• Journal of Chest Surgery
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• v.36 no.4
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• pp.242-254
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• 2003

Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of 25℃ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups. All hearts were perfused at 37℃ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained. Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37℃, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4℃) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at 25℃, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minutes (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37℃ normothermic ischemia and 30 minutes of reperfusion (n=6). Group 4 served as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, improving the LVSP, LVEDP, RPP, and LVdp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.36 no.5
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• pp.242-254
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• 2003

Background: Most of the studies conducted have investigated the beneficial effects of ischemic preconditioning on normothermic myocardial ischemia. However, the effect of preconditioning could be attenuated through the use of multidose cold cardioplegia as practiced in contemporary clinical heart surgical procedures. The purpose of this study was to investigate whether preconditioning improves postischemic cardiac function in a model of $25^{\circ}C$ moderate hypothermic ischemic heart induced by cold cardioplegia in isolated rat hearts. Material and Method: The isolated Sprague-Dawley rat hearts were randomly assigned to four groups All hearts were perfused at 37$^{\circ}C$ for 20 minutes with Krebs-Henseleit solution before the baseline hemodynamic data were obtained, Group 1 consisted of preconditioned hearts that received 3 minutes of global ischemic preconditioning at 37$^{\circ}C$, followed by 5 minutes of reperfusion before 120 minutes of cardioplegic arrest (n=6). Cold (4$^{\circ}C$) St. Thomas Hospital cardioplegia solution was infused to induce cardioplegic arrest. Maintaining the heart at $25^{\circ}C$, infusion of the cardioplegia solution was repeated every 20 minutes throughout the 120 minutes of ischemic period. Group 2 consisted of control hearts that underwent no manipulations between the periods of equilibrium and 120 minutes of cardioplegic arrest (n=6). After 2 hours of cardioplegic arrest, Krebs solution was infused and hemodynamic data were obtained for 30 minuts (group 1, 2: cold cardioplegia group). Group 3 received two episodes of ischemic preconditioning before 30 min of 37$^{\circ}C$ normothermic ischemia and 30 minutes of reperfusion (n=6) Group 4 soloed as ischemic controls for group 3 (group 3, 4: warm ischemia group). Result: Preconditioning did not influence parameters such as left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP) and left ventricular dp/dt (LV dp/dt) in the cold cardioplegia group. (p=NS) However, preconditioning before warm ischemia attenuated the ischemia induced cardiac dysfunction, Improving the LVSP, LVEDP, RPP, and LV dp/dt. Less leakage of CPK and LDH were observed in the ischemic preconditioning group compared to the control group (p<0.05). Conclusion: Ischemic preconditioning improved postischemic cardiac function after warm ischemia, but did not protect cold cardioplegic hearts.

• Journal of Chest Surgery
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• v.41 no.2
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• pp.229-238
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• 2008

Background: Protection of the brain is a major concern during thoracic aortic surgery using hypothermic circulatory arrest (HCA). This study compares the surgical outcomes of two different cerebral protection methods in thoracic aortic surgery using HCA: retrograde cerebral protection (RCP) and antegrade cerebral protection (ACP). Material and Method: We retrospectively reviewed data on 146 patients who underwent thoracic aortic surgery from May 1995 to February 2007 using either RCP (114 patients, Group 1) or ACP (32 patients, Group 2) during HCA. There were 104 dissections (94 acute and 10 chronic) and 42 aneurysms (41 true aneurysms and 1 pseudoaneurysm), and all patients underwent ascending aortic replacement. There were 33 cases of hemiarch replacement, 5 of partial arch replacement, and 21 of total arch replacement. Result: The two groups were similar in preoperative and operative characteristics, but Group 2 had more elderly (over 70 years old) patients (34.4% vs. 10.5%), more coronary artery diseases (18.8% vs. 4.4%), more total arch replacements (46.9% vs. 5.3%) and longer HCA time ($50{\pm}24$ minutes vs. $32{\pm}17$ minutes) than Group 1. The operative mortality was 4.4% (5/114) and 3.1% (1/32), the incidence of permanent neurologic deficits was 5.3% (6/114) and 3.1% (1/32), and the incidence of temporary neurologic deficits was 1.8% (2/114) and 9.4% (3/32) in Groups 1 and 2, respectively. There were no statistical differences between the two groups in operative mortality, postoperative bleeding, or neurologic deficits (permanent and temporary). Conclusion: The early outcomes of aortic surgery using HCA were favorable and showed no statistical difference between RCP and ACP. However, the ACP patients endured longer HCA times and more extended arch surgeries. ACP is the preferred brain protection technique when longer HCA time is expected or extended arch replacement is needed.

• Journal of Chest Surgery
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• v.30 no.5
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• pp.471-478
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• 1997

Introduction: The use of rabbits as a cardiopulmonary bypass(CPB) animal model is extremely dif%cult mainly due to technical problems. On the other hand, deep hypothermic circulatory arrest(CA) is used to facilitate surgical repair in a variety of cardiac diseases. Although steroids are generally known to be effective in the treatment of cerebral edema, the protective effects of steroids on the brain during CA are not conclusively established. Objectives of this study are twofold: the establishment of CPB technique in rabbits and the evaluation of preventive effect of steroid on the development of brain edema during CA. Material '||'&'||' Methods: Fifteen New Zealan white rabbits(average body weight 3.5kg) were divided into three experimental groups; control CA group(n=5), CA with Trendelenberg position group(n=5), and CA with Trendelenberg position + steroid(methylprednisolone 30 mglkg) administration group(n=5). After anesthetic induction and tracheostomy, a median sternotomy was performed. An aortic cannula(3.3mm) and a venous ncannula(14 Fr) were inserted, respectively in the ascending aorta and the right atrium. The CPB circuit consisted of a roller pump and a bubble oxygenator. Priming volume of the circuit was approximately 450m1 with 120" 150ml of blood. CPB was initiated at a flow rate of 80~85ml/kg/min, Ten min after the start of CPB, CA was established with duration of 40min at $20^{\circ}C$ of rectal temperature. After CA, CPB was restarted with 20min period of rewarming. Ten min after weaning, the animal was sacrif;cod. One-to-2g portions of the following tissues were rapidly d:ssected and water contents were examined and compared among gr ups: brain, cervical spinal cord, kidney, duodenum, lung, heart, liver, spleen, pancreas. stomach. Statistical significances were analyzed by Kruskal-Wallis nonparametric test. Results: CPB with CA was successfully performed in all cases. Flow rate of 60-100 mlfkgfmin was able to be maintained throughout CPB. During CPB, no significant metabolic acidosis was detected and aortic pressure ranged between 35-55 mmHg. After weaning from CPB, all hearts resumed normal beating spontaneously. There were no statistically significant differences in the water contents of tissues including brain among the three experimental groups. Conclusion: These results indicate (1) CPB can be reliably administered in rabbits if proper technique is used, (2) the effect of steroid on the protection of brain edema related to Trendelenburg position during CA is not established within the scope of this experiment.

• Journal of Chest Surgery
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• v.13 no.4
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• pp.321-337
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• 1980

The increasing use of cardioplegic solution for the reduction of ischemic tissue injury requires that all cardiplegic solution be carefully assessed for any protective or damaging properties. This study describes functional, enzymatic and structural assessment of the efficiency of three cardioplegic solutions (Young & GIK, Bretschneider, and $K^{+}$ Albumin solution) in a Modified Isolated Rat Heart Model of cardiopulmonary bypass and ischemic arrest. Isolated rat heart were subjected to a 2-minute period of coronary infusion with a cold cardioplegic or a noncardioplegic solution immediately before and also at the midpoint of a 60-minute period of hypothermic ($10{\pm}1$. C) ischemic cardiac arrest. The results of this study were as follow: 1. Spontaneous heart beat after ischemic arrest occured 16 seconds later after Langendorff reperfusion in the Young & GIK group (n=6), and 40 second later in the Bretschneider group (n=6) and 6 minute later in the $K^{+}$ Albumin group (n=6), and 16 minute later in the control group (non-cardioplegia). A good recovery state of spontaneous heart beat was shown in the Young & GIK and Bretschneider groups. 2. The percentage of recorveries of heart function at 30 minute after postischemic working heart perfusion were : heart rate $91.6{\pm}3.1$% (P<0.01)m oeaj airtuc oressyre $83{\pm}3$% (P<0.01), coronary flow $70{\pm}8$% (P<0.05) and aortic flow flow rate $39{\pm}9.3$% (P<0.05) in the Young & GIK group. This percentage of recoveries of the Young & GIK group was significantly greater than the control group. In the Bretschneider group, the percentage of recoveries were : heart rate $87.8{\pm}7.5$%(P<0.05), peak aortic pressure $71{\pm}2.3$% (P<0.05) and aortic flow rate $33.2{\pm}6.6$%(P<0.05). hte percentage of recoveries were significantly greater than in the control group. In the $K^{+}$ Albumin group, recoveries of heart function were poor. 3. Total CPK leakage was $131.2{\pm}12.75$IU/30 min/gm. dry weight in the control group, $50.65{\pm}12.75$IU in the Young & GIK gruop, $69.40{\pm}32.21$Iu in Bretschneider group, and $103.65{\pm}15.47$IU in the $K^{+}$ Albumin group during the 30 minute postischemic Langendorff reperfusion. Total CPK leakage was significantly less (P<0.001) in the Young & GIK group, than in the control group. 4. Direct correlatin between percentage recovery of aortic flow rate and total amount of CPK leakage from Myocardium was noticed.(Correlation Coefficient r = 0.76, P<0.001). 5. Mild perivascular edema was the only finding of light microscopic study of myocardium after 60 minute ischemic arrest with cold cardioplegic solutions and hypothermla.

• Journal of Chest Surgery
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• v.36 no.12
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• pp.970-974
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• 2003

There has been an improvement in the prognosis of tumor thrombi invading the inferior vena cava(IVC) and the right atrium(RA) of renal cell carcinoma with radical nephrectomy and tumor thrombectomy with the aid of cardiopulmonary bypass in the last 10 years. A 30 year old woman was diagnosed with right renal tumor with tumor thrombi invading the right renal vein and the IVC above the right renal vein to the RA. She received radical nephrectomy and removal of tumor thrombi in the infrarenal IVC under hypothermic total circulatory arrest using the cardiopulmonary bypass. The tumor recurred 12 months after the initial operation, she received a second operation for tumor removal from the retroperitoneum, suprarenal IVC, and RA. She died 11 months after the second operation due to lung metastases and recurred hepatic vein tumor extended to the RA and right ventricle.

• Journal of Chest Surgery
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• v.37 no.9
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• pp.774-780
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• 2004

Although traumatic thoracic aortic rupture is potentially a fatal condition requiring surgical attention, the presence of concomitant injury involving other parts of the body may greatly increase the risk of cardio-pulmonary bypass. We report our experience of treating associated injuries prior to the thoracic aortic rupture in these patients. Material and Method: From 1997 to 2003, the medical records of 24 traumatic aortic rupture patients were retrospectively reviewed and checked for the presence of associated injury, surgical method, postoperative course, and complications. Surgical technique comprised thoracotomy with proximal anastomosis under deep hypothermic circulatory arrest followed by side arm perfusion to reestablish cerebral circulation. CSF drainage was performed to prevent lower extremity paraplegia. Result： Major concomitant injuries (n=83) were noted in all of the reviewed patients, Of these, there were 49 thoracic injuries, 18 musculoskeletal injuries, and 13 abdominal injuries, Operations for associated injuries (n=16) were performed in 12 patients on mean 7.6$\pm$12.6 days following the injury. The diagnosis of aortic rupture at the time of injury was detected in only 18 patients. Delayed surgery of the thoracic aorta was performed on average 695$\pm$1350 days after injury and there were no deaths or progression of rupture in any of these patients during the observation period. There were no operative deaths and no major postoperative complications. Conclusion: Treating concomitant major injuries prior to the aortic injury in traumatic aortic rupture may reduce surgical mortality and morbidity.

• Journal of Korean Neurosurgical Society
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• v.29 no.2
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• pp.167-179
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• 2000

Objective : We studied to clarify the effective time zone of mild hypothermic neural protection during ischemia and/or reperfusion after middle cerebral artery occlusion. Methods : In a reversible cerebral infarct model which maintained reperfusion of blood flow after middle cerebral artery occlusion for two hours, the size of cerebral infarction, cerebral edema and the extent of neurological deficit were observed and analyzed for comparison between the control and the experimental groups under hypothermia($33.5^{\circ}C$). The temporalis muscle temperature was reduced to $33.5^{\circ}C$ by surface cooling for two hours during middle cerebral artery occlusion for study group I. The following groups applied hypothermia for two-hour periods after reperfusion : group II(0-2 hours), group III(2-4 hours), and group IV(4-6 hours). They were rewarmed to $36.5^{\circ}C$ until sacrified at 2, 4, 6, 12, and 24 hours after reperfusion. Control group was maintained at normothermia without hypothermia. Results : In the experimental groups with hypothermia, the average value of the size of cerebral infarction($mean{\pm}SD$) was $1.97{\pm}1.65%$, which was a remarkable reduction over that of the control, $4.93{\pm}3.79%$. In the control, a progressive increase was shown in the size of infarction from point of reperfusion to 6 hours after reperfusion without further changes in size afterward. Intra-ischemic hypothermia(group I) prevented ischemic injury but did not prevent reperfusion injury. Group II examplified the most neural protective effect in comparison to the control group and group IV(p<0.05). The cortex was more vulnerable to reperfusion injury than the subcortex. Mild hypothermia showed more neural protective effects on the cortex than subcortex. Conclusion : The most appropriate time zone for application of mild hypothermia was defined to be within four hours following reperfusion.

• Journal of Chest Surgery
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• v.30 no.3
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• pp.253-253
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• 1997

Hypothermia during lung preservation decreases metabolic processes. After the rabbit lung was flushed with modified Euro-Collins solution, heart-lung block was harvested and the left lung was assessed after ligation of the right pulmonary artery and right main-stem bronchus. Heart-lung block was immersed in the same solution for 6 hours. The modified Euro-Collins solution and storage temperature of group 1(10 cases) was 4t, roup 2(10 cases) was l0℃. On completion of the storage period, the left lung was ventilated and reperfused with blood u:high used a cross-circulating paracorporeal rabbit as a "biologic deoxygenator" for 60 minutes. Pulmonary artery pressure, airway pressure, difference in oxygen tension between mow and outflow perfusate and degree of pulmonary edema were assessed at 10-minute intervals while the left lung was ventilated at 0.8 of the inspired oxygen fraction. The mean pulmonary venous oxygen tensions at 10 and 60 minutes after reperfusion were 209.52±42.46 and 103.48± 15.96 mmHg in group I versus 247.78±36.19 and 147.91 ± 11.07 mmHg in group II(p=0.049, (0.0001). The mean alveolar-arterial oxygen differences at 20 and 60 minutes after reperfusion were 357. 95± 12.84 and 437.31 14.26 mmHg in group I versus 310.88±3).47 and )90.93± 15.86 mmHg in group II (p=0.0092, (0.0001). The mean pulmonary arterial pressures at 10 and 60 minutes after reperfusion were 40.56± 18.66 and 87. 2± 17.22 mmHg in group I versus 31.22±6.84 and 65.78± 11.02 mmHg in group rl (p : 0.048, 0.0062). The mean pulmonary vascular resistances at 10 and 60 minutes after reperfusion were 2.69±0.85 and 4.36±0.86 mmHg/ml/min in group I versus 1.99±0.39 and 3.29±0.55 mmHg/ml/min in group II(p : 0.0323, 0.0062). There were no difference between groups in peak airway pressure, lung compliance and degree of pulmonary edema. In conclusion that preservation of lung at l0℃ was superior to preservation at 4℃.

• Journal of Chest Surgery
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• v.31 no.12
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• pp.1226-1229
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• 1998

50 days old, 4.5kg male patient was admitted at department of pediatrics due to congenital heart disease with congestive heart failure. The echocardiographic finding was perimembranous type ventricular septal defect. The patient underwent open heart surgery for patch closure of VSD. Immediately postoperatively, junctional ectopic tachycardia developed and the patient was in hemodynamically unstable state with decreased urine output. We used inotropics, digitalis and diuretics, however these treatments were not effective in recovering the unstable state. Therefore, we tried a mild hypothermic treatment(34℃). During the POD #2, mild hypothermia method was repeated four times. The junctional ectopic tachycardia was converted to normal sinus rhythm, hemodynamic state was stable, and urine output was increased. The patient was discharged at POD #8.