Kim, Jae-Do;Kim, Sang-Jin;Jung, Cheoul-Yun;Hong, Young-Gi;Kim, Ghi-Chan
The Journal of the Korean bone and joint tumor society
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v.3
no.2
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pp.80-88
/
1997
Malignant tumors of extremeties involving major neurovascular structures have been treated by amputation. However recent development of diagnostic tools(CT, MRI etc.), surgical techniques, anticancer chemotherapeutic agents, and radiation techniques allow surgeons to treat malignant tumors in the limb without amputation. It has been reported that a local application of low-heat to the tissue with tumor can kill tumor cells. It is, however, not known if the attendant neural and vascular injuries may be recovered. The present study was, therefore, undertakn to address this question in rabbit sciatic nerves. A low-heat injury to the sciatic nerve was induced by perfusing the nerve with $60^{\circ}C$ saline for 30 minutes and the courses of functional and morphological recovery of the nerve were evaluated for 16 weeks. The results are summerized as follows : 1. In the electromyographic nerve conduction test the average amplitude was markedly attenuated at 4 and 8 weeks after the low-heat treatment, but it progressively increased to the level 89.5% of the control at 16 week post-treatment. The average latency in the control group was 0.62 msec. The latency in the experimental group was much longer than this at 4 and 8 week post-treatment, but it progressively reverted to the control level, showing 0.622 msec at 16 weeks. 2. In the needle EMG, many fibrillation potentials and positive sharp waves were appeared until 8 weeks post-treatment. After 16 weeks, however, no fibrillation potential was observed. 3. In the early phase of post-treatment period, the myelinated nerve fibers contained many vacuoles and the number of myelinated nerve fibers appeared to be considerably reduced. However, as time goes myelinated nerve fibers were regenerated, such that after 16 weeks the histologic appearance of the nerve was similar to that of the control group.
Objectives : Hypothyroidism is a relatively common endocrinologic disease, especially among older women. Western medical doctors treat hypothyroidism with levothyroxine, however there are several side effects, including thyrotoxicosis, atrial fibrillation, osteoporosis, etc. Therefore, traditional Korean medicine(TKM) offers an appealing alternative therapy for hypothyroidism. In this study, Cuscuta Semen was used to analyze its possible effect on a hypothyroidism rat model induced by propylthiouracil(PTU). Methods : 24 two-month-old Sprague-Dawley(SD) rats were divided into 4 groups: normal (n=6), PTU-induced hypothyroidism control(n=6), hypothyroidism rat treated with Cuscuta Semen (n=6), and hypothyroidism rat treated with levothyroxine(n=6). PTU was administered for 4 weeks, Cuscuta Semen and levothyroxine was administered 2 weeks after PTU was initiated for a total duration of 2 weeks. Blood samples from all the rats were taken from their hearts and analyzed. Results : When compared to the normal group, the PTU-induced control group showed significantly lower $T_4$, $T_3$ levels and significantly higher TSH level, which is indicative of hypothyroidism. The Cuscuta Semen group had significantly higher $T_4$ and significantly lower TSH than the control group(p<0.05). There was no significant difference in biochemical labs and weight between the Cuscuta Semen and control groups. Conclusions : These results suggest that Cuscuta Semen could be effective in increasing thyroid hormone production, and be powerful enough to affect the hypothalamus-pituitary-thyroid axis. Also, no adverse effects related with Cuscuta Semen were found, suggesting that it is relatively safe to administer. In conclusion, it seems that Cuscuta Semen is a safe alternative medicine for hypothyroidism.
The aim of this study was to explore the role of IL-6-miR-210 in the regulation of Tregs function and atrial fibrosis in atrial fibrillation (AF). The levels of interleukin (IL)-6 and IL-10 in AF patients were detected by using ELISA. Proportions of Treg cells were detected by fluorescence activated cell sorting analysis in AF patients. The expression of Foxp3, α-SMA, collagen I and collagen III were determined by western blot. The atrial mechanocytes were authenticated by vimentin immunostaining. The expression of miR-210 was performed by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was used to predict potential targets of miR-210. The cardiomyocyte transverse sections in AF model group were observed by H&E staining. The myocardial filaments were observed by masson staining. The level of IL-6 was highly increased while the level of IL-10 (Tregs) was significantly decreased in AF patients as compared to normal control subjects, and IL-6 suppressed Tregs function and promoted the expression of α-SMA, collagen I and collagen III. Furthermore, miR-210 regulated Tregs function by targeting Foxp3, and IL-6 promoted expression of miR-210 via regulating hypoxia inducible factor-1α (HIF-1α). IL-6-miR-210 suppresses regulatory T cell function and promotes atrial fibrosis by targeting Foxp3.
There appears some conduction defects frequently after total correction of Tetralogy of Fallot. Common defect is right bundle branch block due to surgical intervention. We experienced complete A-V block which occured 3 months later after total correction of Tetralogy of Fallot in a 8 year old boy. The patient was completely free of any A-V block after the operation for 3 months, and sudden onset of A-V block with coupled premature ventricular contractions resulted him in shock state during the attack of severe bronchopneumonia for 4 days prior to the second visit. Emergency implantation of Cordis demand type temporary pacemaker was necessary to control the complete heart block with bradyarrhythmia and frequent ventricular fibrillation. Permanent cardiac pacemaker was implanted two weeks later as indicated with Cordis Stanicor lambda demand pacemaker, and the patient was discharged uneventfully on the 8th post implantation day with the heart rate of 72/min. Another 3 months after the implantation, the patient was transported to this hospital as dead on arrival after an accidental fall from a 2 meter height, and all possible cardiopulmonary resuscitation was performed for 60 minutes at the emergency room in vain. Autopsy was done to find out the cause of sudden death and the etiology of complete heart block. Microscopic focal infarctions with scar formation were noted along the course of conduction system in the interventricular septum, which might be the main cause of complete heart block during the attack of severe bronchopneumonia complicated with acute bacterial endocarditis. The tip of the pacemaker wire was slipped from the granulation scar at the apex of the right ventricular cavity, and this might be the direct cause of pacing failure and death.
Proceedings of the Korean Society of Applied Pharmacology
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2003.11a
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pp.112-112
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2003
Voltage-gated $K^{+}$ (Kv) channels represent a structurally and functionally diverse group of membrane proteins. These channels play an important role in determining the length of the cardiac action potential and are the targets for antiarrhythmic drugs. Many $K^{+}$ channel genes have been cloned from human myocardium and functionally contribute to its electrical activity. One of these channels, Kv1.5, is one of the more cardiovascular-specific $K^{+}$ channel isoforms identified to date and forms the molecular basis for an ultra-rapid delayed rectifier $K^{+}$ current found in human atrium. Thus, the blocker of hKv1.5 is expected to be an ideal antiarrhythmic drug for atrial fibrillation. Chelidonine was isolated from Chelidonium majus L. We examined the effect of chelidonine on the hKv1.5 current expressed in Ltk-cells using whole cell mode of patch clamp techniques. Chelidonine selectively inhibited the hKv1.5 current expressed in Ltk-cells in a concentration-dependent manner, whereas did not affect the HERG current expressed in HEK-293 cells. Additionally, chelidonine reduced the tail current amplitude recorded at -50 mV after 250 ms depolarizing pulses to +60 mV, and slowed the deactivation time course resulting in a 'crossover' phenomenon when the tail currents recorded under control conditions and in the presence of chelidonine were superimposed. We found that chelidonine also inhibited the $K^{+}$ current in isolated human atrial myocytes where hKv1.5 channels were predominantly expressed. Furthermore, we examined the effects of chelidonine on the action potentials in rabbit hearts using conventional microelectrode technique. Chelidonine prolonged the action potential durations (APD) of atrial, ventricular myocytes and Purkinje fibers in a dose-dependent manner. However, the effect of chelidonine on atrial APD was frequency-dependent whereas the effect of chelidonine on the APDs of ventricular myocytes and Purkinje fibers was not frequency- dependent. Also, the selective action of chelidonine on heart was more potent than dofetilide, $K^{+}$ channel blocker.
For the induction of arthropathy, 5% hydrogen peroxide($H_2O_2$) was injected for 5 weeks into the intraarticular space of the New Zealand white rabbits to damage articular cartilage. Alginic acid of low molecular weight (2%) made from macromolecular alginate treated with enzyme was administered into articular space at the dose of 5 mg/kg twice a week for 3 and 6 weeks using 1 ml syringe and 26 G needle. Saline was injected for the control. Tissues surrounding the articulation were obtained for the measurements of superoxide dismutase(SOD) activity as a major antioxidant enzyme and malondialdehyde (MDA) as a lipid peroxidation level. Histopathologic examination on the surface of articular cartilage was carried out. Data showed that injection of hydrogen peroxide for 5 weeks had led to the induction of free radical damage and of articular cartilage change as confirmed by microscopic observation. The application of hydrogen peroxide caused a gradual increase in the SODs and MDA. These patterns were similar after 3 and 6 weeks of alginate treatment. Furthermore, microscopic examinations revealed that hydrogen peroxide caused flaking, fibrillation, fissuring, denudation, and hypocellularity in the articular surfaces. In conclusion, lipid peroxidation was demonstrated in the articular cartilage by the administration of hydrogen peroxide in the rabbit model. This lipid peroxidation could be caused by oxygen free radicals. The histologic and enzymatic correlations on lipid peroxidation in the articulation have provided a better understanding of arthropathy. It is possible to take advantage of these findings to evaluate effective alginate dosage more efficiently.
To evaluate the effect of oxygenation[95% O2+5% CO2] of St. Thomas Hospital No.2 cardioplegic solution[Plegisol], 20 isolated perfused rat hearts were studied under hyp-othermic[20oC] ischemic arrest for 2 hours with infusion of cardioplegic solution every 30 minutes throughout the ischemic period. Ten isolated hearts were studied with the oxygenated cardioplegic solution and 10 another isolated hearts with the nonoxygenated one. Mean oxygen tensions of the nonoxygenated and oxygenated cardioplegic solutions were 150mmHg and 470mmHg, respectively. Two in 10 hearts infused with the nonaxygenated cardioplegic solution were not recovered from nonworking heart due to persistent ventricular fibrillation. In comparing hem-odynamic parameters between both groups, the mean postischemic recovery[expressed as a percentage of its preischemic control value] was significantly greater with the oxygenated solution[in 10 recovered hearts] than the nonoxygenated solution[in 8 recovered hearts] [95.9$\pm$1.8% compared with 88.5$\pm$2.9% in peak aortic pressure, p<0.05, 75.7$\pm$5.2% compared with 43.5$\pm$6.5% in aortic flow, p<0.01, 75.5$\pm$4.6% compared with 54.1$\pm$5.6% in cardiac output, p<0.01, 78.3$\pm$4.6% compared with 60.3$\pm$4.6% compared with 60.3$\pm$6.2% in stroke volume, p<0.05, and 80.4$\pm$5.3% compared with 58.6$\pm$7.0% in dP/dT, p<0.05]. It is concluded that oxygenation of St. Thomas Hospital No.2 cardioplegic solution improves cardiac electrical stability and postischemic hemodynamic recovery after ischemic arrest in the isolated perfused rat heart.
Muhammad Ali Tariq;Minhail Khalid Malik;Qazi Shurjeel Uddin;Zahabia Altaf;Mariam Zafar
Journal of Chest Surgery
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v.56
no.6
/
pp.374-386
/
2023
Background: The heightened morbidity and mortality associated with repeat cardiac surgery are well documented. Redo median sternotomy (MS) and minimally invasive valve surgery are options for patients with prior cardiac surgery who require mitral valve surgery (MVS). We conducted a systematic review and meta-analysis comparing the outcomes of redo MS and minimally invasive MVS (MIMVS) in this population. Methods: We searched PubMed, EMBASE, and Scopus for studies comparing outcomes of redo MS and MIMVS for MVS. To calculate risk ratios (RRs) for binary outcomes and weighted mean differences (MDs) for continuous data, we employed a random-effects model. Results: We included 12 retrospective observational studies, comprising 4157 participants (675 for MIMVS; 3482 for redo MS). Reductions in mortality (RR, 0.54; 95% confidence interval [CI], 0.37-0.80), length of hospital stay (MD, -4.23; 95% CI, -5.77 to -2.68), length of intensive care unit (ICU) stay (MD, -2.02; 95% CI, -3.17 to -0.88), and new-onset acute kidney injury (AKI) risk (odds ratio, 0.34; 95% CI, 0.19 to 0.61) were statistically significant and favored MIMVS (p<0.05). No significant differences were observed in aortic cross-clamp time, cardiopulmonary bypass time, or risk of perioperative stroke, new-onset atrial fibrillation, surgical site infection, or reoperation for bleeding (p>0.05). Conclusion: The current literature, which primarily consists of retrospective comparisons, underscores certain benefits of MIMVS over redo MS. These include decreased mortality, shorter hospital and ICU stays, and reduced AKI risk. Given the lack of high-quality evidence, prospective randomized control trials with adequate power are necessary to investigate long-term outcomes.
Twenty white rabbits anesthetized with nembutal (30 mg/kg) were employed in this experiment. Five of them served as controls; the remaining rabbits as experimental group were subjected to irreversible hemorrhagic shock. Shock was induced by bleeding the animals until mean blood pressure decreased to a level of 50-40 mmHg. This level of pressure was maintained for 3-4 hours, after which the drawn blood was reinfused. The reinfusion of blood caused the elevation of arterial pressure almost the control level for some minutes, after which a gradual and progressive decline of blood pressure became evident. This decline was thought to be the result from irreversible hemorrhagic shock. When mean blood pressure declined to less than 50 mmHg, chest was opened and samples of arterial blood and left ventricular muscle were taken. Left ventricular muscle and blood plasma were analyzed for potassium, sodium, chloride and water content. Blood glucose concentration was determined by Somogyi-Nelson's method. Extracellular and intracellular myocardial water and electrolyte content were calculated on the basis that electrolytes are distributed between plasma water and interstitial water according to Gibbs-Donnan equilibrium. In this calculation extracellular water was substituted for Na space. The findings obtained were as follows: 1. The concentration of blood glucose was 87mg% in the controls and it rose to 222 mg% in shock (P<0.01). 2. Plasma potassium elevated significantly from 3.3 mEq/l in controls to 8.0 mEq/l in shock (P<0.01), while small decreases in sodium (151-146 mEq/l) and chloride (102-96 mEq/l) were observed (P<0.3, P<0.1), 3. The changes of blood water content (83.1-84.3%) and cardiac water content (77.5-78.3 gm/100gm WT) were observed. 4. In control animals myocardial potassium levels which averaged 30.2 mEq/100 gmDT rose significantly to 40.3 mEq/100 gmDT in shock (P<0.01), while moderate decreases in sodium(16.3-14.3 mEq/100 gmDT) were observed in shock. 5. The calculated transmembrane resting potential of left ventricular muscle of control animals averaged 95 mV, while rabbits in shock averaged 77 mV. (P <0.01). The findings of this experiment do not correspond with the conclusions that myocardial depression seems to be the cause of irreversible hemorrhagic shock, because the excitability of heart muscle is elevated. From the point of view that the lowered transmembrane resting potential, the cause of death in terminal stage of irreversible hemorrhagic shock may be ventricular fibrillation. It can't be said, however, that the lowered transmembrane resting potential is responsible for the transition from reversible to irreversible hemorrhagic shock. The marked increase in blood glucose suggested that glycogenolysis in the liver is favorably active in shock.
Park, Jeong-Hyun;Im, Hee-Kyung;Kim, Jee-Hee;Lee, Young-Il
The Korean Journal of Emergency Medical Services
/
v.20
no.2
/
pp.7-19
/
2016
Purpose: To investigate the effect of early hypothermia on post-resuscitation myocardial recovery and survival time after cardiac arrest and resuscitation in a rat model of myocardial infarction(MI). Methods: Thoracotomies were performed in 10 male Sprague Dawley rats weighing 450-455g. Myocardial infarction was induced by ligation of the left anterior descending coronary artery. Ninety minutes after arterial ligation, ventricular fibrillation was induced, cardiopulmonary resuscitation was subsequently performed before defibrillation was attempted. Animals were randomized to control group and experimental group(acute MI-normothermia)($32^{\circ}C$ for 4 hours). Duration of survival was recorded. Myocardial functions, including cardiac output, left ventricular ejection fraction, and myocardial performance index were measured using echocardiography. Results: Myocardial function was significantly better in hypothermia group than the control group during the first 4 hours post-resuscitation. The survival time of the experimental group was greater than that of the control group(p<.050). Conclusion: This study suggests that early hypothermia can attenuate post-resuscitation myocardial dysfunction after acute myocardial function, and may be a useful strategy in post-resuscitation care.
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