• 대한한의학회지
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• 제18권1호
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• pp.456-469
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• 1997

The cerebral infarction arised from occulsion of cerebral artery has a high mortality rate and fatal sequelae. Sohabhyangwon(蘇合香元) is generally regarded to have a effect of walking up the patient from unconsiousness and promoting the flow of Qj(氣) by warming channel. METHOD The purpose of this study is to find out the effections of Sohabhyangwon(蘇合香元) on regional cerebral blood flow and relative cerebral infarction area in the experimentally induced infartion in rats In this experiment, 12 Spraque-Dawley rats weighting 280-350g were used. Cerebral ischemia induced by intraluminal suture technique of Kozumi's and Zea-Longer's method. $Co_{2},\;O_2$, pH, arterial blood pressure in rats were checked by Blood Gas Analyzer every 30 minutes for 2 hours. And regional cerebral blood flow were checking by hydrogen clearance technique, cerebral infarcted area was megsured by Image Analysis System. RESULTS 1. During the experiment, $CO_{2},\;O_2$, pH, arterial blood pressure in rats had no change in both sample group and control group. 2. Cortical cerebral blood flow decreased at same rate in both sample group and control group after inducing cerebral infarction. 3. On comparison of relative cerebral infarcted area, Sohabhyangwon(蘇合香元) perfused group showed a significant decrease. CONCLUSION According to the result above, Sohabhyangwon has a protection effect on cranial nerve and-has no effect on cerebral blood flow.

• Journal of Chest Surgery
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• 제54권1호
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• pp.9-16
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• 2021

Background: The deposition of monomeric C-reactive protein (mCRP) in the myocardium aggravates ischemia-reperfusion injury (IRI) and myocardial infarction. Ischemic preconditioning (IPC) is known to protect the myocardium against IRI. Methods: We evaluated the effects of IPC on myocardium upon which mCRP had been deposited due to IRI in a rat model. Myocardial IRI was induced via ligation of the coronary artery. Direct IPC was applied prior to IRI using multiple short direct occlusions of the coronary artery. CRP was infused intravenously after IRI. The study included sham (n=3), IRI-only (n=5), IRI+CRP (n=9), and IPC+IRI+CRP (n=6) groups. The infarcted area and the area at risk were assessed using Evans blue and 2,3,5-triphenyltetrazolium staining. Additionally, mCRP immunostaining and interleukin-6 (IL-6) mRNA reverse transcription-polymerase chain reaction were performed. Results: In the IRI+CRP group, the infarcted area and the area of mCRP deposition were greater, and the level of IL-6 mRNA expression was higher, than in the IRI-only group. However, in the IPC+IRI+CRP group relative to the IRI+CRP group, the relative areas of infarction (20% vs. 34%, respectively; p=0.079) and mCRP myocardial deposition (21% vs. 44%, respectively; p=0.026) were lower and IL-6 mRNA expression was higher (fold change: 407 vs. 326, respectively; p=0.376), although the difference in IL-6 mRNA expression was not statistically significant. Conclusion: IPC was associated with significantly decreased deposition of mCRP and with increased expression of IL-6 in myocardium damaged by IRI. The net cardioprotective effect of decreased mCRP deposition and increased IL-6 levels should be clarified in a further study.

• Journal of Chest Surgery
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• 제15권3호
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• pp.331-337
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• 1982

Complete TGA is a common congenital cardiovacular anomaly, and without palliative or corrective surgery, the infant born with TGA rarely survives the first year of life. Hemodynamically, recirculated blood flow in the systemic and pulmonary circuit has a key role in systemic arterial oxygen saturation and the status of the pulmonary vascular bed. Recently a d-TGA with VSD and PS, in a 12 year old male patient had been tried for inversion of the ventricular flow with Rastelli operation. An intracardiac tunnel was constructed between the VSD and the aortic orifice to connect the ventricle to the aorta. The right ventricle was connected with the pulmonary circulation by anastomosis of an valved conduit between the right ventricle and the distal end of the pulmonary artery. During the postop, period, the irreversible renal failure, accompanied by metabolic acidosis and pulmonary edema, occured under relative stabilized cardiac performance state. The autopsy was done, which revealed diffuse infarcted area in both kidney and preserved intra & extracardiac graft constructed.

• The Korean Journal of Physiology and Pharmacology
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• 제24권3호
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• pp.259-266
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• 2020

Cardiovascular diseases are the primary reason of mortality, among which myocardial infarction (MI) is the most dominant and prevalent. This study was considered to examine D-Limonene protective action against isoproterenol (ISO) induced MI. Wister male rats were dispersed into four groups. Normal and D-Limonene control group in which rats administered saline or D-Limonene. ISO control animals were administered saline for 21 days then challenged with ISO (85 mg/kg, subcutaneously) on 20th and 21st day for MI induction. D-Limonene pretreated group in which animals were pretreated with D-Limonene 50 mg/kg orally for 21 days then administered ISO on 20th and 21st day. MI prompted variations were assessed by myocardial infarction area determination, blood pressure (BP) alterations, cardiac injury biomarkers and inflammatory mediators measurements. For more depth investigation, both the apoptotic status was evaluated via measuring mRNA expression of Bcl-2 and Bax as well as mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) signal transduction were investigated via Western blotting. MI group revealed significant infarcted area, blood pressure alterations, myocardial injury enzymes intensification together with inflammatory cytokines amplification. MI was associated with activation of MAPK-ERK signal pathway and apoptotic status within the myocardium. On the other hand, pretreated with D-Limonene demonstrated deterred infracted area, reduced myocardial enzymes, improved BP indices, lessened inflammatory levels. Furthermore, D-Limonene pretreatment caused a decline in MAPK proteins pathway and Bax relative mRNA expression, while intensifying Bcl-2 mRNA expression promoting that D-Limonene may constrain MI induced myocardial apoptosis. D-Limonene mitigated MI injury through MAPK/NF-κB pathway inhibition and anti-apoptotic effect.