• Journal of Chest Surgery
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• v.30 no.1
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• pp.27-33
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• 1997

Retrograde myocardial protection is widely accepted in CABG operation because of the limitations of the antegrade method in the coronary arterial stenosis lesions. We analyzed 76 c ses of retrograde myocardial protection among 96 cases of CABG operation performed between April 1994 and August 1995, There were 48 males and 25 females, and the mean age was 58.2 $\pm$ 8.3 years. 53 patients (70%) were operated for unstable angina, 14 (18%) for stable angina, 6 (8%) for post-infarct angina, 1 (1%) for acute myocardial infarction, and 2()%) for failed PTCA. Preoperative coronary angiography revealed 3-vessel disease in 42 cases, 2-vessel disease in 11, 1-vessel disease in 10, and left main disease in 13 cases. We used SVG(63 cases), LIMA(69 cases), RIMA(11 cases), radial artery(6 cases), and gastroepiploic artery(1 case) for the grafts. Mean anastomosis was 3.2 $\pm$ 1.1. We protected the myocardium with antegrade induction and retrograde maintenance in all the cases except a case of retrograde induction and maintenance. During the aortic cross-clamping, blood cardioplegia was administered intermittently in 19 cases, and continuously in 57 In 39 cases, we used retrograde ardioplegia and antegrade perfusion of RCA graft simultaneously. We had no operative motality. Perioperative complications were arrhythmia in 15 cases, perioperatve myocardial infarction in 10, low cardiac output syndrome In 8, transient neurologic problem in 7, transient psychiatric problem in 6, ARF in 3, bleeding in 2, pneumonia in 2, wound infection in 1, and duodenal ulcer perforation in 1 . In this report, we experienced 76 cases of CABG operation with retrograde myocardial protection under the acceptable operative risk without operative mortality.

• Journal of Chest Surgery
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• v.41 no.3
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• pp.329-334
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• 2008

Background: Percutaneous cardiopulmonary support. (PCPS) has the potential to rescue patients in cardiogenic shock who might otherwise die. PCPS has been a therapeutic option in a variety of the clinical settings such as for patients with myocardial Infarction, high-risk coronary intervention and postcardiotomy cardiogenic shock, and the PCPS device is easy to install. We report our early experience with PCPS as a life saving procedure in cardiogenic shock patients due to acute myocardial infarction. Material and Method: From January 2005 to December 2006, eight patients in cardiogenic shock with acute myocardial infarction underwent PCPS using the CAPIOX emergency bypass system($EBS^{(R)}$, Terumo, Tokyo, Japan). Uptake cannulae were inserted deep into the femoral vein up to the right atrium and return cannulae were inserted into the femoral artery with Seldinger techniques using 20 and 16-French cannulae, respectively. Simultaneously, autopriming was performed at the $EBS^{(R)}$ circuit. The $EBS^{(R)}$ flow rate was maintained between $2.5{\sim}3.0L/min/m^2$ and anticoagulation was performed using intravenous heparin with an ACT level above 200 seconds. Result: The mean age of patients was $61.1{\pm}14.2$ years (range, 39 to 77 years). Three patients were under control of the $EBS^{(R)}$ before percutaneous coronary intervention (PCI), three patients were under control of the $EBS^{(R)}$ during PCI, one patient was under control of the $EBS^{(R)}$ after PCI, and one patient was under control of the $EBS^{(R)}$ after coronary bypass surgery. The mean support time was $47.5{\pm}27.9$ hours (range, 8 to 76 hours). Five patients (62.5%) could be weaned from the $EBS^{(R)}$ after $53.6{\pm}27.2$ hours. (range, 12 to 68 hours) of support. All of the patients who could successfully be weaned from support were discharged from the hospital. There were three complications: one case of gastrointestinal bleeding and two cases of acute renal failure. Two of the three mortality cases were under cardiac arrest before $EBS^{(R)}$ support, and one patient had an intractable ventricular arrhythmia during the support. All of the discharged patients are still surviving at $16.8{\pm}3.1$ months (range, 12 to 20 months) of follow-up. Conclusion: The use of $EBS^{(R)}$ for cardiogenic shock caused by an acute myocardial infarction could rescue patients who might otherwise have died. Successfully recovered patients after $EBS^{(R)}$ treatment have survived without severe complications. More experience and additional clinical investigations are necessary to elucidate the proper installation timing and management protocol of the $EBS^{(R)}$ in the future.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.879-890
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• 2006

Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.