These experiments were designed to study the influence of protein undernutrition during lactation period(3 wks) or after-weaning period(8 wks) on growth of organs, and on brain and liver composition of the experimental rats. The following experimental groups were studied. Group No. Rats Lactation(3 wks) (Diet of mother rat) After-weaning period(8wks) Rehabilitation Period(17wks) I 8 25% Casein diet 25% Casein diet 25% Casein diet II 8 12% Casein diet 25% Casein diet 25% Casein diet III 8 25% Casein diet 5% Casein diet 25% Casein diet IV 8 12% Casein diet 5% Casein diet 25% Casein diet After the perriod of rehabilitation(17 wks) with 25% casein diet, the following results were obtained. 1. Most of the organs except the spleen could not catch up with the normal group in their weights for the group of protein undernutrition during lactation(3 wks), even after 17 weeks of rehabilitation. For the group of protein undernutrition during after-weaning period(8 wks) brain, lung, heart, spleen and pancreas could catch up with the normal group after rehabilitation. According to this result it is assumed that the growth of brain, lung, heart and pancreas might be developed mostly during lactation and that the growth of liver and kidney might be developed after-weaning period continuously. 2. For the groups of protein underuntrition during lactation period or after-weaning period the amounts of total lipid, cholesterol and phospholipid of brain were lower than those of normal group. Especially, cholesterol level was significantly lower than normal group. And there was also a significant difference in the phospholipid level of the after-weaning(8 wks) deprivation group. 3. The groups of protein undernutrition during lactation or after-weaning period(8 wks) showed lower level of liver nitrogen and higher level of liver fat. Especially, protein undernutriton during lactation gave a greater influence on the lever of liver fat.
Voltage-sensitive release mechanism was pharmacologically dissected from the $Ca^{2+}-induced\;Ca^{2+}\;release$ in the SR $Ca^{2+}$ release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR $Ca^{2+}$ release process was monitored by using forward-mode $Na^+-Ca^{2+}$ exchange after restriction of the interactions between $Ca^{2+}$ from SR and $Na^+-Ca^{2+}$ exchange within micro-domains with heavy cytosolic $Ca^{2+}$ buffering with 10 mM BAPTA. During stimulation every 10 s with a pulse roughly mimicking action potential, the initial outward current gradually turned into a huge inward current of $-12.9{\pm}0.5\;pA/pF$. From the inward current, two different inward $I_{NCX}s$ were identified. One was $10\;{\mu}M$ ryanodine-sensitive, constituting $14.2{\pm}2.3%$. It was completely blocked by $CdCl_2$ (0.1 mM and 0.5 mM) and by $Na^+-depletion$. The other was identified by 5 mM $NiCl_2$ after suppression of $I_{CaL}$ and ryanodine receptor, constituting $14.8{\pm}1.6%$. This latter was blocked by either 10 mM caffeine-induced SR $Ca^{2+}-depletion$ or 1 mM tetracaine. IV-relationships illustrated that the latter was activated until the peak in $30{\sim}35\;mV$ lower voltages than the former. Overall, it was concluded that the SR $Ca^{2+}$ release process in the rat ventricular myocytes is mediated by the voltage-sensitive release mechanism in addition to the $Ca^{2+}-induced-Ca^{2+}\;release$.
Cardiac fibroblasts constitute one of the largest cell populations in the heart, and contribute to structural, biochemical, mechanical and electrical properties of the myocardium. Nonetheless, their cardiac functions, especially electrophysiological properties, have often been disregarded in studies. $Ca^{2+}$-activated $K^+\;(K_{Ca})$ channels can control $Ca^{2+}$ influx as well as a number of $Ca^{2+}$-dependent physiological processes. We, therefore, attempted to identify and characterize $K_{Ca}$ channels in rat Cardiac fibroblasts. First, we showed that the cells cultured from the rat ventricle were cardiac fibroblasts by immunostaining for discoidin domain receptor 2 (DDR-2), a specific fibroblast marker. Secondly, we detected the expression of various $K_{Ca}$ channels by reverse transcription polymerase chain reaction (RT-PCR), and found all three family members of $K_{Ca}$ channels, including large conductance $K_{Ca}$ (BK-${\alpha}1-\;and\;-{\beta}1{\sim}4$subunits), intermediate conductance $K_{Ca}$ (IK), and small conductance $K_{Ca}$ (SK$1{\sim}4$ subunits) channels. Thirdly, we recorded BK, IK, and SK channels by whole cell mode patch clamp technique using their specific blockers. Finally, we performed cell proliferation assay to evaluate the effects of the channels on cell proliferation, and found that the inhibition of IK channel increased the cell proliferation. These results showed the existence of BK, IK, and SK channels in rat ventricular fibroblasts and involvement of IK channel in cell proliferation.
Yangkyuksanhoa-tang is frequently used for cerebrovascular accident(CVA). The present study was performed to investigate the effect of Yangkyuksanhoa-tang on the peri vascular immunoreactive nerve fiber of the basilar artery after experimentally induced subarachnoid hemorrhage(SAH). Sprague Dawley rats weighing between 350-400g were used. The SAH induced by injection of the fresh autologus heart blood(0.3-0.4ml) into the cisterna magna through the posterior atlanto-occipital membrane. Sample group was given a $3.3m{\ell}/kg/day$ of Yangkyuksanhoa-tang extracts for 2 days after SAH. The experimental animals divided into 48hrs after SAH. The changes of perivascular immunoreactive nerve fiber was examined by using indirect immunofluorescence method. The meshlike perivascular nerve fiber appeared in the basilar artery of normal rats. In basilar artery of SAH elicitated rat, the distribution of calcitonin gene-related peptide (CGRP)-immunoreactivity(IR) and vasoactive intestinal polypeptide(VIP)-IR of the perivascular nerve fiber were remarkably diminished, also dopamine beta hydroxylase(DBH)-IR, neuropeptide Y(NPY)-IR and serotonin-IR were diminished. In SAH elicitated rat with Yangkyuksanhoa-tang treatment, the CGRP-IR and VIP-IR degree were repaired as well as normal rat's, but DBH-IR, NPY-IR and serotonin-IR had no changes. These results provide the basic data to investigate the effect of Yangkyuksanhoa-tang on the vasospasm after SAH.
The aim of this study was to evaluate the preventive role of epigallocatechin-3 gallate (EGCG, a derivative of green tea) in ischemia/reperfusion (I/R) injury of isolated rat hearts. It has been suggested that EGCG has beneficial health effects, including prevention of cancer and heart disease, and it is also a potent antioxidant. Rat hearts were subjected to 20 min of normoxia, 20 min of zero-flow ischemia and then 50 min of reperfusion. EGCG was perfused 10 min before ischemia and during the whole reperfusion period. EGCG significantly increased left ventricular developed pressure (LVDP) and increased maximum positive and negative dP/dt (+/-dP/dtmax). EGCG also significantly increased the coronary flow (CF) at baseline before ischemia and at the onset of the reperfusion period. Moreover, EGCG decreased left ventricular end diastolic pressure (LVEDP). This study showed that lipid peroxydation was inhibited and Mn-SOD and catalase expressions were increased in the presence of EGCG. In addition, EGCG increased levels of Bcl-2, Mn-superoxide dismutase (SOD), and catalase expression and decreased levels of Bax and increased the ratio of Bcl-2/Bax in isolated rat hearts. Cleaved caspase-3 was decreased after EGCG treatment. EGCG markedly decreased the infarct size while attenuating the increase in lactate dehydrogenase (LDH) levels in the effluent. In summary, we suggest that EGCG has a protective effect on I/R-associated hemodynamic alteration and injury by acting as an antioxidant and anti-apoptotic agent in one.
The purpose of the present study is to investigate the effects of green tea catechin on microsomal phospholipase $A_2(PLA_2)$ activity and the arachidonic acid (AA) cascade in hearts of microwave exposed rats. Sprague-Dawley male rats weighing $100{\pm}10$ g were randomly assigned to one normal group and three microwave exposed groups. The microwave exposed groups were subdivided into three groups: catechin free diet (MW) group, 0.25% catechin (MW-0.25C group and 0.5% catechin (MW-0.5C) group according to the levels of dietary catechin supplementation. Rats were sacrificed $6^{th}$ day after microwave irradiations (2.45 GHz, 15 min). The heart microsome $PLA_2$ activity in the MW group was 130% greater than that of normal groups, whereas there was no significant difference between normal group and MW-0.25C, MW-0.5C group. The per- centage phosphatidyl ethanolamine (PE) hydrolyzed in the heart microsome in the MW was increased 54% by microwave irra- diation, whereas there was no significant difference between normal group and MW-0.5C group. The percentage phosphatidyl choline (PC) hydrolyzed in the heart microsome in the MW group was increased by 104% and by microwave irradiation, whereas there was no significant difference between normal group and MW-0.5C group. The formation of thromboxane $A_2(TXA_2)$ in the heart microsome was 70% greater in the MW group than in the normal group. However, the MW-0.25C and MW-0.5C group maintained the normal level. The formation of prostacyclin ($PGI_2$) in the heart microsome was 21% lower in the MW group than in the normal group, while that of MW-0.25C and MW-0.5C group were maintained in the normal group. The heart microsomal thiobarbituric acid reactive substances (TBARS) concentrations, as an index of lipid peroxide, were 71% greater in the MW group, as compared with normal group. However, the MW-0.25C and MW-0.5C group were 4.6% and 9.2% lower, respectively, than that of MW group. In conclusion, heart function appeared to be improved by green tea catechin supplementation due to its antithrombus action, which in return controls the AA cascade system.
This study was undertaken to search for a new antiarrhythmic agent in natural plants. Extracts of Buxus microphylla var. koreana Nakai have been used as folk remedies of several diseases, including malaria and venereal disease, but any study on the pharmacological actions of this plant has not yet been carried out and its active ingredients have not been identified. In our laboratory, we isolated buxuletin (nonalkaloid) and cyclobuxine D (steroidal alkaloid) from Buxus microphylla var. koreana Nakai and reported their pharmacological actions: diuretic effects of buxuletin in rabbits and hypotensive effect of cyclobuxine D in rats. In the present study, we investigated the effect of cyclobuxine D on isolated frog heart and heart rate in urethane anesthetized rats. In order to clarify the mechanism of bradycardic effect of cyclobuxine D, we examined the changes of the ECG parameters (PR, QRS and R ${\alpha}$ T interval) produced by intravenous injection of cyclobuxine D in anesthetized rats. Cyclobuxine D depressed the contractile force in isolated frog heart and exerted a dose-dependent bradycardic effect in anesthetized rats. Intracerebroventricular injection of cyclobuxine D caused a fall in blood pressure and an increase in heart rate, but those effects were not significant. Cyclobuxine D prolonged the PR interval and RaT interval (${\alpha}$ Tindicates the apex of T), but was without significant effects on the duration of the QRS complex and PRc in urethane anesthetized rats.
Bolus intravenous injection of adenosine resulted the temporal decrease of systemic blood pressure and heart rate in the anesthetized rats. Adenosine also resulted the persistent decrease of contractility and heart rate in the isolated spontaneously beating rat right atria. Both of the above inhibition effets of adenosine were increased by the pretreatment of NBI (nitrobenzylthioinosine), whitch is an adenosine transport inhibitor, but decreased by the pretreatment of 8- phenyltheophy1line, which is an adenosine antagonist. In isolated thoracic aorta ring segment of normotensive rats, intact rings were relaxed by adenosine ($42.3{\pm}8.7%$) and ATP ($85.9{\pm}15.8%$) in the concentration of $10^{-4}M$, but rubbed rings were relaxed by adenosine ($35.2{\pm}1.9%$) and ATP ($11.3{\pm}9.0%$) in $10^{-4}M$. After pretreatment of L-NAME (N-Nitro-Larginine methyl ester), which is an NO inhibitor, adenosine-induced relaxation was not affected, but ATP-induced relax ation was significantly inhibited (P<0.01). Meanwhile, adenosine resulted almost same as vasorelaxation in isolated thoracic aorta of SHR comparing to those of normotensive rats. But, vasodilation responses of ATP in intact rings of SHR are significantly inhibited comparing to those of normotensive rats. Adenosine-induced relaxation is attenuated after 8-phenyltheophylline pretreatment, but increased after NBI pretreatment. However, ATP-induced relaxations are not affected by 8-phenyltheophylline or NBI pretreatment. These results suggested that the hypotensive effects of adenosine was due to the decrease of contractile force and heart rate through the A1 receptor and vasodilation are mediated by A2 receptor of the vascular smooth muscle. And, the heart protective and vasodilation effects of adenosine might suggest that it would be useful in the acute treatment of coronary artery disease.
Although the effects of adenosine on the heart, including the clinical suppression of cardiac arrhythmias, have been recognized for more than half a century, it is only in the last decade that the therapeutic potential of adenosine has been recognized. The objective of this study was to determine if augmentation of myocardial adenosine levels during global ischemia improves functional recovery after reperfusion. We used to modified Langendonf system to evaluate myocardial protective effect. Isolated rat hearts were subjected to 90 minutes of deep hypothermic arrest(15$^{\circ}C$) with modified St. Thomas'Hospital cardioplegic solution used to provide myocardial protection. Myocardial adenosine levels were augmented during ischemia by providing exogenous adenosine in the cardioplegic solution. Two groups of hearts w re studied: (1) control group(n=10) cardioplegia alone; (2) adenosine group(n=10) adenosine(0.75mg/kg/min) added to the cardioplegic solution. Significantly better percent recovery(p<0.01) in hemodynamics(except heart rate) at 60 minutes after reperfusion was evident compared to baseline values in the adenosine group. (systolic no란ic pressure : 78.5$\pm$3.6% vs 66.6$\pm$5.9%, airtic overflow volume : 61.7$\pm$ 11.6% vs 37.2$\pm$ 15.4%, coronary flow volume 77.1$\pm$7.5% vs 57.2$\pm$ 11.1%, and cardiac output : 65.6$\pm$ 11.5% vs 44.2$\pm$ 12.4%). Heart rate was similar in two groups(94.4$\pm$4.8% vs 95.3 $\pm$ 6.8%). Adenosine groups resulted in significantly rapid recovery time of heart beat after reperEusion(p<0.01) (24.5$\pm$7.6 sec. vs 179.0$\pm$ 131.1sec.). In biochemical study, CPK levels(0.1 $\pm$0.3U/L vs 1.4$\pm$0.8U/L) and lactic acid levels(0.08$\pm$0.Immol/L vs 0.34$\pm$0.2 mmol/L) were significantly low in adenosine groups(p<0.01). We concluded that adenosine included cardioplegia have better recovery effects after r perfusion in myocardial ischemia compared to adenosine free cardioplegia.
Journal of the Korean Society of Food Science and Nutrition
/
v.16
no.2
/
pp.63-68
/
1987
The effects of various levels of copper(Cu) intake on the concentrations of copper, iron (Fe) and 3inc(Zn) in rat tissues were studied in growing rats. For different groups the drinking water was supplemented with 0(control), 25, 50, 100 and 200ppm Cu(as copper sulphate) for 1 day respectively. All animal groups were fed with the control diet (Cu contents, 12.8%mg/kg diet) during the experiment. At the end of the 4 week experiment, body weight gain was slightly lower in the Cu supply groups than in control group. Liver and serum Cu were significantly higher in 50, 100 and 200ppm Cu of male and in 200ppm Cu of female than in control groups. Spleen Cu was significantly increased by the supplementation of Cu. Liver and heart Fe of male and heart Fe of female were increased by incresing supplementary Cu levels. In 50ppm Cu group, liver, spleen and kidney Fe of female increased but the others did not. Fe of tissues was different in male and female rats according to Cu levels supplied. Serum Zn of male and female was significantly lower in 50, 100 and 200ppm Cu groups than in control and 25ppm Cu groups. When supplemented with Cu levels there were no significant differences among groups for liver, kidney, spleen and heart Zn as well as heart and kidney Cu.
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