventilation during a tracheobronchial stenting procedure are challenging given that mandatory positive pressure ventilation cannot be fully achieved while using a rigid bronchoscope due to leakage from the scope tip. Biphasic cuirass ventilation is a negative pressure ventilation method using an external cuirass fitted to the anterior chest, which could assist in spontaneous breathing and ventilation support. We report 3 successful anesthesia cases in which we could maintain adequate ventilation and oxygenation, supported by biphasic cuirass ventilation, in patients undergoing tracheobronchial stent placement or removal procedures using rigid bronchoscopy.

Does the Rewarmed Heart Restore the Myocardial Proteome to That of the Pre-Cooled State?--A Proteomic Analysis of Surgical Samples.

BACKGROUND: Hypothermia is utilized in cardiac and aortic surgery to protect organs from ischemic reperfusion injury. Although the cooled body is invariably rewarmed after the procedure, it is still unknown whether the rewarmed body regains its former biological state. This study determined the modulatory effects of hypothermia on the human myocardial proteome and whether subsequent rewarming restores the proteome to the state prior to cooling. METHODS AND RESULTS: A quantitative proteomic analysis was performed using isobaric tags for relative and absolute quantification labeling tandem mass spectrometry. Right atrial samples were taken 3 times (pre, during and post cooling) during deep hypothermic cardiopulmonary bypass (CPB) from 8 patients with aortic arch aneurysms and 3 corresponding time points during normothermic CPB from 8 patients with ascending aortic or valsalva aneurysms. In total, 697 proteins were identified, with 222 proteins having high protein confidence. Bioinformatic analyses revealed significant downregulation of 19 proteins associated with energy production at hypothermic cardioplegic arrest. On rewarmed beating, 10 proteins remained downregulated, including those regulating cardiac contraction and adaptor proteins, although levels of the aforementioned 19 downregulated proteins returned to their initial values. Additional echocardiographic evaluation demonstrated that hypothermia preserved the variables of diastolic function to a greater extent than normothermic surgery. CONCLUSIONS: Rewarming restores the human myocardial proteome to the pre-cooled state, except for proteins regulating cardiac contraction and adaptor proteins.

[Full Recovery from Cardiopulmonary Arrest caused by Traumatic Asphyxia].

Traumatic asphyxia is a crush injury of the chest characterized by facial edema, cyanosis, conjunctival hemorrhage, and petechiae on the face and chest. The prognosis depends on the duration of chest compression and early cardiopulmonary resuscitation after cardiopulmonary arrest. Here we report a case of full recovery from cardiopulmonary arrest caused by traumatic asphyxia. The chest of a 56-year-old man was compressed by a machine while working. Immediately, his colleague started cardiopulmonary resuscitation, which was successful. When he was admitted to our hospital, his consciousness level was E1V2M2(Glasgow coma scale). Our treatment included therapeutic hypothermia, the duration of which was 24 hours at 34 °C. Rewarming his body to 36 °C took place over 48 hours. Thereafter, he recovered completely and was discharged on the 12th hospital day without neurologic sequela. Therapeutic hypothermia was possibly effective in this case.

Plasma proteomic changes during hypothermic and normothermic cardiopulmonary bypass in aortic surgeries.

Deep hypothermic circulatory arrest (DHCA) is a protective method against brain ischemia in aortic surgery. However, the possible effects of DHCA on the plasma proteins remain to be determined. In the present study, we used novel high­throughput technology to compare the plasma proteomes during DHCA (22˚C) with selective cerebral perfusion (SCP, n=7) to those during normothermic cardiopulmonary bypass (CPB, n=7). Three plasma samples per patient were obtained during CPB: T1, prior to cooling; T2, during hypothermia; T3, after rewarming for the DHCA group and three corresponding points for the normothermic group. A proteomic analysis was performed using isobaric tag for relative and absolute quantification (iTRAQ) labeling tandem mass spectrometry to assess quantitative protein changes. In total, the analysis identified 262 proteins. The bioinformatics analysis revealed a significant upregulation of complement activation at T2 in normothermic CPB, which was suppressed in DHCA. These findings were confirmed by the changes of the terminal complement complex (SC5b­9) levels. At T3, however, the level of SC5b­9 showed a greater increase in DHCA compared to normothermic CPB, while 48 proteins were significantly downregulated in DHCA. The results demonstrated that DHCA and rewarming potentially exert a significant effect on the plasma proteome in patients undergoing aortic surgery.

[Recipient of living kidney transplantation during which heparin-induced thrombocytopenia (HIT) was suspected: a case report].

A 67-year-old woman with a diabetic renal failure was scheduled for a living kidney transplantation. Heparin was first used during hemodialysis 5 days before operation. Thrombocytopenia was found immediately after induction of general anesthesia, and the diagnosis of HIT was wade based on clinical symptom and 4 T's scoring. The surgery was continued because of the progress of donor surgery. Argatoroban was administered based on APTT measurement as an anticoagulation therapy during and after the operation. Although deep vein thrombosis was found 13 days after the operation, the transplanted kidney was established successfully. It is necessary to take a great caution in HIT development after heparin use.

[A case report: perioperative management of adenotonsillectomy in a morbidly obese patient with severe obstructive sleep apnea syndrome].

A male patient in his thirties was scheduled to undergo adenotonsillectomy due to dyspnea from bilateral tonsillar hypertrophy. He was morbidly obese (body mass index 56 kg x m(-2)) with severe obstructive sleep apnea syndrome (OSAS), and thus was evaluated with extreme risk for difficult ventilation and intubation. We planned awake intubation via video-assisted laryngoscopy and fiberoptic bronchoscopy under dexmedetomidine sedation, and the intubation was successfully performed. After adenotonsillectomy, upper airway obstruction due to hemorrhage and oropharyngeal swelling can be life-threatening requiring emergent airway management. Thus for postoperative airway management, due to the possibility of "cannot intubate, cannot ventilate" (CICV) and presumed difficult tracheotomy, we scheduled to perform tracheotomy during adenotonsillectomy, right after anesthetic induction and awake intubation. On postoperative day 1, he started walking with no need of sedative drugs. On day 4, after confirmation of minimal oropharyngeal swelling, tracheal cannulae was removed, and no further complications were observed in his postoperative course. We conclude that careful preoperative evaluation of the airway, retention of spontaneous breathing via awake intubation, and preventive tracheotomy for postoperative airway management are important points in perioperative management of a morbidly obese patient with severe obstructive sleep apnea syndrome.

Intravenous infusion of remifentanil induces transient withdrawal hyperalgesia depending on administration duration in rats.

BACKGROUND: Recent studies suggest that remifentanil, similar to other µ-opioid agonists, may induce hyperalgesia. We performed animal experiments to determine whether IV remifentanil infusion, the mode of administration used in clinical practice, induces hyperalgesia and the conditions in which this phenomenon occurs. We also determined whether remifentanil-induced hyperalgesia is related to extracellular signal-regulated protein kinase 1/2 (ERK1/2) phosphorylation. METHODS: Remifentanil was administered through a catheter in the tail vein of male Sprague-Dawley rats for 10 minutes (30 µg · kg(-1) · min(-1)), 30 minutes (0.1, 1, and 10 µg · kg(-1) · min(-1)), or 120 minutes (0.1, 1, 3, and 10 µg · kg(-1) · min(-1)). The von Frey test and a tail-flick test were performed, followed by ERK1/2 immunohistochemistry. We examined whether intrathecal preadministration of the mitogen-activated protein kinase inhibitor U0126 suppresses hyperalgesia. RESULTS: Remifentanil had a dose-dependent antinociceptive effect that rapidly diminished. Ten- or 30-minute remifentanil infusion did not induce hyperalgesia. However, tail-flick latency and mechanical pain threshold after infusion termination were significantly lower in the 120-minute remifentanil administration group than those in the control group, regardless of dose. Hyperalgesia duration was no longer than 60 minutes. Significantly more phospho-ERK1/2-immunoreactive neurons in the superficial spinal dorsal horn were observed in the remifentanil 120-minute groups with hyperalgesia than in the 30-minute remifentanil groups without hyperalgesia, although U0126 did not suppress hyperalgesia. CONCLUSIONS: IV remifentanil induces transient withdrawal hyperalgesia soon after its termination. This hyperalgesia is strongly associated with the duration of exposure to remifentanil. Contrary to our hypothesis, ERK1/2 by itself was not the essential factor involved in the induction of the hyperalgesia.

[Perioperative management of total laryngectomy for a patient with cold agglutinin disease].

Cold agglutinin disease is possible to cause thromboembolism of various organs due to changes in red blood cells by exposure to low temperature. Safety standards for perioperative management of patients with cold agglutinin have not been established. A patient with cold agglutinin disease was scheduled to undergo total laryngectomy and greater pectoral muscle flap. We thought it important to perform intensive temperature control to prevent a decrease in temperature below the thermal amplitude, which induces agglutinin in the vessel. We tried to keep the temperature of the patient with the warming equipment aggressively and monitored the shift of temperature in detail. It was also important to shorten the surgery with less hemorrhage and anesthetic management which can avoid a large shift in body temperature. We could keep peripheral and deep temperature above the critical point causing agglomeration. We did not find any symptoms of microembolism due to cold agglutination during the operation.

[Case report of paradoxical arousal-like EEG changes during pediatric laparotomy].

An 8-year-old boy with Chiari malformation and myelomeningocele received total cystectomy and ileal neobladder surgery under general anesthesia with sevoflurane, nitrous oxide, and intravenous fentanyl. Bispectral index (BIS) suddenly decreased from 50 to 7 with large slow delta waves during ileal anastomosis, although there was no change regarding blood pressure and heart rate. This EEG change was considered first as 'paradoxical arousal', of which mechanism is commonly due to the unexpected noxious stimulation. In spite of additional intravenous fentanyl, this EEG pattern did not change at all, but disappeared spontaneously. This episode repeated two times under the similar condition during surgery. The patient recovered from anesthesia without any neurological complications. The effect-site fentanyl concentration simulated later was supposed to suppress the noxious stimulation adequately during this procedure. Although we can not elucidate the mechanism of paradoxical arousal-like EEG change, our case report suggests that paradoxical arousal may occur by factors other than inadequate anesthesia.

Profound reduction of somatic and visceral pain in mice by intrathecal administration of the anti-migraine drug, sumatriptan.

Sumatriptan and the other triptan drugs target the serotonin receptor subtypes1B, 1D, and 1F (5-HT(1B/D/F)), and are prescribed widely in the treatment of migraine. An anti-migraine action of triptans has been postulated at multiple targets, within the brain and at both the central and peripheral terminals of trigeminal "pain-sensory" fibers. However, as triptan receptors are also located on "pain-sensory" afferents throughout the body, it is surprising that triptans only reduce migraine pain in humans, and experimental cranial pain in animals. Here we tested the hypothesis that sumatriptan can indeed reduce non-cranial, somatic and visceral pain in behavioral models in mice. Because sumatriptan must cross the blood brain barrier to reach somatic afferent terminals in the spinal cord, we compared systemic to direct spinal (intrathecal) sumatriptan. Acute nociceptive thresholds were not altered by sumatriptan pre-treatment, regardless of route. However, in behavioral models of persistent inflammatory pain, we found a profound anti-hyperalgesic action of intrathecal, but not systemic, sumatriptan. By contrast, sumatriptan was completely ineffective in an experimental model of neuropathic pain. The pronounced activity of intrathecal sumatriptan against inflammatory pain in mice raises the possibility that there is a wider spectrum of therapeutic indications for triptans beyond headache.

Spider toxins activate the capsaicin receptor to produce inflammatory pain.

Bites and stings from venomous creatures can produce pain and inflammation as part of their defensive strategy to ward off predators or competitors. Molecules accounting for lethal effects of venoms have been extensively characterized, but less is known about the mechanisms by which they produce pain. Venoms from spiders, snakes, cone snails or scorpions contain a pharmacopoeia of peptide toxins that block receptor or channel activation as a means of producing shock, paralysis or death. We examined whether these venoms also contain toxins that activate (rather than inhibit) excitatory channels on somatosensory neurons to produce a noxious sensation in mammals. Here we show that venom from a tarantula that is native to the West Indies contains three inhibitor cysteine knot (ICK) peptides that target the capsaicin receptor (TRPV1), an excitatory channel expressed by sensory neurons of the pain pathway. In contrast with the predominant role of ICK toxins as channel inhibitors, these previously unknown 'vanillotoxins' function as TRPV1 agonists, providing new tools for understanding mechanisms of TRP channel gating. Some vanillotoxins also inhibit voltage-gated potassium channels, supporting potential similarities between TRP and voltage-gated channel structures. TRP channels can now be included among the targets of peptide toxins, showing that animals, like plants (for example, chilli peppers), avert predators by activating TRP channels on sensory nerve fibres to elicit pain and inflammation.

TRPA1 mediates the inflammatory actions of environmental irritants and proalgesic agents.

TRPA1 is an excitatory ion channel targeted by pungent irritants from mustard and garlic. TRPA1 has been proposed to function in diverse sensory processes, including thermal (cold) nociception, hearing, and inflammatory pain. Using TRPA1-deficient mice, we now show that this channel is the sole target through which mustard oil and garlic activate primary afferent nociceptors to produce inflammatory pain. TRPA1 is also targeted by environmental irritants, such as acrolein, that account for toxic and inflammatory actions of tear gas, vehicle exhaust, and metabolic byproducts of chemotherapeutic agents. TRPA1-deficient mice display normal cold sensitivity and unimpaired auditory function, suggesting that this channel is not required for the initial detection of noxious cold or sound. However, TRPA1-deficient mice exhibit pronounced deficits in bradykinin-evoked nociceptor excitation and pain hypersensitivity. Thus, TRPA1 is an important component of the transduction machinery through which environmental irritants and endogenous proalgesic agents depolarize nociceptors to elicit inflammatory pain.

[A case of severe coronary artery spasm associated with anaphylactic reaction caused by protamine administration].

A 65-year-old man with mitral regurgitation and atrial fibrillation underwent mitral valve plasty and Maze's operation. Cardiopulmonary bypass (CPB) was finished uneventfully. But after protamine administration, severe systemic hypotension occurred suddenly with electrocardiographic ST-segment elevation and wide QRS intervals. We thought that this reaction had been caused by coronary spasm and not by anaphylactic reaction because he was without typical anaphylactic manifestations such as general rash and bronchospasm. We administered epinephrine, methylprednisolone, heparin for restarting CPB, and used IABP support to assist systemic circulation. We again tried to administer protamine to neutralize the anticoagulative effect of heparin when his vital sign had recovered, but the same reaction occurred immediately with small amounts of protamine. The second CPB was necessary for some time. This case suggests that coronary artery spasm associated with anaphylactic reaction was induced by administration of protamine. It is known that intravenous protamine administration sometimes causes adverse events. As in this case, we should consider the possibility of severe coronary spasm associated with anaphylactoid reaction even if other symptoms of anaphylactic reactions such as cutaneous manifestation and bronchospasm are not present.

[Surgical stress in perioperative period of combined off-pump coronary artery bypass grafting and abdominal aortic aneurysm repair].

OBJECTIVES: It is still controversial whether we should choose simultaneous operation or two-staged operation for patients who need both coronary artery bypass grafting (CABG) and abdominal aortic aneurysm (AAA) repair. Some reports suggest that combined CABG without cardiopulmonary bypass and AAA repair is less invasive than those with cardiopulmonary bypass. We estimated surgical stress of combined off pump CABG and AAA repair (CABG + AAA) in perioperative period compared with simple AAA repair retrospectively. METHODS: Seven patients (mean 60 years) underwent simultaneous operation of off pump CABG and AAA repair in our institution. We gathered data associated with circulatory, respiratory, renal function, recovery, and so on. We also examined postoperative complication and mortality. RESULTS: All parameters, except operation time and amount of catecholamine used, were not significantly different between the two groups. There were no operative mortality and only a slight morbidity in CABG + AAA. CONCLUSIONS: Our findings suggest that careful circulatory management with adequate transfusion and catecholamine use under precise monitoring is necessary during operation, but recovery after surgery, complication, and mortality in this combined operation are almost equivalent to those of simple AAA repair. We suggest that combined operation of CABG and AAA repair can be performed effectively.