• Biomedical Science Letters
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• v.2 no.1
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• pp.71-90
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• 1996

There is considerable current interest in the effect of regular vigorous exercise and in particular endurance-running as a possible measure in improving myocardial function. Some data indicate that the aging heart may actually suffer from vigorous endurance exercise. On the contrary appropriate exercise in aged animals improves myocardial function and aerobic energy metabolism. So far there is relatively little data to indicate that endurance exercise is in fact beneficial in improving myocardial function or damaging to heart of aged animals. The present investigation aimed to study the possible effect of a long range treadmill training program on the heart in aging rats. Male rats aged 3, 10, and 20 months were divided at random into a control (sedentary) and an exercise group. The training group was exercised for 5 days a week on an automated treadmill for 20minutes at 18m/min over a period of 5 months. The exercise regimen of our experiments did not cause any significant changes in the tissues and ultrastructural as com-pared with sedentary age-matched control. Tissues and ultrastructures of myocardial cells in trained group aged 8 months are intact and well organized as well as sedentary control group. Age associated tissue and ultrastructural changes of trained group aged 15 months included : an increase in transformed mitochondria, vacuoles, lysosomes, lipid droplets and early lipofuscin. But the trained heart did not show significant difference in tissue and ultrastructural properties from those of sedentary controls. Endurance-trained group aged 25 months showed significant qualitative tissue and ultrastructural difference as compared with age-matched controls. In addition to those found in 25 months control group, focal necrosis, myofibril fraying, hypercontraction band, seperation of intercalated discs, degenerating nucleus and infiltration of collagenous fiber into myocyte were noted in trained 25 months group. The stereological examination of the mi-crographs disclosed no significant difference in the myoflbril, mitochondrion, sarcotubule and in-terstitium volume density and surface density of mitochondrial cristae and numerical density of mitochondria between trained and control group aged 8 and 15 months. In the trained 25 months group, significant increase in volume density of interstitium, lipofucsin granule were shown as compared to untrained age-matched control. On the other hand, significant decrease in mitochondrion volume density was shown. The myofibril volume density did not differ between trained and control group although trained group showed slight increase. From the data obtained a reduced mitochondria/myofibrils ratio was found in trained rat heart aged 25 months and there was no difference between trained and control rat aged 15 months. But a slight but not significant increase was found in the trained group aged 8 months as compared with same age control group. Such increase in the ratio in young animals is considered to be of great importance to cardiac pumping and adaptability. Whereas such adaptations don't seem to occur in aged heart muscle. This study proposed that repeated endurance exercise do not cause any significant qualitative and quantitative ultrastructural change of heart muscle in young(3months) and adult (10months) suggesting that the heart is able to adapt to the exercise. On the contrary, the repeated endurance exercise stress may actually induce degenerative changes in the aged heart muscle(20months).

• Clinical and Experimental Pediatrics
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• v.50 no.5
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• pp.476-483
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• 2007

Purpose : The objective of this study was to assess ventricular function by tissue Doppler imaging (TDI) in children with congenital heart disease (CHD) who have been undergoing open heart surgery (OHS) using cardiopulmonary bypass. We tried to compare the parameters of tissue Doppler imaging before and after OHS in patients with congenital heart disease. Methods : This study was conducted on 32 patients with CHD after OHS from January 2005 to December 2005 at Kyungpook National University hospital. Patients who underwent 2-D echocardiography before and after their OHS. All patients were divided into three groups, left ventricular volume overloading group (group 1), and right ventricular volume overloading group (group 2), and right ventricular pressure overloading group (group 3). The TDIs were examined before and 1 to 3 months after OHS. Peak early diastolic (E), and peak late diastolic (A) velocity of transmitral flow were measured by pulsed wave Doppler examination. Peak systolic (Sm), peak early diastolic (Em), and peak late diastolic (Am) velocity in apical 4-chamber and 2-chamber views were measured by TDI. The author calculated E/Em ratio. Results : The patients were 14 boys and 18 girls and the average age of patients was 2 years and 3 months. The congenital heart diseases which have to get OHS were ventricular septal defect (13 cases), atrial septal defect (7), atrioventricular septal defect (3), isolated pulmonary stenosis (2) and tetralogy of Fallot (7). There were significant decrease of Sm, Em, Am measured on tricuspid annulus and E/Em measured on mitral annulus in apical 4 chamber view (P<0.05). Conclusion : This study showed significant decrease of Sm, Em, Am measured on tricuspid annulus and E/Em measured on mitral annulus in apical 4 chamber view after OHS. These changes might be due to the effects of cardiopulmonary bypass in OHS and/or hemodynamic changes after correction of congenital heart disease. To clarify these changes, further study on more patients is needed.

• Childhood Kidney Diseases
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• v.3 no.2
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• pp.109-116
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• 1999

Purpose: Insulin-like growth factor(IGF)-I and -II are peptide growth factor whose activity is modulated by interaction with the family of six IGF-binding proteins(IGFBPs). IGF-I is detected in rat kidney and has metabolic and growth effects. This study was designed to examine temporal expression of IGFBPs in kidney during renal development and postischemic regeneration in rat. Method: The expression of IGFBPs in kidney during renal development from 15th day of gestation to adult life by using Northern blot analysis. We also examined the renal IGF-IGFBP axis in uremic rat by using Northern blot and immunohistochemistry. Results: The mRNA of IGFBP-1 and -3 were not or barely detected in fetal stages. However, the mRNA level of IGFBP-1 and -3 were increased gradually from day 7 after birth to adult. In contrast, the mRNA of IGFBP-2 and -5 were highly expressed in fetal stages and maintained almost same levels until day 7 (IGFBP-2) or day 30 (IGFBP-5) after birth, then their levels decreased markedly. The mRNA of IGFBP-4 were expressed moderately in fetal kidney and increased gradually after birth. Interestingly, the mRNA of IGFBP-1 and-4 were induced up to 3-5 fold during maximum regeneration period and were recovered to normal levels after acute ischemic injury. In contrast, the mRNA level of IGFBP-3 and-IGFBPrP-1 were decreased slightly at 1 day after ischemic injury, then recovered to normal level during maximum regeneration period. Conclusion: There were differential expressions of IGFBPs in kidney that can modulate IGF action on developing, differentiating, maintaining, and regenerating renal structure and function.

• Journal of Chest Surgery
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• v.6 no.2
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• pp.131-142
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• 1973

Studies of cardiopulmonary function and acid-base balance were performed on 29 dogs during control period, during oligemic hypotension and following return of blood to the animals. Intravenous morphine and local anesthesia were used. Fifteen of the 29 animals survived the complete experiment. The 14 animals that failed to survive the experimental period died between 15 to 90 minutes after the onset of bleeding. The results were as follows. 1. The heart rate increased after the onset of bleeding and failed to return to control level following reinfusion. Stroke volume decreased markedly after bleeding and failed to recover after return of blood from the reservoir. Cardiac output also decreased during oligemic hypotension and was maintained at this level after re-infusion. Total peripheral resistance decreased significantly immediately after bleeding, however it increased soon over the pre-bleeding level. Central venous pressure decreased after the onset of bleeding and remained at lower level for the rest of the experimental period. Arterial blood pressure, clown to 40-45 mmHg by acute hemorrhage, was elevated near to control level. Left ventricular work decreased tremendously during oligemic hypotension and failed to return to control level with the re-infusion of blood. Hematocrit value showed no significant decrease after bleeding and increased after re-infusion. Hemoglobin decreased after the onset of bleeding and recovered to control value after re-infusion. 2. The respiratory rate fell rapidly after bleeding from 124 to 29 and remained at this lower level for the remainder of the experiment. The tidal volume increased after bleeding and was maintained at this level for the remainder of the experiment. The respiratory minute volume showed no significant changes throughout the experimental period. Oxygen consumption fell lightly in all animals during oligemic hypotension and returned to normal levels following re-infusion. Arterial oxygen content and arterial oxygen saturation decreased following bleeding and the values returned to normal levels after the return of blood from the reservoir The arterio-venous oxygen difference increased after the onset of bleeding. It failed to return to normal values following re-infusion. Arterial $Pco_2$ decreased in all animals after the beginning of the bleeding. Partial pressure of $Co_2$ continued to fall until re-infusion, after which the values returned toward normal. Animals became acidotic. The pH fell to lower level following bleeding. Lactic acid and lactate: pyruvate ratio also increased during same period. Arterial pH and lactic acid failed to return to control value and lactate: pyruvate ratio increased more after re-infusion. Sodium bicarbonate decreased after bleeding and returned to control value following re-infusion.

• Journal of Chest Surgery
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• v.29 no.8
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• pp.867-874
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• 1996

This study was designed to assess the left ventricular peak systolic pressure/end-systolic volume (PSP/ESV) ratio in predicting symptomatic improvement with valve replacement in patients with aortic regurgitation and enlarged left von'lrlcular volume. We studied 21 patients (15 men and 6 women aged 15 to 60 years) with moderate or severe aortic regur- gitation, no other cardiovascular abnormalities and left ventricular end-systolic volume over 60 m11m2. In this group we assessed the preoperative variables which routinely were measured at cardiac catheterlzation to predict symptomatic improvement with valve replacement. Six months after operation, symptoms were alleviated in 13 patients(62%), and unchanged in 8()8%). By multivariate analysis, the PSP/ESV rati was a strong predictor for functional class 6 months after surgery(p=0.005) and also for change- in functional class prior to an operation to 6 months postoperatively(p=0.0)2). By 6 months after receiving valve replacement, all patients with a ratio over 1. 71 mmHglml/m'were in functional class I or II , in contrast, of those with a ratio < 1.71 mmHg/ml/m2, 40% were in functional class III. The PSP/ESV ratio may help to predict which patients with aortic regurgitation and enlarged left ven- tricular end-systolic volume will have symptomatic improvement with valve replacement.

• The Korean Journal of Nuclear Medicine
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• v.26 no.1
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• pp.58-64
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• 1992

We performed exercise radionuclide ventriculography to evaluate left ventricular (LV) function in 35 patients with pure mitral stenosis (MS). There were 6 males and 29 females ranging from 21 to 63 years of age (mean $37{\pm}10$ years). We also studied 8 healthy men as control group (mean age $27{\pm}5$ years). Each patients was evaluated at rest and during maximal exercise on an isokinetic bicycle ergometer. Peak filling rate (PFR), peak ejection rate (PER), ejection fracion (EF), end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and cardiac output (CO) were determined by the radionuclide technique. The results were summarized as follows: 1) LV systolic dysfunction and reduced PFR were noted in patients with MS. 2) EDV as well as SV decreased with exercise in patients with MS. 3) No significant increase in EF during exercise compared to rest value was observed because it was caused by reduced EDV and SV during exercise in patients with MS. 4) CO increased with exercise was significantly lower than normal in patients with MS. 5) Patients with MS were divided into two groups according to whether SF increased more than 5% druing exercise compared to resting state or decreased. Significant difference were found between these two groups. Patients with a fall in EF with exercise were older, had larger left atrial size, and had lesser decreased in ESV during exercise.

• Journal of Chest Surgery
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• v.31 no.3
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• pp.221-225
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• 1998

From February 1996 to May 1997, 18 patients underwent mitral valve repair for mitral regurgitation. There were 9 male and 9 female patients aged from 19 to 68 years(mean, 53). Thirteen patients were in New York Heart Association(NYHA) class III and IV. The cause of mitral regurgitation was degenerative in 12 patients, rheumatic in 5 patients and infective in 1 patient. Fifteen patients were in Carpentier's functional classification II, 2 patients in Carpentier's class III and 1 patient in Carpentier's class I. Surgical procedures included prosthetic ring annuloplasty(16 cases), rectangular resection of posterior leaflet(15 cases), chordal shortening(5 cases), triangular resection of anterior leaflet(2 cases), commissurotomy(2 cases), partial transposition of posterior leaflet(1 case). These procedures were combined in most patients. There was no operative death. These patients have been followed from 1 to 15 months, mean of 6.7 months. There was one late death resulted from low cardiac output following mitral valve replacement. The function of the repaired valve in other 17 patients has remained satisfactory during the observed interval. We consider that mitral valve repair is highly satisfactory in patients with mitral regurgitation.

• Science of Emotion and Sensibility
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• v.14 no.4
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• pp.653-662
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• 2011

As technology in 3D industry has rapidly advanced, a lot of studies primarily focusing on visual function and cognition have become vigorous. However, studies on effect of 3D visual fatigue on autonomic nervous system have not less been conducted. Thus, this study was to identify and determine the effect that might have a negative influence on sympathetic nervous system, parasympathetic nervous system, and cardiovascular system. Fifteen undergraduates (female: 9, mean age: $22.53{\pm}2.55$) participated and were sat on a comfortable chair, viewing a 3D content during about 1 hour. Cardiac responses like SDNN(standard deviation of RR intervals), RMS-SD(root mean squared successive difference), and HF/LF ratios extracted from the measured PPG(Photo-PlethysmoGram) before viewing 3D were compared to those after viewing 3D. The results showed that after subjects watched the 3D, responses in sympathetic nervous system and parasympathetic nervous system were activated and deactivated, respectively relative to those before watching the 3D. The results showed that HF/LF ratio, Ln(LF), and Ln(HF) after viewing 3D were significantly reduced relative to those before viewing 3D. No significant effects were observed in SDNN and RMS-SD. Results obtained in this study showed that visual fatigue induced by watching 3D adversely influenced autonomic nervous system, and thereby reduced heart rate variability causing sympathetic nervous acceleration.

• Journal of Korean Medical classics
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• v.3
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• pp.151-217
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• 1989

In this thesis, I intend to study the translational and clinical interpretation through the theory of Ja-Yeol, and reached the following conclusions. 1. Liver-Heat-Disease due to absess of the function of expelling and lifting off, that Liver-Yang cannot lift up to upper-warmer, and stagnate liver. I think the symptoms of yellowish urine, abdominal pain, somnolence, fever belong to the syndrome of 'Gi-Bun(氣分)', and the symptoms of ravings with surprising, distending pain of hypochondrium, restless involuntary movement of the limbs, unable to lie flat belong to the syndrome of 'Hyeol-Bun(血分)'. 2. Heart-Heat-Disease due that 'Eum-Gi(陰氣)' in heart cannot lay down and reach to stagnate at heart, inner part. I think the symptoms of unjoy, acute cardiac pain, fidgetiness, well-nausea, headeche, reddish face, anhidrosis, etc. reveal with Heart-Heat-Disease. 3. Spleen-Beat-Disease due that 'Eum-Gi' in spleen cannot lay down and Yin of spleen changs heat. I think the symptoms of heaviness of head, cheek pain, fidgetiness, cyanosis, well-nausea, fever, not to let flex and reflex with back pain, diarrhea with abdominal pain, left and right cheek pain reveal with Spleen-Heat-Disease. I think symptoms of fever, diarrhea with abdominal pain belong to the syndrome of Yin-exhausion. 4. Lung-Heat-Disease due to that 'Eum-Gi' in lung cannot lay down. When 'Wi-Gi(衛氣)' stagnates at external part, I think, the symptoms of intolerance to wind and cold, yellowish fur, fever reveal. When Wi-Gi stagnates at lung, inner part, I think, the symptoms of dispnea with cough, pain on chest and back, unable to breath deeply, hydrosis and chilling reveal. 5. Kidney-Heat-Disease, in that the symptoms of back pain, leg aching, extreme thirst and frequently drink, fever, pain and stiffness of nape, cooling and aching leg, heat on plantar pedis, not trying to speak reveal is regarded external heat disease of 'Tai-Yang-Gyeong's(太陽經)' disease that asthenic fever open 'Tai-Yang-Gyeong' and lift by not enough of 'Yang-Gi(陽氣)' lifeing up from Kidney space, the water space of five elements.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.89-102
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• 1982

The $Na^+-and\;K^+-induced\;Ca^{++}$ release was measured isotopically by millipore filter technique in pig heart mitochondria. With EGTA-quenching technique, the characteristics of mitochondrial $Ca^{++}-pool$ and the sources of $Ca^{++}$ released from mitochondria by $Na^+\;or\;K^+$ were analyzed. The mitochondrial $Ca^{++}-pool$ could be distinctly divided into two components: internal and external ones which were represented either by uptake through inner membrane, or by energy independent passive binding to external surface of mitochondria, respectively. In energized mitochondria, a large portion of $Ca^{++}$was transported into internal pool with little external binding, while in de-enerigzed state, a large portion of transported $Ca^{++}$ existed in the external pool with limited amount of $Ca^{++}$ in the internal pool which was possibly transported through the $Ca^{++}-carrier$ present in the inner membrane. $Na^+$ induced the $Ca^{++}$ release from both internal pool and external pool and external binding pool of mitochondria. In contrast, $K^+$ did not affect $Ca^{++}$ of the internal pool, but, displaced $Ca^{++}$ bound to external surface of the mitochondria. When the $Ca^{++}-reuptake$ was blocked by EGTA, the $Ca^{++}$ release from the internal pool by $Na^+$ was rapid; the rate of $Ca^{++}-efflux$ appeared to be a function of $[Na^+]^2$ and about 8mM $Na^+$ was required to elicit half-maximal velocity of $Ca^{++}-efflux$. So it was revealed that $Ca^{++}-efflux$ velocity was particulary sensitive to small changes of the $Na^+$ concentration in physiological range. Energy independent $Ca^{++}-binding$ sites of mitochondrial external surface showed unique characteristics. The total number of external $Ca^{++}-binding$ sites of pig heart mitochondria was 29 nmoles per mg protein and the dissociation constant(Kd) was $34{\mu}M$. The $Ca^{++}-binding$ to the external sites seemed to be competitively inhibited by $Na^+\;and\;K^+$; the inhibition constant(Ki) were 9.7 mM and 7.1 mM respectively. Considering the intracellular ion concentrations and large proportion of $Ca^{++}$ uptake in energized mitochondria, the external $Ca^{++}-binding$ pool of the mitochondria did not seem to play a significant role on the regulation of intracellular free $Ca^{++}$ concentration. From this experiment, it was suggested that a small change of intracellular free $Na^+$ concentration might play a role on regulation of free $Ca^{++}$ concentration in cardiac cell by influencing $Ca^{++}-efflux$ from the internal pool of mitochondria.