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Biomedical subjects

J Y Su

Publications and source records attributed to J Y Su.

At least 109 records · Page 6Linked to original sources
PubMed1983

Experimental study in rabbits of the antishock effect of anisodamine (654-2), and its mechanism of action.

The antishock effect of anisodamine (654-2) was observed in different kinds of experimental shock in groups of rabbits--due to late hemorrhage, superior mesenteric artery occlusion, and septic shock from peritonitis. The drug 654-2 significantly alleviated the progress of shock and increased the survival rate of the animals. The therapeutic effect of 654-2 was much better than that of other vasoactive drugs commonly used, such as norepinephrine, phenoxybenzamine, dopamine, and aramine. The antishock mechanism of 654-2 is probably partly due to its protective action on intestinal shock in preventing its effects becoming irreversible. The antishock action of 654-2 both by basic research workers and clinicians merits further study.

Animals↗
PubMed1983

Salutary effects of anisodamine in murine traumatic shock.

Anisodamine, an alkaloid originally extracted from the Chinese herb Anisodus tanguticus, has been reported to possess beneficial actions in septic, superior mesenteric artery occlusion, and hemorrhagic shock. We have investigated its actions in traumatic shock in rats. Anisodamine (2.5 mg/kg) increased survival time from 1.4 +/- 0.2 h to 3.1 +/- 0.3 h (P less than 0.001) in traumatized rats with 50% of the drug-treated animals surviving at least 3.5 h. Drug treatment had no significant effect on plasma cathepsin D activity (12.0 +/- 2.3 vs 10.4 +/- 1.7; vehicle- vs drug-treated, respectively). However, plasma myocardial depressant factor accumulation was significantly blunted by anisodamine, 62 +/- 5 vs 41 +/- 5 U/ml (P less than 0.02), indicating that prevention of MDF formation may be one protective mechanism of this substance.

Animals↗
PubMed1982

Mechanism of adenosine 3',5'-monophosphate (cAMP)-induced increase in Ca2+ uptake by the sarcoplasmic reticulum in functionally skinned myocardial fibers.

The increased rate of Ca2+ uptake and ATPase activity in isolated cardiac sarcoplasmic reticulum (SR) by adenosine 3',5'-monophosphate (cAMP) has been shown to be activated by a cAMP-dependent protein kinase (cAMP kinase). Functionally skinned myocardial fiber preparations were used to study the mechanisms of cAMP action on the SR at the same time that tension was monitored. cAMP effects were studied on Ca2+ -activated tension of the contractile proteins, and on Ca2+ uptake and release from the SR using caffeine-induced tension transients. Neither cyclic AMP (0.1-5 microM) nor the catalytic subunit of cAMP kinase (0.1-1 microM) (PK-C) significantly changed either the maximal or the submaximal Ca2+ -activated tension. The areas of the tension transients were unchanged when cAMP was present in the releasing solution (release phase), and were significantly increased up to a mean of about 80% when cAMP or PK-C was present in the Ca2+ loading solutions (uptake phase). The increased tension transient was blocked by heat-stable inhibitor of cAMP kinase. We conclude that cAMP-induced increases in Ca2+ uptake by the SR could play an important role in the positive inotropic effect. cAMP kinase could thus play a crucial role in the regulation of myocardial contractility.

Animals↗
PubMed1980

Effects of circulatory arrest and rewarming on regional blood flow during surface-induced hypothermia.

Regional blood flow and distribution of cardiac output (CO) were evaluated by the radioactive microsphere technique in rhesus monkeys during surface rewarming following the induction of deep hypothermia (20 degrees C.) under deep ether anesthesia. A comparison of animals subjected to 30 minutes of circulatory arrest and those not arrested revealed cerebral, coronary, and renal vascular resistance and flow patterns consistent with a hyperemic response to circulatory arrest at 20 degrees C. Throughout rewarming cerebral and coronary absolute flows tended to be at or above the flows noted at comparable cooling temperatures in a previous study. Renal flow fraction (% Qt) were well preserved during rewarming to 30 degrees C., but a decrease was observed thereafter. Carcass (muscle, skin, bone) %Qt was also reduced following rewarming, especially in arrested animals. CO appeared to be similar to those noted at comparable cooling temperatures until 30 degrees C. during rewarming; thereafter, CO did not fully recover to awake control levels. These data suggest that regional flow is redistributed from the carcass and renal circulations to cerebral and coronary circulations in response to hemodynamic alterations during surface rewarming. It was concluded that autoregulative responses to both circulatory arrest and hemodynamic factors are elicited during surface rewarming from deep hypothermia to 20 degrees C. with the method described.

Animals↗
PubMed1980

Effects of enflurane on functionally skinned myocardial fibers from rabbits.

Enflurance, at clinical concentrations, decreases the contractility of isolated intact cardiac muscle. The authors investigated the intracellular mechanism(s) of this depression by examining the Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum (SR) using functionally skinned fibers from right ventricular papillary muscle of rabbits. This preparation permits control of intracellular ionic composition (pH 7.0, 20 C). The [Ca2+]--tension relationship and caffeine-induced tension transient (as a measure of the amount of Ca2+ release) were analyzed. Enflurane significantly but only slightly depressed the maximum Ca2+-activated tension (10 per cent decrease at 5 per cent enflurane) and did not change the [Ca2+] required for half-maximal activation of the fibers. In contrast, enflurane markedly inhibited the Ca2+ uptake by the SR (30-85 per cent decrease at 2.5-7.5 per cent enflurane). The inhibition was dose-dependent. Ca2+ release from the SR with 25 mM caffeine was not changed at low concentrations of enflurane (1-5 per cent), but was decreased at high concentration (25 per cent decrease at 7.5 per cent enflurane). Enflurane (1-7.5 per cent), however, increased (13-44 per cent) the submaximum caffeine (2 mM)-induced Ca2+ release from the SR, and the effect was not dose-dependent. The aforementioned effects were reversible. These results are similar to those previously reported for halothane. It is concluded that enflurane may induce myocardial depression mainly by inhibiting Ca2+ uptake by the SR.

Animals↗
PubMed1979

Effects of halothane on caffeine-induced tension transients in functionally skinned myocardial fibers.

The effects of halothane on caffeine-induced tension transients in functionally skinned myocardial fibers were investigated. Fiber bundles from mechanically disrupted rabbit right ventricular papillary muscles were mounted on a tension transducer. The fiber preparation was loaded with Ca2+; Ca2+ was then released by the use of caffeine (25 mM); and the area of the resulting tension transient was measured. Each preparation was sequentially transferred from control to test to control solution. The control solutions were equilibrated with 100% N2, and the test solutions with a mixture of N2 and various halothane concentrations. The preparation was exposed to halothane during the Ca2+ uptake or the release phase only, or during both Ca2+ uptake and release phases. The areas of the test tension transients were compared with those of the two control tension transients. It was found that halothane depressed the caffeine-induced tension transient either during the uptake phase or the combined-uptake-and-release phase but not during the release phase. The halothane-induced depression was dose-dependent, reversible, and comparable to the depression observed in intact isolated papillary muscles. We conclude that halothane could induce myocardial depression by inhibiting Ca2+ uptake by the sarcoplasmic reticulum.

Animals↗
PubMed1979

Effects of ether anesthesia and surface-induced hypothermia on regional blood flow.

Regional blood flow and distribution of cardiac output (CO) were evaluated by the radioactive microsphere technique in seven rhesus monkeys prior to anesthesia, following the induction of deep ether anesthesia and throughout the cooling course during surface-induced hypothermia to temperatures of 20 degrees C. As given, deep ether anesthesia alone significantly decreased CO 10% to 15% and output fraction (Qt) was decreased to the carcass, increased to the splanchnic circulation (although not statistically significant), and unchanged to other organs, while total vascular (TVR) and organ resistances were reduced. With the addition of cooling, CO progressively decreased. Individual organ Qt's, however, did not change from anesthetized normothermic values; thus organ flows decreased parallel to the reduction of CO as cooling progressed. TVR and organ vascular resistances increased to levels in excess of 150% of anesthetized precooling values, apparently as the result of viscosity rather than vascular changes.

Anesthesia, Inhalation↗
PubMed1979

The effect of methylmercury on isolated cardiac tissues.

The effect of methylmercury hydroxide (MMH) on the frequency of spontaneously beating atrial-SA node and on the isometric tension of electrically stimulated left atrial (1 Hz) preparation isolated from rats were investigated. The tissues were also fixed for ultrastructural study at the end of the experiments. We found that MMH, at low doses (0.5 and 2ppm), increased the frequency of contractions and the isometric tension of isolated atria and decreased the isometric tension of isolated papillar muscles, and at higher doses (greater than 2ppm), decreased all the above parameter. Morphologically, there were dilation and swelling of mitochondrial and sarcoplasmic reticulum. Occasionally, deposits of amorphous material in the mitochondria and myofibrillary degeneration of myocardial fibers were noted. It is concluded the MMH has direct effect on intracellular organelles (mitochondria, sarcoplasmic reticulum, and myofibril) of myocardial tissue and induces functional changes of atria and papillary muscles

Animals↗
PubMed1978

Effects of halothane on Ca2+-activated tension development in mechanically disrupted rabbit myocardial fibers.

The effect of halothane on maximal and submaximal Ca2+-activated tension in mechanically disrupted right ventricular papillary muscle from rabbits was studied. Steady-state isometric tension generation was measured in the muscle bundle. The relaxing solution contained (in mM) [Mg2+] = 1, [K+] = 70, [MgATP2-] = 2, [creatine phosphate2-] = 15, [EGTA total] = 7 and imidazole proprionate. The contracting solution contained in addition Ca2+ in various concentrations. In all solutions ionic strength was maintained at 0.15 and pH at 7.00 +/- 0.02 at 20 degrees C. Each fiber bundle was immersed in control solutions equilibrated with 100% N2 and test solutions equilibrated with various concentrations of halothane-N2 mixture. Increasing doses of halothane (1--4%) significantly shifted the relationship between Ca2+ and tension towards higher [Ca2+] and depressed the maximum Ca2+-activated tension. The maximum tension generated at pCa = 3.8 was depressed 5% per 1% increase in halothane concentration. The percentage of maximum tension at submaximum Ca2+ concentrations (pCa = 5.6--5.0) was not significantly decreased until halothane concentration was greater than 2%. It is concluded that halothane slightly but significantly depressed the interactions of contractile proteins and to a lesser degree Ca2+-activation of the regulatory proteins. The halothane-induced depression was completely reversible.

Adenosine Triphosphatases↗
PubMed1976

Influence of hyperthyroidism on glycerol-extracted cardiac muscle from rabbits.

The mechanism responsible for the enhancement of myocardial contractility in hyperthyroidism is unclear. The possibility that this mechanism may involve a direct effect on the contractile proteins was investigated using the glycerol-extracted muscle strip from right ventricular papillary muscles of euthyroid rabbits and rabbits made hyperthyroid by the intraperitoneal injection of 0.25 mg/kg 1-thyroxine for 10 d. Intact papillary muscles from the hyperthyroid rabbits had an enhanced rate of tension development, a decreased time to peak tension, and a slight though insignificant increase in active tension compared to control animals. Maximal isometric contractions were induced in glycerol-extracted cardiac muscle strips from the two animal groups by the addition of 5 mmol/litre ATP and 5 mmol/litre MgCl in a buffer solution containing 0.15 mol/litre Tris-HCl (pH 7.1) at 26 degrees C. Peak isometric tension was increased in glycerinated muscle strips from hyperthyroid rabbits (1.52+/-0.10 vs 1.26 +/-0.13g/mm2), but the differences did not reach statistical significance. However, there was a marked increase in the rate of tension development in the hyperthyroid group (62.5+/-5.4 vs 41.8+/-4.7 mg/mm-2/s, P less than 0.01). This increase in the rate of isometric tension development in both intact and glycerinated muscles from hyperthyroid rabbits may be related to changes in the intrinsic turnover of actomyosin cross-bridge links in this condition. Thus, these findings suggest that thyroid hormone may influence cardiac muscle function by a direct effect on the contractile proteins.

Adenosine Triphosphate↗
PubMedDate not supplied

24xi-Methyl 5 alpha-cholestane-3 alpha,6 beta,9 alpha,25-tetrol 24-monoacetate, a novel polyhydroxylated steroid from the soft coral Sarcophyton tortuosum.

A novel polyhydroxylated steroid, named sartortuosterol A, with rare 3 alpha- and 6-hydroxyl groups, was isolated from the South China Sea soft coral Sarcophyton tortuosum Tixier-Durivault, and its structure was established as 24xi-methyl 5 alpha-cholestane-3 alpha, 6 beta, 9 alpha,25-tetrol 25-monoacetate from spectroscopic data and chemical conversions.

Animals↗
PubMedDate not supplied

Substrate- and effector-induced conformational changes in phosphofructokinase from white muscle of rainbow trout (Oncorhynchus mykiss): a fluorescence study.

Results of activity and spectral studies using fluorescence show that AMP and fructose 2,6-bisphosphate (F2,6P2) activate muscle phosphofructokinase (PFK) from rainbow trout (Oncorhynchus mykiss) through specific and similar conformational changes. Inorganic compounds, such as ammonium and phosphate ions, also increase enzyme activity allosterically; however, the structural alterations in the enzyme caused by these effectors are quite different from those caused by AMP and F2,6P2. No effects of the inorganic compounds on the environment of tryptophan residues of the enzyme were observed. Mg-ATP, a substrate of the enzyme, acts as an allosteric inhibitor at high concentrations. Although Mg-ATP and citrate inhibit the enzyme activity in a synergistic way, the conformational effects of these negative effectors are different. Mg-ATP caused a drastic decrease in fluorescence intensity of the enzyme, whereas citrate did not.

Adenosine Monophosphate↗