Effects of suspended silt and clay on the survival of the rearing bivalves, Meretrix lusoria, Cyclina sinensis and Mactra veneriformis were studied. During sixty-five days of experimental cultures in different concentrations of suspended silt and clay and in different time of immersions, mortalities of the bivalves were checked every day, and the rates of shell movement and oxygen consumption were measured. In general, the higher the concentration of silt and clay and the longer the immersion time, the earlier the occurence, and the higher the rate of the mortalities of the experimental bivalves. M. veneriformis was subjected to earlier mortality than the others, and the period of $50\%$ mortality was the shortest of the three species (37 days in 1,000 ppm), and longer was that of C. sinensis(42 days). Mortality of M. lusoria occured latest and $50\%$ mortality was seen at the immersion time of 50-51 days. Particularly, M. lusoria showed no mortality in the sea water with 100 ppm of suspended silt and clay, and even in the concentrations of 500 or 1,000 ppm they were able to survive without mortality only if the immersion time was short (12-18 hours per day). M. veneriformis and C. sinensis were also able to survive without mortality when the immersion time was short (12 hours per day) in low concentration (100 ppm). Shell movements of experimental bivalves varied depending upon species. In the case of M. veneriformis the shell was opened continuously and C. sinensis opened their shells frequently, while M. lusoria maintained their shells closed in any experimental concentrations of sea water with suspended silt and clay. Total metabolic activity of M. veneriformis was found to be highest while that of M. lusoria showed the lowest. Little difference of oxygen consumption in excised gill tissue was shown between the control group and the experimental groups. Consequently, it may be stated that the mortality results from a immersion in sea water with high concentration of suspended silt and clay for long-time although the survival rates of the experimental bivalves depend also upon the species, physiological conditions, concentration of suspended silt and clay and immersion time. The survival percentage of bivalve y in relation to the time (day) of immersion X in sea water of suspended silt and clay was found to be: $$M.\;lusoria\;(1,000\;ppm):\;y=7.7\times10^9\;\chi^{-4.77}\;(500\;ppm):\;y=259\chi^{-0.26}$$$$C.\;sinensis\;(1,000\;ppm):\;y=-21\chi+936\;(\chi<44),\;y=-0.65\;\chi+35\;(\chi>44)$$$$(500\;ppm):\;y=4.4\times10^5\;\chi^{-2.27}$$$$M.\;veneriformis\;(1,000\;ppm):\;y=-18\chi+716\;(\chi<39),\;y=-0.89\chi+39\;(\chi>39)$$
The present study was performed to investigate antioxidant, anticancer, and antimicrobial activities of four Korean sweet potato variaties and to identify the changes in these biological activities under different cooking conditions. Total polyphenol content was 3.8-73.6 mg/g in 80% ethanol extracts of sweet potatoes. The polyphenol content was highest Sinjami variety (p < 0.05). Radical scavenging activity against DPPH and $ABTS^{{\cdot}+}$ was high in Sinjami (p < 0.05) and the ethanol extract from Sinjami also showed effective superoxide dismutase (SOD)-like activity, which decreased significantly by steaming and roasting (p < 0.05). Ethanol extracts from the four sweet potato variaties did not inhibit cancer cell growth in MCF-7 or HepG2 cells at concentrations of 1, 10, and $100\;{\mu}g$/mL. Of the investigated sweet potato variaties, only Sinjami exhibited strong antimicrobial activity against Escherichia coli, Staphylococcus aureus, and Salmonella typhimurium. The antimicrobial activity of Sinjami against E. coli, St. aureus, and S. typhimurium decreased following steaming and roasting (p < 0.05). These results indicate that the Sinjami Korean sweet potato had higher polyphenol content, radical scavenging activity, SOD-like activity, and antimicrobial activity than those of the other variaties and consuming raw Sinjami might be beneficial for maintenance of biological activities.
Antidromically activated spinoreticular tract (SRT) cell units in the lumbosacral enlargement of ${\alpha}-chloralose$ anesthetized cats were classified as medial and lateral SRT units according to the location of their axonal termination. Identified SRT units were tested fer antidromic conduction velocity, laterality of their axonal projection, the location in spinal gray, peripheral receptive field, the response pattern to graded mechanichal stimulation and the responsiveness to $A{\delta}$ and C volley of the peripheral nerve. 1) The 59% of 34 medial SRT units were recorded in ipsilateral side to the antidromic stimulation site, but 60% of the 47 lateral SRT units projected to contralateral side. 2) Most of the medial SRT cells and rostral ventrolateral medulla (RVLM)-projecting lateral SRT cells were recorded in lamina VII & VIII. The LRN (lateral reticular nucleus)-projecting SRT cells, however, distributed through all the laminae except superficial ones (I & II). 3) The identified SRT units were classified as low theshold (LT), deep, high threshold (HT), wide dynamic range (WDR) cells, based on the response patterns to graded mechanical stimuli. The proportion of SRT units which receive noxious input was 37.5%, 25% and 75% in the medial, LRN-projecting and RVLM SRT group, respectively. 4) There was no significant difference in the mean conduction velocities between the 3 groups. But the deep cells had significantly higher velocity than that of the HT cells. The above results show that the peripheral inputs to the SRT units are different in the 3 groups: medial, LRN & RVLM SRT group. Especially in case of the SRT cells projecting to RVLM which is a probable candidate fur the integration center of various pressor reflexes such as somatosympathetic reflex, the noxious informations occupy higher proportion of input to them than in other groups. Therefore the noxious information transmitted through the lateral SRT destined for RVLM is expected to play a role in somatosymapthetic reflex.
From the study of movements of $Ca^{++}$ in frog cardiac muscle, Niedergerke (1963) postulated that $Ca^{++}$ necessary for the cardiac contraction is stored in a specific pool. Langer et al (1967) and DeCaro (1967) also found a close relationship between the change of $Ca^{++}$ flux kinetics and the change of contractile force. According to the studies of several investigators, Ca II (Bailey and Dressel 1968) or phase I and II (Langer 1965, Langer et al 1967, 1971) in the $Ca^{++}$ washout curve was associated with cardiac contractility. This investigation was aimed to elucidate the anatomical region of the contractile active $Ca^{++}$ pool. At the same time, it was assumed in this study that $Ca^{++}$ in the sarcoplasmic reticulumn represents one of the major intracellular $Ca^{++}$ pool and cardiac contractility was also dependent on the intracellular $Ca^{++}$ concentration. Consequently, this experiment was performed at different temperatures to activate to activate inhibit the deactivating process of activated $Ca^{++}$ in the intracellular space to see if changes in the contractility decay curve existed at different temperatures. The isolated hearts of rabbits and turtles (Amyda maackii) were attached to the perfusion apparatus according to the method employed by Bailey and Dressel (1968). The isolated hearts were initally perfused with a full Ringer solution containing 2 mg/ml of inulin for 1 hr, and then $Ca^{++}$ and inulin-free Ringer solution was perfused while the isometric tension was recorded and a serial sample of perfusion fluid dripping from the cardiac apex was collected for 10 sec throughout experimental period. The above procedure was performed at $23^{\circ}C$, $30^{\circ}C$ and $38^{\circ}C$ on the rabbit heart and $10{\sim}13^{\circ}C$, $10^{\circ}C$, $25^{\circ}C$, $30^{\circ}C$ and $35^{\circ}C$ on the turtle heart. After determination of $Ca^{++}$ and inulin concentration of the samples, the $Ca^{++}$, inulin washout curve and the contractile tensin decay curve were analysed according to the method of Riggs (1963). The results were summarized as follows; 1. In the rabbit heart, there are 2 inulin compartments, 3 $Ca^{++}$ compartments and sing1e exponential decay of contractile tension. In the turtle heart, there are $1{\sim}2$ inulin compartments, $1{\sim}2$$Ca^{++}$ compartments and $1{\sim}2$ phases of contractile tension decay. The fact that the inulin space was divided into 3 compartments in the washout curve in these hearts indicates the presence of heterogeneity in cardiac perfusion, i.e., overfused and underperfused area. 2. Ca I a9d Ca II in these hearts were found to have $Ca^{++}$ in the ECF compartments because their half times in the washout curves were far smaller than those of the inulin washout curves in the rabbit heart and similar to those of the inulin washout curves in the turtle heart. Ca III in the rabbit heart may have originated from the intracellular $Ca^{++}$ store. But no Ca III in the turtle heart was found. This may be due to the fact that the iutracellular $Ca^{++}$ pool in the turtle heart was too small to detect using this experimental procedure since sarcoplasmic reticulumn in the turtle heart is poorly developed. 3. In the rabbit heart, there were no chages in the half time of Ca I, Ca II, inulin I and inulin II at different temperatures, but the half time of Ca III was significantly prolonged at lower temperatures, and the half time of the contractile tension decay tended to be prolonged at lower temperatures but this was not significant. In the turtle heart, there were no changes in the half time of Ca I, Ca II, inulin 1, inulin II and phase I of the contractile tension decay at different temperatures, but the half time of phase II of the contractile tension decay was significantly prolonged at lower temperatures. This finding indicates that intracellu!ar $Ca^{++}$ in these hearts was also responsible particulary for maintaining the cardiac contractility at the lower temperatures. 4. The half times of contractile tension decay were shorter than those of Ca II in the $Ca^{++}$ washout curves in both animal hearts. According to the above results it was shown that $Ca^{++}$ in ECF is primarily and $Ca^{++}$ in the intracellular space is partially associated with the cardic contractility.
The extrafetal transfer of $Li^{+}$ in amniotic fluid was studied in 45 pregnant rabbits. LiCl solution was administered either intravenously to mother or directly into the amniotic sac and monitored the appearance and disappearance of $Li^{+}$ in the amniotic fluid, then calculated the transfer rate of $Li^{+}$ of extrafetal origin. To study the transplacental $Li^{+}$ transfer, a solution of 150 mM LiCl was infused continuously via maternal vein (initial dose: 0.7 mmol/kg, maintaining dose: 0.03 mmol/kg/min) and the $Li^{+}$ concentration was measured in maternal blood and amniotic fluid after 60 and 120 minutes of infusion. Change in the volume of aminotic fluid was determined by Congo red dilution method at the same time. Effects of duration of gestation was not considered in this study. Extrafetal transport of $Li^{+}$ into the amniotic fluid was estimated by comparing the $Li^{+}$ concentration and volume of amniotic fluid determined before and after ligating the placental vessels. Extrafetal $Li^{+}$ transport from the amniotic fluid was determined by observing the time dependent disappearance of $Li^{+}$ and Congo red in amniotic fluid after injecting 0.5 ml solution of 15 mM or 90 mM LiCl and 50 mg/ml Congo red. Following are the results obtained: 1) During infusion of LiCl through maternal vein the ratio of the aminotic $Li^{+}$/maternal plasma $Li^{+}$ increased significantly along with the increment of fetal weight. 2) The volume of amniotic fluid of larger fetuses than 20.5 gm increased significantly during administration of LiCl while that of smaller fetuses did not change. 3) After umbilical cord ligation the $Li^{+}$ concentration of amniotic fluid of larger fetuses than 20.5 gm was decreased to $59.9{\pm}10.3%$ and $56.9{\pm}42.9%$$(mean{\pm}S.D.)$ of those of control group after 60 and 120 minutes of LiCl infusion respectively. In amniotic fluid of smaller fetuses than 20.5 gm, there was no significant difference between control and ligation groups. 4) The disappearance rate of Congo red in the amniotic fluid was $45.2{\pm}8.2%/hr$. 5) The disappearance rate of $Li^{+}$ after intraamniotic injection of LiCl depended on the amount injected. On injecting $7.5\;{\mu}mol$ LiCl, $Li^{+}$ disappeared rapidly from the amniotic fluid and the rates after 60 min and 90 min were $97.0{\pm}2.8,\;98.5{\pm}2.0%$ respectively. On injecting $45\;{\mu}mol$ LiCl, the rates were $56.0{\pm}15.4,\;78.9{\pm}14.5%$ at 60 and 90 min. 6) From the above results it was concluded: a) $Li^{+}$ transfer into the amniotic fluid increased along with the fetal growth and one half of $Li^{+}$ influx is through the extrafetal route even after the maturation of fetal kidney. b) One half of the $Li^{+}$ transfer from the amniotic fluid was through swallowing of fetus, while the remaining half was transfered rapidly through amniotic membrane, which was concentration limited.
Park, Hyoung-Jin;Kwon, Hyeok-Yil;Suh, Sang-Won;Kim, Jeong-Mi;Lee, Tae-Hyung
The Korean Journal of Physiology
/
v.24
no.1
/
pp.39-49
/
1990
It has been reported that bombesin induces contraction of the smooth muscle of the gastrointestinal tract. Thus, the present investigation was undertaken to see an influence of bombesin on electrical activity of the gastric smooth muscle, since electrical activity is associated with contractile activity in the smooth muscle of the stomach. Smooth muscle strips $(5\;{\times}\;1.5\;cm)$ that included the corpus and antrum were prepared from the ventral and dorsal portion of the feline stomach along the greater curvature. Circular muscle strips $(1\;{\times}\;0.3\;cm)$ of the corpus were also obtained. Electrical activity of the corpus and antrum of the muscle strip was monophasically recorded by using Ag-AgCl capillary electrodes placed on the circular muscle layer. Contractile activity of the circular muscle strip was also recorded. The recordings were performed in Krebs-Ringer solution that was continuously aerated with $O_{2}$ containing 5% $Co_{2}$, and kept at $36^{\circ}C$. Dose-related responses of electrical activity and contractility to bombesin was studied after frequency of slow waves and contraction of each strip reached to a steady state. An action of $D-leu^{13}-{\psi}\;(CH_{2}NH)-D-leu^{14}-bombesin,\;D-pro^{2}-D-trp^{7,9}-substance\;P$, tetrodotoxin, hexamethonium, atropine, phentolamine or propranolol on the effect of bombesin was also observed. 1) Bombesin increased frequency of slow waves and contractions dose-dependently at concentrations from $10^{-9}\;M\;to\;3\;{\times}\;10^{-8}\;M$. 2) The bombesin analogue at a concentration of $3\;{\times}\;10^{-7}\;M$ antagonized the effect of bombesin on frequency of slow waves. 3) The effect of bombesin on frequency of slow waves was inhibited by tetrodotoxin $(10^{-6}\;M)$ and hexamethonium $(10^{-3}\;M)$ but unaffected by atropine $(10^{-6}\;M)$, phentolamine $(10^{-5}\;M)$ and propranolol $(10^{-5}\;M)$. 4) The effect of bombesin on frequency of slow waves was blocked by the substance P analogue at a concentration of $10^{-5}\;M$. 5) Substance P at a concentration of $10^{-5}\;M$ failed to change frequency of slow waves. It is concluded from the above results that bombesin increases the frequency of slow waves as well as contractions of the smooth muscle strip from the feline stomach, and the effect of bombesin might be mediated by non-cholinergic or non-adrenergic mechanism at neuromuscular junction. However, enteric nerves that have substance P as a neurotransmitter do not appear to participate in the action of bombesin on frequency of slow waves.
The effects of electrolytes, adenosine, ATP, 5-hydroxytryptamine (5-HT, serotonin) and ketanserin on the inhibitory junction potentials (IJPs) were investigated to clarify the interactions of these drugs with the neurotransmitters released from non-adrenergic, non-cholinergic nerves in the antrum of guinea-pig stomach. Electrical responses of antral circular muscle cells were recorded intracellularly using glass capillary microelectrode filled with 3 M KCI. All experiments were performed in Tris-buffered Tyrode soluition which was aerated with 100% $O_{2}$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) Inhibitory junction potential (IJP) was recorded in antral strip, while excitatory junction potential (EJP) was recorded in fundic strip. 2) IJP recorded in antral strip was not influenced by atropine $(10^{-6}\;M)$ and guanethidine $(5{\times}10^{-6})$. 3) The amplitude of IJP increased in high $Ca^{2+}$ solution, while that of IJP decreased in high $Mg^{2+}$ solution or by $Ca^{2+}$ antagonist (verapamil). Apamin, $Ca^{2+}$-activated $K^{+}$ channel blocker blocked IJP completely. 4) ATP and adenosine decreased the amplitude of IJP. 5) 5-HT decreased the amplitude of IJP with no change of the amplitude of slow waves, while ketanserin (5-HT type 2 blocker) decreased the amplitude of slow waves markedly with no change in that of IJP. From the above results, the following conclusions could be made. 1) IJP recorded in antral strip is resulted from neurotransmitters released from non-adrenergic, non-cholinergic nerves. 2) An increase in the concentration of external $Ca^{2+}$ enhances the release of neurotransmitters from non-adrenergic, non-cholinergic nerves which activate the $Ca^{2+}$-dependent $K^{+}$ channel.
Park, Hyoung-Jin;Lee, Yun-Lyul;Kwon, Hyeok-Yil;Shin, Won-Im;Suh, Sang-Won
The Korean Journal of Physiology
/
v.23
no.1
/
pp.79-87
/
1989
Molecular property as well as biological activities of bombesin-like substance (BBS-LS) isolated from the skin of B. orientalis in Korea was compared with those of synthetic BBS-14. BBS-LS in the crude extract was applied on a Sephadex G-50, superfine column $(1.6{\times}112\;cm)$. On chromatogram, the first peak (3.5% of BBS-LS) was found ahead of synthetic GRP-27, and the second peak (rest) between synthetic GRP-27 and synthetic BBS-14. The main form of BBS-LS was successfully purified by using a column of alkaline alumina followed by sequential gel-filtrations on a column of Sephadex G-10, fine and a column of Sephadex G-50, superfine. Chromatographic analysis of the purified BBS-LS using a column of Sephadex G-50, superfine and reversed phase HPLC revealed that the main form of BBS-LS in the skin of B. orientalis could be distinctly different from either BBS-14 or GRP-27 in molecular size. The purified BBS-LS exerted biological activities quite identical to those of synthetic BBS-14. The results of the present investigation indicate that the skin of B. orientalis contains BBS-LS composed of two distinct forms. The main form of BBS-LS purified in the present study is heterogenous to both synthetic BBS-14 and GRP-27 in molecular size but identical to BBS in biological activities.
The effects of ouabain on the contractile and electrical activities were investigated in the isolated preparations of guinea-pig taenia coli, and compared with those of vanadate. Spontaneous contractions were recorded with force transducer, and electrical activites were measured by use of suction electrode, or single sucrose-gap technique. The contractions were induced by the electrical stimulation for 5 seconds every 1 minute with alternating current (60 Hz, 3.0 V/cm) through the platinum electrodes located in parallel with the long axis of the preparation. All experiments were performed in tris-buffered Tyrode solution which was aerated with $100%{\;}O_2$ and kept at $35^{\circ}C$. The results obtained were as follows: 1) Responses of spontaneous contractions to ouabain were concentration-dependent; $10^{-7}M$ ouabain caused a rise of basal tone. Above the concentration of $10^{-6}M$ ouabain, an initial increase followed by a decrease in tension was observed. 2) A continuous spike discharge was induced by the administration of $10^{-7}M$ ouabain. Above $10^{-6}M$ ouabain, a transient initial increase followed by a decrease in spike frequency and amplitude was produced, and finally membrane potential was sustained at a certain level without a spike discharge. 3) The characteristic response to $10^{-7}M$ ouabain was not blocked by the pretreatment with $10^{-7}M$ atropine. 4) The electrically induced contractions were completely suppressed at the concentration of $2{\times}10^{-7}M$ ouabain. These contractions were blocked more rapidly in paralled with the increase in ouabain concentration. 5) Effects of vanadate on the spontaneous activities were quite different from those of ouabain; $10^{-6}M$ vanadate increased the amplitude of contractions and $10^{-5}M$ vanadate increased slightly both amplitude and frequency of spontaneous contractions. $10^{-4}M$ vanadate showed irregular phasic contractions superimposed on the increased basal tone. 6) $10^{-5}M$ vanadate depolarized the membrane potential and shortened the interval between the bursts of spike discharge, whereas $10^{-4}M$ vanadate induced continuous spike discharge with membrane depolarization. 7) Vanadate caused a characteristic inhibitory response to the contractions induced by electrical stimulation; An initial rapid inhibition of tension development and then gradual recovery to a certain level. From the above results, the following conclusions could be made: 1) The rise of basal tone at $10^{-7}M$ ouabain is due to continuous spike discharge without a silent period. The continuous spike discharge is likely to be associated with a slight membrane depolarization caused by the blockage of Na pump. 2) The biphasic response induced by above $10^{-6}M$ ouabain seems to occur by the different mechanisms. The initial increase in tension is associated with depolarization along with an increase in spike frquency, whereas the subsequent relaxation occurs through a non-electrical mechanism. 3) The characteristic response to $10^{-7}M$ ouabain is resulted not from the action on intrinsic nerve terminal, but from its direct action on the membrane of smooth muscle cells. 4) The phasic contractions superimposed on the increased basal tone at the concentration of $10^{-4}M$ vanadate is resulted from the continuous spike discharge with membrane depolarization, of which mechanism remains unknown. 5) The inhibitory action of ouabain on the electrically induced contractions suggests that the increasein intracellular Na in some way inhibits the electrically induced $Ca^{2+}$ influx. The mechanism of vanadate action on the induced contractions remains unknown.
Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.
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