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Biomedical subjects

J Y Su

Publications and source records attributed to J Y Su.

At least 55 records · Page 3Linked to original sources
PubMed1994

An accurate method for open reduction and internal fixation of high and low condylar process fractures.

OBJECTIVE: This study was undertaken to evaluate a protocol for open reduction of both high and low condylar fractures that consistently produces accurate reductions, uses rigid internal fixation, and allows immediate function. MATERIALS AND METHODS: This protocol was retrospectively evaluated in 22 consecutive patients (23 fractures). RESULTS: All patients functioned immediately. There were no inaccurate reductions, malocclusions, wound infections, neurosensory deficits, or reports of chronic pain. No patients required reoperation. CONCLUSION: The results of this study indicate that this protocol consistently produces accurate reduction of condylar process fractures and allows immediate function with a minimum of morbidity.

Adolescent↗
PubMed1994

Mechanisms of action of enflurane on vascular smooth muscle. Comparison of rabbit aorta and femoral artery.

BACKGROUND: This study was performed to elucidate the mechanisms of action of enflurane by comparing the vascular smooth muscle responses of conduit arteries of larger (aorta) and smaller (femoral artery) diameter to enflurane using isolated rings and skinned strips. METHODS: Isolated intact rings (endothelium denuded) of aorta and femoral artery from rabbits were activated by various concentrations of norepinephrine (NE) and the effects of enflurane were examined at the steady-state force. In a separate study, the rings were pretreated with verapamil before the NE activation and tested with enflurane. In the saponin-treated arterial strips ("skinned"), the effects of enflurane on Ca2+ uptake or release from the sarcoplasmic reticulum were studied using caffeine-induced tension transients. RESULTS: In isolated aortic rings, enflurane (0.9%-5%) enhanced tension development at low NE concentrations (5 and 30 nM) but depressed it at highest concentration (10 microM). In contrast, enflurane depressed tension development in the femoral artery at all NE concentrations. Enflurane caused significant increase in the NE-activated force in rings pretreated with verapamil. In skinned strips, enflurane (1%-3%) decreased Ca2+ uptake (concentration resulting in 50% depression: 1.8% for aorta and 2.5% for femoral artery) and increased Ca2+ release from the sarcoplasmic reticulum (59%-208% for aorta and 10%-55% for femoral artery). These effects were dose-dependent. Enflurane potentiated ryanodine depression of caffeine-induced tension transients. CONCLUSIONS: Enflurane has similar mechanisms of action in aorta and femoral artery: blocking Ca2+ influx, and causing, at least in part, Ca2+ release from the sarcoplasmic reticulum through the ryanodine-receptor channel. These cellular actions of enflurane account for the depression in femoral artery and enhancement in aorta of NE-activated force in isolated rings.

Animals↗
PubMed1994

Regulation of phosphofructokinase from muscle and liver of rainbow trout by protein phosphorylation.

Phosphofructokinase (PFK) from both white skeletal muscle and liver of trout is controlled by reversible phosphorylation. In vitro phosphorylation of purified muscle PFK with the catalytic subunit of cAMP-dependent protein kinase led to a 25% decrease in the S0.5 F6P and reduced inhibition by Mg.ATP and citrate. Phosphorylation of trout liver PFK lowered the I50 Mg.ATP (by 27%) but in vitro treatment with acid phosphatase reduced S0.5 F6P by 40% and increased I50 Mg.ATP by 50%. Thus, dephosphorylated trout liver PFK appears to be the more active enzyme form. Compared with mammalian PFK, the less rigorous effects of phosphorylation on trout liver PFK and relatively stronger phosphorylation control of skeletal muscle PFK may serve different patterns of carbohydrate metabolism in lower vertebrates, in particular the in situ processing of lactate in post-exercise muscle.

Adenosine Triphosphate↗
PubMed1994

The experience of two-epidural-catheter for painless labor.

'Two epidural-catheters' method was used to relieve labor pain during the first and second stage of labor course. Six milliliters of a mixture of '0.15% bupivacaine +0.03% xylocaine +0.0005% fentanyl' was the main agent given through the epidural catheter every 2 hours when the cervix was 3-4 cm dilated with 4 ml of 1% xylocaine as test dose. Addition doses of the mixture were given when needed. Fifty two, ASA I-II, parturients (primigravida: 43, multipara: 9) were included in this study. The mode of delivery was: 59.6% by vacuum, 36.4% by normal spontaneous delivery (NSD), and 4% by Cesarean Section (C/S). 88.5% of newborns had Apgar score > or = 7 at 1 minute and all had Apgar score > or = 7 at 5 minutes. 38(73%) of 52 parturients were fully satisfied with the analgesic effect during the whole labor course and 14(27%) of 52 parturients were partially satisfied with the analgesic effect owing to 1) intolerable lower abdominal pain (11 cases), 2) mild painful episiotomy (1 case), and backache (2 cases). No motor block was noted. Good analgesic effect during the second stage labor course could be obtained by our 'Two-Epidural-Catheter' method and no significant complications of newborns and parturients were noted in our study.

Adolescent↗
PubMed1994

Role of regulatory peptide in pathogenesis of shock.

The present study evaluated the pathogenetic roles of three kinds of regulatory peptide. The results showed that (i) plasma endothelin (ET) level elevated significantly in septic shock rats, persistent intravenous drip of low doses ET caused development of shock state in normal rats and the irreversible outcome of light hemorrhagic shock. Furthermore, i. v. administration of specific ET-antiserum was significantly effective to septic shock rats. (ii) Plasma calcitonin gene-related peptide (CGRP) increased by 260% in septic shock rats, i. v. drip of low doses CGRP both in early and late sepsis were effective to shock rats. (iii) Angiotensin-II (ANG-II) contents of heart and aorta increased dramatically both in early and late septic shock, and inhibiting its increase with Captopril in late sepsis significantly improved the shock state, but results were inverse in early sepsis. It could be concluded that ET was one of the most important factors participating in the pathogenesis of shock, CGRP had a compensatory regulatory role in shock and the role of tissue ANG-II was different during different periods of shock.

Angiotensin II↗
PubMed1993

Phosphofructokinase from liver of the rainbow trout, Oncorhynchus mykiss.

Phosphofructokinase (PFK) from liver of the rainbow trout Oncorhynchus mykiss was purified to homogeneity with a recovery of 35% of total activity. The purified enzyme was a homotetramer with a native molecular weight of 297,000 +/- 16,000 and a subunit M(r) of 76,000 +/- 3000. Arrhenius plots of enzyme activity were linear over 5-27 degrees C with an activation energy of 52.3 +/- 2.1 kJ/mol. The binding of fructose 6-phosphate was cooperative. High ATP increased the Hill coefficient and produced a marked allotropic inhibition of the enzyme activity. The affinity of the enzyme for fructose 6-phosphate was increased by the addition of the enzyme activators such as inorganic phosphate, ammonium ions, AMP, and fructose 2,6-bisphosphate; the activators also reduced the inhibitory effect of ATP. Trout liver PFK was activated by phosphoenolpyruvate at physiological concentrations but was not affected by citrate.

Adenosine Monophosphate↗
PubMed1993

Mechanisms of action of 7-O-ethyl tetrandrine in isolated vascular smooth muscle of the rabbit aorta.

Tetrandrine is an alkaloid from a Chinese herb which has been used to treat hypertension in humans. The mechanism(s) of its antihypertensive action is not clear. The goal of this study was to examine the direct effects of a derivative of tetrandrine, 7-O-ethyl tetrandrine (TD), on vascular smooth muscle. In particular, the goals were to study (1) the involvement of the endothelium in the responses of isolated aortic rings to TD, and (2) the effects of TD at intracellular sites involved in muscle contraction in skinned aortic strips treated with saponin. TD (1-100 mumol/l) decreased noradrenaline (NA) and K(+)-evoked contraction of isolated aortic rings with or without endothelium in a concentration-dependent manner although to a lesser degree with the K(+)-evoked contraction. In NA-contracted rings, the IC50 for TD was approximately 28-30 mumol/l, at which a 20% decrease in K(+)-force development of aortic rings was observed. The slope of the concentration-relaxation curve was steeper in aortic rings with endothelium than without endothelium (1.09 vs. 0.88) in NA-contracted rings. TD increased tone in acetylcholine (ACh)-relaxed rings but did not change the force in aortic rings relaxed by sodium nitroprusside (NaNP) or ATP. In TD pretreated rings, TD blocked ACh-induced relaxation, but not NaNP or ATP-induced relaxation. In skinned aortic strips, TD decreased Ca2+ uptake by the SR (IC50 approximately 77.4 mumol/l, slope = 0.88), did not affect Ca2+ release from the SR, and decreased Ca2+-activation of the contractile proteins at 300 mumol/l TD.

Alkaloids↗
PubMed1993

Modulation of sarcoplasmic reticulum Ca(2+)-release channels by caffeine, Ca2+, and Mg2+ in skinned myocardial fibers of fetal and adult rats.

Ryanodine causes depression of the caffeine-induced tension transient (ryanodine depression) in skinned muscle fibers, because it blocks the sarcoplasmic reticulum (SR) Ca(2+)-release channels [Su, J. Y. (1988) Pflügers Arch 411:132-136, 371-377; (1992) Pflügers Arch 421:1-6]. This study was performed to examine the sensitivity of SR Ca(2+)-release channels to ryanodine in fetal compared to adult myocardium and to investigate the influence of Ca2+, caffeine, and Mg2+ on ryanodine depression in skinned fibers. Ryanodine (0.3 nM-1 microM) caused a dose-dependent depression in skinned myocardial fibers of the rat, and the fetal fibers (IC50 approximately 74 nM) were 26-fold less sensitive than those of the adult (IC50 approximately 2.9 nM). The depression induced by 0.1 microM or 1 microM ryanodine was a function of [caffeine], or [Ca2+] (pCa < 6.0), which was potentiated by caffeine, and an inverse function of [Mg2+]. At pCa > 8.0 plus 25 mM caffeine, a 20% ryanodine depression was observed in both the fetal and adult fibers, indicating independence from Ca2+. Ryanodine depression in skinned fibers of the fetus was less affected than that seen in the adult by pCai, [caffeine]i, or 25 mM caffeine plus pCai or plus pMgi (IC50 approximately pCa 4.5 versus 5.1; caffeine 12.7 mM versus 2 mM; pCa 6.7 versus 7.3; and pMg 3.9 versus 3.3 respectively). The results show that the SR Ca(2+)-release channel in both fetal and adult myocardium is modulated by Ca2+, caffeine, and Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The effect of halothane on the sarcoplasmic reticulum in normal and right ventricular hypertrophy in rabbits.

Calcium accumulation and storage by the sarcoplasmic reticulum is affected adversely by both inhaled anesthetics and hypertrophy. The interaction of these two conditions in right ventricular muscle was examined in a skinned fiber preparation whereby the sarcolemma was disrupted mechanically to permit external control of the chemical composition of the cytoplasm. Skinned fibers were obtained from the right ventricles of rabbits 4 mo after surgical banding of the pulmonary artery (n = 5) or sham banding (n = 4). Right ventricles after pulmonary artery banding weighed an average of twice that of normal right ventricles. The sarcoplasmic reticulum of the skinned fibers was permitted to accumulate Ca2+ and then maximal or submaximal Ca2+ release was induced with 25 mM or 2 mM caffeine, respectively. The magnitude of the Ca2+ release was estimated by the area of the ensuing tension over time. When 1%, 2%, or 3% halothane accompanied the 2 mM caffeine, both normal and hypertrophied muscle exhibited an area of the tension transient twice that of the tension transients without halothane (control). When present during Ca2+ accumulation, 1%, 2%, and 3% halothane reduced the 25 mM caffeine-induced tension transient in normal and hypertrophied muscle to 36%, 17%, and 11%, respectively, of the controls. The equal depression in normal and hypertrophied right ventricles was in contrast to a previous study in which hypertrophy provided some protection against the decrease in sarcoplasmic reticulum Ca2+ storage by halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1993

Possibility of targeting treatment for ischemic heart disease with liposome (II).

Studies on the isolated rat heart perfusion model have proved that perfusion with high Ca2+ (4.5 mmol/L), high K+ (8.7 mmol/L) or free radical generating system (FRGS) significantly increases myocardial uptake of liposomes. Intravenous injection of liposomes covalently combined with antibody of rat myocardial cells obviously elevates the target action of liposomes to myocardium. Liposome-carried SOD for treatment of rat myocardial ischemia-reperfusion injury is much more effective than simple SOD. The results evidence that the liposome as drug carrier for treatment of ischemic heart diseases shows a broad prospect for its clinical use.

Animals↗
PubMed1993

[Changes of calcium transport capacity of myocardium and myocardial mitochondria during sepsis].

On the isolated perfused heart model of septic rats, the present study showed that: (1) Calcium content and 45Ca-influx of myocardium increased 190%, 208% (P < 0.01) and that of mitochondria elevated 332%, 178% (P < 0.01) respectively with no change of myocardial 45Ca-release during sepsis. (2) 10(-8) mol/L calcitonin gene-related peptide (CGRP) or 10(-7) mol/L atriopeptin (ANP) added into the Krebs-Henseleit solution could effectively reduce 45Ca-influx to myocardium and mitochondria with no effect on myocardial 45Ca-release. (3) The calcium uptake reserve of mitochondria evaluated in vitro showed that the maximal calcium uptake and uptake velocity of mitochondria during sepsis were reduced 34.6%, 33.3% (P < 0.01) respectively. The data suggested that the net increase of myocardial Ca2+ content resulted from increase of 45Ca-influx with no change of 45Ca-efflux and the reduction of mitochondrial Ca2+ buffering capacity during sepsis were key events in the pathogenesis of intracellular Ca(2+)-overload. CGRP and ANP could effectively alleviate Ca(2+)-overload of myocardium and mitochondria. This may have some cellular protection action during sepsis.

Animals↗
PubMed1993

Possibility of targeting treatment for ischemic heart disease with liposome (I).

This paper reports the basic research on the possibility of using targeting treatment for ischemic heart disease with liposome as drug carrier. Studies have been performed on isolated rat cardiomyocytes, or isolated perfused rat and rabbit hearts. Results show that cardiomyocytes may interact with liposome through fusion, endocytosis, adsorption and molecular exchange of phospholipid. Forms of cellular uptake of liposome depend chiefly on the physicochemical properties of liposomes. Anoxia changes the pattern of liposome uptake by cardiomyocytes and increases uptake of liposomes. Uptake of liposomes, especially of positively charged liposomes by ischemic myocardium is significantly increased. The quantity of increase of liposome uptake is in the following order: ischemia-reperfusion area > peripheral area of the infarct > non-ischemic area > infarcted area. The above results indicate that liposome as drug carrier might promote the delivery of drug into ischemic myocardium and cardiomyocytes.

Animals↗
PubMed1992

Influence of caffeine, Ca2+, and Mg2+ on ryanodine depression of the tension transient in skinned myocardial fibers of the rabbit.

Ryanodine, a blocker for Ca(2+)-release channels of the sarcoplasmic reticulum (SR Ca(2+)-release channels), induces depression of myocardial contraction in isolated intact muscle, which is consistent with depression of the caffeine-induced tension transient in skinned muscle fibers. In isolated SR, ryanodine binds to a specific receptor with high affinity, and this binding is enhanced by caffeine and increasing Ca2+ and decreased by increasing Mg2+. The aim of this study was to test the hypothesis that depression of myocardial contraction is mediated by changes in ryanodine-receptor binding properties. Accordingly, factors (caffeine, Ca2+, and Mg2+) affecting ryanodine-receptor binding properties in the isolated SR membrane were studied in skinned myocardial fibers from adult rabbits. The depression of the caffeine-induced tension transient by ryanodine (ryanodine depression) influenced by these three factors was measured. In a dose-dependent manner, increasing caffeine or Ca2+ concentrations enhanced the ryanodine depression. The concentrations for 50% ryanodine depression (IC50) approximated 7 mM for caffeine, and pCa 5.25 for Ca2+. When 1 microM ryanodine and 25 mM caffeine were combined, ryanodine depression was independent of Ca2+ at low Ca2+ concentrations (20%-30% at pCa greater than 8 and 7.5) and was a direct function of Ca2+ at higher concentrations (pCa 7.5-6.0 with IC50 approx. pCa 6.75). In contrast, increasing Mg2+ reduced the ryanodine depression with IC50 approximately equal to pMg 3.3. In conclusion, the caffeine- or Ca(2+)-enhanced, and Mg(2+)-reduced ryanodine depression observed in this study is consistent with known ryanodine-receptor binding properties.

Animals↗
PubMed1992

Scalarane-type bishomosester terpenes from the sponge Phyllospongia foliascens.

Five new 20,24-bishomoscalarane sesterterpenes, phyllactones A [1], B [2], C [3], D [4], and E [5], are reported from the sponge Phyllospongia foliascens collected in the waters of the Nansha Islands in the South China Sea. Structural elucidation of these compounds is based on spectral data and chemical conversions. Phyllactones A and B show moderate cytotoxicity against KB cells (IC50 20 micrograms/ml).

Acetylation↗
PubMed1992

Left ventricular hypertrophy in rabbits does not exaggerate the effects of halothane on the intracellular components of cardiac contraction.

Inhalational anesthetics and ventricular hypertrophy have adverse effects on cardiac muscle contraction. The effects of 1, 2, and 3% halothane on the contractile protein and sarcoplasmic reticulum, but not the sarcolemma, were examined in normal left ventricular tissue from rabbits that underwent a sham surgical procedure (n = 5) and in left ventricular hypertrophied tissue from surgically induced aortic coarctation (n = 7). Muscle samples were mechanically "skinned" to disrupt the sarcolemma. Fiber bundles were mounted in photodiode transducers and bathed in a series of solutions designed to examine the contractile protein [Ca2+]-tension responses or to examine Ca2+ storage by and release from the sarcoplasmic reticulum. Hill equation analysis of the [Ca2+]-tension relationship of the contractile protein was performed. Compared to normal muscle, hypertrophied muscle was associated with an 8.2% decrease in the [Ca2+] necessary for 50% maximum tension (more sensitive to Ca2+) (P less than 0.001) and an increase in the slope constant of 23% (P less than 0.001). In normal and hypertrophied tissue, each 1% of halothane incrementally decreased the contractile protein response to maximal [Ca2+] by 5% (P less than 0.01), increased the [Ca2+] at 50% maximum tension by 5% (P less than 0.01), and had no effect on the slope of the Hill equation. Halothane also inhibited Ca2+ storage by the sarcoplasmic reticulum. In normal muscle, 1, 2, and 3% halothane decreased the stored Ca2+ to 42, 22, and 9%, respectively, of Ca2+ storage without halothane (P less than 0.001). However, hypertrophied muscle demonstrated slightly less depression (P less than 0.05 by analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗