In this study, the effects of tauroursodeoxycholic acid (TUDCA) on ischemia/ reperfusion injury were investigated on isolated heart perfusion models. Hezrts were perfused with oxygenated Krebs-henseleit solution (pH 7.4, $37^{\cire}C$) on a Langendorff apparatus. After equilibration, isolated hearts were treated with TUDCA 100 and 200 $\mu\textrm{M}$ or vehicle (0.02% DMSO) for 10 min before the onset of ischemia in single treatment group. In 7 day pretreatment group. TUDCA 50, 100 and 200 mg/kg body weight were given orally for 7 days before operation. After global ischemia (30 min), ischemic hearts were reperfused for 30 min. The physiological (i.e. heart rate, left ventricdular developed pressure, coronary flow, double product, time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 810 sec during ischemia, LVDP was 34.0 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 34.3 U/L. Single treatment with TUDCA did not change the postischemic recovery of cardiac function, LDH and time to contractur compared with ischemic control group. TUDCA pretreatment showed the tendency to decrease LDH release and to increase time to contracture and coronary flow. Our findings suggest that TUDCA does not ameliorate ischemia/reperfusion-reduced myocardial damage.
Amlodipine, a calcium channel blocker of the dihydropyridine group, is commonly used in management of hypertension, angina, and myocardial infarction. Amlodipine overdose, characterized by severe hypotension, arrythmias, and pulmonary edema, has seldom been reported in Korean literature. We report on a fatal case of amlodipine intoxication with complications including rhabdomyolysis and oliguric acute kidney injury. A 70-year-old woman with a medical history of hypertension was presented at the author's hospital 6 hours after ingestion of 50 amlodipine (norvasc) tablets (total dosage 250 mg) in an attempted suicide. Her laboratory tests showed a serum creatinine level of 2.5 mg/dL, with elevated serum creatine phosphokinase and myoglobin. The patient was initially treated with fluids, alkali, calcium gluconate, glucagon, and vasopressors without a hemodynamic effect. High-dose insulin therapy was also started with a bolus injection of regular insulin (RI), followed by continuous infusion of RI and 50% dextrose with water. Despite intensive treatment including insulin therapy, inotropics, mechanical ventilation, and continuous venovenous hemodiafiltration, the patient died of refractory shock and cardiac arrest with no signs of renal recovery 116 hours after her hospital admission.
A clinical analysis was performed on 97 cases of chest injuries experienced at Department of Thoracic and cardiovascular Surgery, Armed Forces Capital Hospital during 2 years period from 1986 to 1988. Of 97 patients of chest trauma, 39 cases were result from penetrating injuries whereas 58 cases were from non-penetrating injuries, and there were 77 cases of hemothorax and / or pneumothorax, 47 of rib fracture, 8 of foreign body, 6 scapular and clavicle fracture, 5 of diaphragmatic injuries, 4 of paraplegia. The majority of chest injuries were encounted in the age group between 21 and 30 years-old, mean age was 25.9 years-old and all cases were male except one. Gun-shot wound was the most common cause in the penetrating injuries and the majority of non-penetrating chest injury patients were traffic accident and fist or kick accounted for next. The principles of therapy for chest trauma were rapid expansion of the lung by closed thoracostomy[45 cases] and thoracentesis only[3 cases] but thoracotomy done at 27 cases because of massive bleeding or intrapleural hematoma, foreign body, cardiac injury, diaphragmatic injury and bronchial rupture. The over-all mortality was 2.07 percent[2 cases among all], a case was from penetrating injuries and another was from non-penetrating injuries.
Purpose: Arterial injury in children is a challenging problem for its special characteristics. It is rare even during warfare. This review described a personal experience in the management and outcome of acute pediatric arterial injuries of extremities. Methods: Thirty-six children below age of 13 years were studied during period from 2004 through 2014 in Iraq. Results: Male patients were 27 (75%) and female were 9 (25%). Seven to twelve years old was the most affected age group. The incidence of iatrogenic injuries was greater in infants and toddlers while penetrating injuries were the most common in older children. Upper limbs arteries were affected in 17 (47.2%) and lower limb in 19 (52.8%) patients. Hard signs were the commonest mode of presentation (83.3%). Lateral wall tear and complete transection were the most frequent types of arterial injury (36.1% and 27.8% respectively). The most frequent procedures performed were end-to-end anastomosis and lateral arteriorrhaphy. Surgical outcome was good. In 27 cases distal pulsations were regained. Seven cases had impalpable distal pulses but still viable limbs. Limb length discrepancy was detected in one case. One case was complicated with limb loss. No death was recorded. Conclusion: Arterial injuries in children are age related. The proper treatment of arterial injuries in children requires high index of suspicion, early operative intervention and continuous postoperative follow-up throughout years of active growth. Angiogram has a limited role as a diagnostic tool in acute arterial injuries.
In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.
Chung, Eui Suk;Lee, Jae Hoon;Seo, Jong Kwon;Kim, Byung Gyu;Kim, Gwang Sil;Lee, Hye Young;Byun, Young Sup;Kim, Hyun Jung
Journal of Yeungnam Medical Science
/
v.37
no.4
/
pp.345-348
/
2020
Papillary fibroelastomas are the second most common primary cardiac tumor in adults. Over 80% of fibroelastomas occur on the cardiac valves, usually on the left side of the heart, while the remaining lesions are typically scattered throughout the atria and ventricles. Although the optimal timing for surgery is controversial and depends on tumor size and location, prompt surgical resection is warranted in patients at high risk of embolism. A tumor on the cardiac valve can be removed using the slicing excision technique without leaflet injury. Here we present two cases of papillary fibroelastomas occurring on the ventricular surface of the aortic valve and in the right ventricle.
A clinical evaluation was performed on 11 cases of the cardiac rupture by blunt chest trauma at the department of thoracic and cardiovascular surgery, Yeungnam University Hospital during the period from July, 1993 to May, 1995. The results were as follows ; The sex distribution was 8 mem and one women, and mean age was 41 years old. The causes of accident was traffic accident in most cases. And then one case was cultivator accident and another one was fall down. The average times from trauma to admission was 139 minutes and the patients that transferred via other hospitals have relatively long average times to 227 minutes. The average times from admission to operation was 117 minutes and we consumed 25 minutes for the preoperative preparation. The sites of injury were 7 cases in the right heart and 3 cases in the left heart. There were symptoms and signs of the cardiac tamponade(dyspnea, chest pain, nausea/vomitus, neck vein distention & hypovolemic shock) at admission and in most of them typical symptoms and signs of a tamponade appeared. Surgical approach was performed with median sternotomy in 10 cases. Subxiphoid pericardial window was created in one case. Another case which was very difficult in surgical procedure was operated under cardiopulmonary bypass and the result was good.
An in vitro model for ischemia/reperfusion injury has not been well-established. We hypothesized that this failure may be caused by serum deprivation, the use of glutamine-containing media, and absence of acidosis. Cell viability of H9c2 cells was significantly decreased by serum deprivation. In this condition, reperfusion damage was not observed even after simulating severe ischemia. However, when cells were cultured under 10% dialyzed FBS, cell viability was less affected compared to cells cultured under serum deprivation and reperfusion damage was observed after hypoxia for 24 h. Reperfusion damage after glucose or glutamine deprivation under hypoxia was not significantly different from that after hypoxia only. However, with both glucose and glutamine deprivation, reperfusion damage was significantly increased. After hypoxia with lactic acidosis, reperfusion damage was comparable with that after hypoxia with glucose and glutamine deprivation. Although high-passage H9c2 cells were more resistant to reperfusion damage than low-passage cells, reperfusion damage was observed especially after hypoxia and acidosis with glucose and glutamine deprivation. Cell death induced by reperfusion after hypoxia with acidosis was not prevented by apoptosis, autophagy, or necroptosis inhibitors, but significantly decreased by ferrostatin-1, a ferroptosis inhibitor, and deferoxamine, an iron chelator. These data suggested that in our SIR model, cell death due to reperfusion injury is likely to occur via ferroptosis, which is related with ischemia/reperfusion-induced cell death in vivo. In conclusion, we established an optimal reperfusion injury model, in which ferroptotic cell death occurred by hypoxia and acidosis with or without glucose/glutamine deprivation under 10% dialyzed FBS.
Aprotinin, a serine protease inhibitor, has been used to ameliorate the inevitable consequences, including blood component injury after cardiac surgery with cardiopulmonary bypass (CPB). However, there are many arguments on its dosage or usage. We assessed whether administration of low dose of aprotinin in only priming solution has any beneficial effect or reduces its side effects on cardiac surgery. Thirty patients scheduled for elective cardiac surgery were randomly assigned to aprotinin group (n=15) which received aprotinin in priming solution (two million kallikrein inhibitory unit, KIU) and added one million KIU at 1 hour after the beginning of CPB or control group (n=15) which did not receive it. Hematological and biochemical variables, cytokines and cardiac marker levels, and postoperative outcomes were compared between two groups at before, during or after operation. Platelet count in aprotinin group was higher than that of control group at postoperative 24 hr. Activated partial thromboplastin time in aprotinin group was longer than that of control group at intensive care unit (ICU). Troponin-I level and postoperative blood loss volumes in aprotinin group were lower than those of control group at ICU. There were no significant differences between the two groups on the others. These results showed that low dosage of only priming solution during cardiac surgery with CPB reduced platelet destruction and postoperative bleeding, and attenuates myocardial damage. However, further studies need to be carried out with more population or pediatric patients for evaluating various aprotinin usage.
Panax Ginseng C.A. Meyer has been known for hundreds of years as the most valuable drug having mysterious effects among all the herbal medicines and plants in Korea. Also, many experimental studies have been performed recently that the various effects were identified and applied clinically. So we attempted an experimental study on the effect of ginsenoside Rg1 mixtures in an isolated rat heart with the use of the Langendorff model. The objective of this study was to determine whether this ginsenoside Rg1 mixtures would protect the myocardial injury after ischemic arrest and reperfusion. Isolated rat hearts were allowed to equilibrate for 20 minutes and were then subjected to 15 minutes of normothermic ischemia. After this ischemic period, isolated rat hearts were allowed to reperfusion for 10 minutes(Ischemic Group). In other group , isolated rat hearts were perfused for 60 minutes continuously with normothermia( Normothermic Group). Hemodynamic and biochemical parameters such as heart rate, left ventricular pressure, +dp/dt max, coronary blood flow and cardiac enzymes were measured during initial perfusion, ischemia, reperfusion period (Ischemic group) and 20, 40 and 60 minutes after continuous perfusion(Normothermic group). After completion of the experiment, this data was evaluated and the following results were obtained. 1. Heart rates showed an increase in both ischemic and normothermic experimental groups, but statistically significant differences were not identified. 2. LVP(Left Ventricular Pressure) showed statistically significant differences in both ischemic and normothermic experimental groups(p<0.005, p<0.01). 3. +dp/dt max showed statistically significant differences in both ischemic and normothermic experimental groups(p<0.01, p<0.01). 4. There were no statistically significant differences in coronary blood flow and cardiac cenzymes in all groups, but experimental groups seemed to have better protection and recovery. These results suggest that ginsenoside Rg1 mixtures has a protective effect on the myocardial injury after ischemia and reperfusion.
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