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Biomedical subjects

J Y Su

Publications and source records attributed to J Y Su.

At least 73 records · Page 4Linked to original sources
PubMed1992

[Alteration of calcium uptake and Ca(2+)-ATPase activity of cardiac sarcoplasmic reticulum in rat during ischemia-reperfusion].

Using Langendorff's perfusion model of isolated rat heart, the effect of period of ischemia, ischemia-reperfusion and changes in perfusate pH on the function of calcium uptake of cardiac sarcoplasmic reticulum (SR) was observed. The initial rate and capacity of calcium uptake by SR decreased significantly after 25 min ischemia, and were further worsened when ischemia was prolonged to 40 min. When hearts were subjected to 15 min reperfusion after 25 min ischemia, calcium uptake capacity and initial rate decreased even more in comparison with that of 40 min ischemia. In addition, the calcium dependent ATPase activity of SR was also markedly inhibited. Reperfusion with acid (pH 6.8) or alkaline (pH 8.0) made no significant difference on the aforementioned reperfusion induced changes. The results indicated that myocardial ischemia depressed the calcium transport activity of SR, and this depression was further aggravated with prolonging ischemia. Reperfusion after ischemia exacerbated the ischemic injury. Reperfusion with either acid or alkaline Krebs-Henseleit solution could not improve the calcium uptake function of SR, implying that the pH change does not seem to be an important factor in inducing the SR dysfunction during ischemia-reperfusion.

Animals↗
PubMed1992

Cell protection mechanism of antishock action of anisodamine.

Anisodamine was used as an antishock (chiefly septic) drug beginning in the early 1960s in China. Its underlining mechanism was believed to be due to its vasodilative action. But in normal animals it only produces slight vasodilation. Our work during the recent 15 years proved that anisodamine is not only beneficial in the treatment for septic shock, but also for hemorrhagic, traumatic, and SMAO shock, and its mechanism of action are based on its following biological actions: (1) it has membrane stabilization and cell protection action, which was probably related to its calcium antagonist action; (2) it protects ischemia intestine from releasing shock factors; and (3) its inhibition of endotoxin binding to cells and tissue at the membrane level probably makes it an special antishock drug for septic shock.

Animals↗
PubMed1992

[Effect of endothelin on isolated myocytes from rat heart].

The mechanism of endothelin (ET) action on isolated myocytes of rat heart was investigated. Administration of 10(-9)-10(-7) mol/L ET caused dose-dependently severe contracture of myocytes, increase in cytosolic lactate dehydrogenase leakage and increase of cellular total calcium. ET also enhanced 45Ca2+ influx in myocytes, that could be antagonized by calcium channel blocker verapamil. Incubation of Fura-2 -preloaded myocytes with ET would induce a significant increase of cytosolic free Ca2+, and this effect of ET could also be partly antagonized by verapamil. These results suggest that ET enhances Ca2+ influx in myocytes mainly through voltage-dependent calcium channel, by which ET exerts its biological action.

Animals↗
PubMed1992

[Effect of NO-like relaxing factor (NO-LRF) in rat tourniquet shock].

On tourniquet shock (ToS) rat model, it was found that the reactivity of isolated perfused aortic ring to noradrenaline was decreased, while the cGMP content of the aortic tissue was increased. These ToS-induced changes could be potentiated or attenuated respectively by perfusion with NO-precursor, L-arginine, or NO-synthesis inhibitor L-NNA independent of the presence of vascular endothelium. Guanylate cyclase inhibitor, methylene blue, could also attenuate the aortic reactivity. All these results suggest that the aortic musculature can produce a NO-LRF factor capable of lowering the vascular reactivity of the ToS animals. That L-arginine can ameliorate while L-NNA can exacerbate ToS, suggest that NO-LRF do play an adaptive role in the protective mechanism of the organism during ToS.

Animals↗
PubMed1992

Instrumented laxity test for the evaluation of posterior cruciate ligament reconstructed knee.

By making anterior and posterior drawer tests using "Laxity tester" is an objective way to evaluate the resting position of tibia plateau and knee laxity. This study followed up 16 cases of PCL reconstructed or pull-out repaired knees for an average of two years and seven months. A force of 20 1b was applied to evaluate knee laxity at 30 degree and 90 degree knee flexion. From paired t-test, the stability of reconstructed knees was not statistically different from that of control contralateral normal knees. The functional scores measured by the Gillquist scoring system for injured knees after reconstruction were satisfactory. Therefore the restabilized PCL deficient knees by the modified Clancy method or pull-out repair yielded good evaluation scores. The data of contralateral normal knee laxity obtained in this study was used as reference in pre-operative and post-operative evaluation of PCL injured knee.

Female↗
PubMed1991

Molecular cloning and expression of the human deoxythymidylate kinase gene in yeast.

(Deoxy)thymidylate (dTMP) kinase is an enzyme which phosphorylates dTMP to dTDP in the presence of ATP and magnesium. This enzyme is important in cellular DNA synthesis because the synthesis of dTTP, either via the de novo pathway or through the exogenous supply of thymidine, requires the activity of this enzyme. It has been suggested that the activities of the enzymes involved in DNA precursor biosynthesis, such as thymidine kinase, thymidylate synthase, thymidylate kinase, and dihydrofolate reductase, are subjected to cell cycle regulation. Here we describe the cloning of a human dTMP kinase cDNA by functional complementation of a yeast dTMP kinase temperature-sensitive mutant at the non-permissive temperature. The nucleotide sequence of the cloned human cDNA is predicted to encode a 24 KD protein that shows considerable homology with the yeast and vaccinia virus dTMP kinase enzymes. The human enzyme activity has been investigated by expressing it in yeast. In this work, we demonstrate that the cloned human cDNA, when expressed in yeast, produces dTMP kinase activity.

Amino Acid Sequence↗
PubMed1991

Role of Na(+)-Ca2+ exchange system in the pathogenesis of myocardial ischemia-reperfusion damage.

Results from a systematic experiment on isolated perfused rat heart and isolated myocytes of adult rat showed that the mechanism of calcium influx during myocardial ischemia-reperfusion is due to the development of intracellular sodium overload during ischemic period; on reperfusion, the high intracellular Na+ content activated the reverse direction of Na(+)-Ca2+ exchange over myocardial sarcolemma (SL), thus a large quantity of extracellular Ca2+ fluxed over the SL to the intracellular space, forming a condition of intracellular Ca2+ overload, which leads to irreversible damage of the myocardium.

Animals↗
PubMed1990

Genetic and molecular analysis of the SOE1 gene: a tRNA(3Glu) missense suppressor of yeast cdc8 mutations.

The CDC8 gene of Saccharomyces cerevisiae encodes deoxythymidylate (dTMP) kinase and is required for nuclear and mitochondrial DNA replication in both the mitotic and meiotic cell cycles. All cdc8 temperature-sensitive mutants are partially defective in meiotic and mitochondrial functions at the permissive temperature. In a study of revertants of temperature-sensitive cdc8 mutants, the SOE201 and SOE1 mutants were isolated. The SOE201 mutant is a disome of chromosome X to which the cdc8 gene maps. Using the chromosome X aneuploids to vary cdc8 gene dosage, we demonstrate that different levels of dTMP kinase activity are required for mitotic, meiotic or mitochondrial DNA replication. The SOE1 mutant contains a dominant suppressor that suppresses five different cdc8 alleles but does not suppress a complete cdc8 deletion. The SOE1 gene is located less than 1.5 cM from the CYH2 gene on chromosome VII and is adjacent to the TSM437-CYH2 region, with the gene order being SOE1-TSM437-CYH2. SOE1 is an inefficient suppressor that can neither suppress the cdc8 hypomorphic phenotype nor restore dTMP kinase activity in vitro. SOE1 is a single C to T mutation in the anticodon of a tRNA(3Glu) gene and thereby, produces a missense suppressor tRNA capable of recognizing AAA lysine codons. We propose that the resultant lysine to glutamate change stabilizes thermo-labile dTMP kinase molecules in the cell.

Alleles↗
PubMed1990

Effects of alfentanil on isolated cardiac tissues of the rabbit.

Alfentanil causes cardiac stimulation or depression in intact animals and in clinical practice; there is no information concerning its direct effects on the heart. Therefore, we studied the effects of alfentanil on isolated cardiac tissues from young adult rabbits. The right atrium with sinoatrial node (SA node) was beating spontaneously, and the left atrium and papillary muscle were stimulated. Isometric contraction was monitored. Alfentanil, in concentrations of 0.05-0.5 mM, decreased by 6%-55% the frequency of contractions of the right atrial-SA node in a dose-related manner. In left atria and right atrial-SA node, but not in papillary muscle, alfentanil in concentrations greater than or equal to 0.01 mM increased the peak developed force and its maximum rate of increase. The time-to-peak developed force was prolonged in papillary muscle but not in right atrial-SA node and left atria. The maximum rate of fall of peak developed force was increased in left atria and decreased in papillary muscle by the administration of alfentanil. The time-to-50% relaxation of peak developed force was not consistently affected by alfentanil in all three muscle preparations. The same concentrations of alfentanil (greater than or equal to 0.01 mM) increased resting force in papillary muscle but not in left atria or right atrial-SA node. It is concluded that alfentanil has direct positive inotropic and negative chronotropic effects on the heart and that it causes contracture of ventricular myocardium.

Alfentanil↗
PubMed1990

[Antagonism of verapamil on the injurious action of endothelin of isolated rat heart].

Isolated rat hearts perfused with endothelin at a concentration of 10(-8) mol/L showed serious functional and cellular myocardial deterioration as manifested by a significant increase of mean perfusion and left ventricular pressure, decrease of +/- LV dp/dtmax, leakage of myocardial protein, formation of lipid peroxides, increase of myocardial calcium content, etc. Calcium channel blocker, verapamil, effectively antagonized the injurious action of endothelin on rat heart whether administered along with or after endothelin perfusion.

Animals↗
PubMed1989

Comparison of the effects of halothane on skinned myocardial fibers from newborn and adult rabbit. I. Effects on contractile proteins.

The effect of halothane on maximal and submaximal Ca2+-activated tension development of the contractile proteins of newborn and adult cardiac muscle from rabbits was determined. Right ventricular muscle was removed from newborn and adult rabbits, and the sarcolemma was disrupted (skinned) by homogenization. Fiber bundles were dissected from the homogenate and mounted on tension transducers. Fiber bundles were alternately immersed in relaxing solution [( Ca2+] less than 10(-9) M) and contracting solutions (various [Ca2+] from 10(-5.6) to 10(-3.8) M), which were saturated with 100% N2 alone or with three concentrations of halothane-N2 mixture. In the absence of halothane, newborn skinned myocardial fibers were slightly more sensitive to submaximal Ca2+ concentrations than were adult myocardial fibers. [Ca2+] required for 50% maximum tension were 10(-5.43) M and 10(-5.31) M, respectively (P less than 0.05). Halothane (1-3%) decreased the maximal Ca2+-activated tension (at [Ca2+] = 10(-3.8) M) similarly in adult and newborn myocardial fibers in a dose-dependent fashion. Tension was reduced by 5.9% for each 1% increase in halothane concentration. Halothane also decreased the sensitivity of adult myocardial skinned fibers to submaximal Ca2+ concentrations (10(-5.6) M to 10(-5.0) M) by shifting the Ca2+-tension response curve to the right. Only 3% halothane decreased the sensitivity of newborn myocardial skinned fibers to Ca2+. The authors conclude that halothane causes less depression of Ca2+ activation of the contractile proteins in newborn than adult rabbit myocardium and that this effect of halothane cannot account for greater negative inotropy of halothane in the newborn.

Animals↗
PubMed1989

Comparison of the effects of halothane on skinned myocardial fibers from newborn and adult rabbit: II. Effects on sarcoplasmic reticulum.

The effect of halothane on Ca2+ uptake or release by the sarcoplasmic reticulum (SR) was compared in the newborn and adult rabbit myocardium. The sarcolemma of right ventricular myocardium was disrupted (skinned) by homogenization. Fiber bundles were dissected from the homogenate, mounted on tension transducers, and immersed sequentially in five solutions that loaded Ca2+ into the SR, then in solutions containing either 2 or 25 mM caffeine to release SR-stored Ca2+, resulting in transient tension development. Experimental solutions were saturated with halothane in N2 gas during Ca2+ uptake by SR, Ca2+ release by SR, or during both SR Ca2+ uptake and release. Halothane (0.5-1.7%) resulted in dose-dependent depression of SR Ca2+ uptake in both newborn and adult skinned fibers. Less tension transient depression resulted in newborn (35%) than adult skinned fibers (49.5%, P less than 0.05) with 0.5% halothane exposure during SR Ca2+ uptake. Similar depression resulted in newborn (53.7% and 73.4%) and adult fibers (65.2% and 77.9%) with 1.0% and 1.7% halothane. Halothane had little effect on SR Ca2+ release by 25 mM caffeine but enhanced submaximal SR Ca2+ release by 2 mM caffeine more in newborn than adult myocardium. Increased Ca2+ efflux from newborn SR may contribute to the greater sensitivity of intact newborn cardiac muscle to exposure to halothane.

Aging↗
PubMed1989

Intracellular mechanisms of halothane's effect on isolated aortic strips of the rabbit.

The intracellular mechanisms of halothane action were examined in vascular smooth muscle from the aorta. Medial layers of the aorta from rabbits were mounted on photodiode tension transducers, stretched to 20 mg resting tension, and "skinned" with saponin. The skinned fiber preparations were then immersed in bathing solutions to study the effects of halothane (0.5-2%) on Ca2+ activation of the contractile proteins, and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using caffeine-induced tension transients. For comparison, isolated intact aortic rings were mounted on Blinks' dual tissue bath and attached to force transducers. The preparations were contracted with either 40 mM KCl, or norepinephrine (NE) followed by acetylcholine (ACh)- or sodium nitroprusside (SNP)-induced relaxation. At steady state contraction or relaxation, the effects of halothane (1-3%) were studied. The steady state tension during halothane was expressed as a percentage of the steady state tension before administration of halothane. In the isolated intact aortic rings, halothane (1-3%) produced biphasic effects on KCl-induced tension, i.e., an initially slight increase followed by decreases, independent of endothelium. Halothane markedly increased tension in the ACh- or SNP-relaxed state. The effects were dose-dependent. In the skinned aortic strips, halothane slightly decreased maximum Ca2+-activated tension development of the contractile proteins. Halothane decreased Ca2+ accumulation in the SR and increased Ca2+ release from the SR in a dose-dependent manner. The halothane-induced increases in Ca2+ release from the SR were blocked by ryanodine, an SR Ca2+ release channel blocker. It is concluded that halothane directly causes vascular contraction or relaxation, depending on the condition, and that halothane's effects on the SR may play a role.

Acetylcholine↗
PubMed1989

[Factors affect Na(+)-Ca2+ exchange in rat's cardiomyocytes and protein-reconstituted liposomes].

Rat's Ca-resistant ventricular myocytes and reconstituted liposomes of canine cardiac sarcolemma were used in analysing factors affecting Na(+)-Ca2+ exchange system. Decrease in extracellular (extravesicular) Na+ or increase in intracellular Na+ by inhibition of the Za(+)-K(+)-ATPase with ouabain stimulated the Na(+)-Ca2+ exchange. Mn2+, an antagonist of Na(+)-Ca2+ exchange, dose-dependently inhibited the Na(+)-dependent Ca2+ uptake. However, verapamil had no effect on it. Arachidonic acid and lipid peroxides caused by incubation with-H2O2 significantly stimulated Na(+)-Ca2+ exchange in a dose-dependent fashion.

Animals↗
PubMed1989

[Significance of endothelin in shock pathogenesis].

Endothelin is a recently discovered bioactive peptide produced by vascular endothelial cells. By means of specific radioimmunoassay we found that plasma endothelin level in patients with late septic shock was significantly increased. And a typical shock model in healthy rats was reproduced by continuous infusion of endothelin (endothelin shock). Infusion of endothelin at a small dose to hemorrhagic shocked rats deteriorated the shock process and resulted in an irreversible development. From these results it is suggested that endothelin may be an endogenous injury-inducing factor, acting as one of the important humoral factors involved in shock pathogenesis.

Animals↗
PubMed1989

[Anoxia-reoxygenation injury in isolated rat myocytes is modulated by cell sodium during the anoxia period].

Using the model of anoxia-reoxygenation injury in isolated rat myocytes, we observed that incubation of myocytes with ouabain, inhibitor of Na+-K+ ATPase, during anoxia period significantly increased the cell sodium content. These myocytes demonstrated severe injury and intracellular calcium overload during reoxygenation period. The sodium content of myocytes at the end of anoxia period was positively correlated with the overload of intracellular calcium at reoxygenation (r = 0.882, P less than 0.01). Mn2+, an inhibitor of Na+-Ca2+ exchange, significantly attenuated the anoxia-reoxygenation injury when given during reoxygenation period. Mn2+ also inhibited the cell injury caused by incubation of myocytes with Na+-free medium. These results suggest that anoxia-reoxygenation injury of rat myocytes is modulated by cell sodium during the anoxia period, and the Na+-Ca2+ exchange mechanism plays an important role in influx of extracellular calcium during reoxygenation period.

Animals↗
PubMed1988

Intracellular mechanisms of verapamil and diltiazem action on striated muscle of the rabbit.

Skinned fibers from striated muscle were used to study the intracellular mechanisms (contractile proteins and sarcoplasmic reticulum [SR]) of action of diltiazem (DT) and verapamil (VP) on muscle contraction. Rabbit papillary muscle (PM), and the skeletal muscles adductor magnus (AM, fast-twitch) and soleus (SL, slow-twitch) were used. The muscles were skinned by homogenization and fibre bundles for PM and single fibres for AM and SL were dissected from the homogenate and mounted on photodiode force transducers. VP (0.1-3.0 mmol/l) (and to a lesser degree DT) increased Ca2+-activated tension development of the contractile protains in PM and SL and decreased it in AM (+[4-20]%, +4%, -[14-28]%, respectively). Both drugs increased the submaximal Ca2+-activated tension development at the order of PM = SL greater than AM in a dose-dependent manner. The changes of half-maximal pCa50 at 1 mmol/l VP were 0.25, 0.25, and 0.15, respectively. For Ca2+ uptake and release from the SR, VP as well as DT (0.1-3.0 mmol/l) in the uptake phase decreased caffeine-induced tension transients in a dose-dependent fashion. At 0.01-3.0 mmol/l, the drugs directly induced Ca2+ release from the SR or enhanced caffeine-induced tension transients with the exception that in PM, DT attenuated caffeine-induced tension transients. Thus, VP and DT have similar intracellular mechanisms of action in striated muscle. Both drugs induced calcium release from the SR and increase Ca2+ sensitivity of the contractile proteins, and thus could be the underlying mechanisms for potentiating twitch tension, and inducing contracture in skeletal muscle.

Animals↗