ABSTRACT
Two isomers of nitrochlorobenzene (o-, and p-NCB) were treated by a Pd/Fe catalyst in aqueous solutions through catalytic amination and dechlorination. Nitrochlorobenzenes are rapidly converted to form chloroanilines (CAN) first through an amination process, and then rapidly dechlorinated to become aniline (AN) and Cl(-), without the involvement of any other intermediate reaction products. The amination and dechlorination reaction are believed to take place predominantly on the surface site of the Pd/Fe catalysts. The dechlorination rate of the reductive degradation of the two isomers of nitrochlorobenzene (o-, and p-NCB) in the presence of Pd/Fe as a catalyst was measured experimentally. In all cases, the reaction rate constants were found to increase with the decrease in the Gibbs free energy (correlation with the activation energy) of NCBs formation; the activation energy of each dechlorination reaction was measured to be 95.83 and 77.05 kJ/mol, respectively for o- and p-NCB. The results demonstrated that p-NCBs were reduced more easily than o-NCBs.
Subject(s)
Catalysis , Industrial Waste , Iron , Chemistry , Isomerism , Kinetics , Metals , Chemistry , Nitrobenzenes , Chemistry , Palladium , Chemistry , Structure-Activity Relationship , Waste Disposal, Fluid , Methods , Water , Chemistry , Water Purification , MethodsABSTRACT
The Na(+)-Ca(2+) exchange is a major pathway for removal of cytosolic Ca(2+) in cardiac myocytes. To explore the effects of temperature, intracellular Na(+), ATP and pH on Na(+)-Ca(2+) exchange currents (I(Na/Ca)) of intact guinea-pig myocytes, the whole-cell patch-clamp technique was used to record I(Na/Ca) in isolated guinea-pig ventricular myocytes. We found that I(Na/Ca) at 34 degrees C was four times higher than that at 22 degrees C. However, intracellular acidification had no obvious influence on bidirectional I(Na/Ca). At 22~24 degrees C , intracellular ATP depletion and intracellular acidification did not markedly affect bidirectional I(Na/Ca) either. At 34~37 degrees C , intracellular ATP depletion and intracellular acidification synergistically inhibited the outward and inward currents of I(Na/Ca), and blocked the inward currents of I(Na/Ca)more potently than the outward currents of I(Na/Ca). The effect of ATP on I(Na/Ca) is temperature-dependent. Intracellular higher sodium increased the outward currents of I(Na/Ca) however it did not increase, even sometimes decreased the inward currents of I(Na/Ca). These results suggest that intracellular ATP depletion and intracellular acidification synergistically impair Ca(2+) extrusion via forward mode Na(+)-Ca(2+) exchange, and intracellular sodium overload increases Ca(2+) influx via reverse mode Na(+)-Ca(2+) exchange, leading to calcium overload respectively.
Subject(s)
Animals , Male , Adenosine Triphosphate , Physiology , Calcium , Metabolism , Guinea Pigs , Heart Ventricles , Cell Biology , Pathology , Hydrogen-Ion Concentration , Hypoxia , Intracellular Fluid , Physiology , Myocytes, Cardiac , Metabolism , Physiology , Patch-Clamp Techniques , Sodium , Physiology , Sodium-Calcium Exchanger , Physiology , TemperatureABSTRACT
<p><b>AIM</b>To elucidate the possible mechanisms underlying antiarrhythmia of the non-selective Na+/H+ exchanger inhibitor--amiloride.</p><p><b>METHODS</b>Single ventricular cells were isolated using a double-enzyme method. Effects of amiloride on voltage-dependent potassium and calcium currents in isolated guinea pig ventricular myocyte were recorded by using whole-cell patch clamp techniques.</p><p><b>RESULTS</b>Exposure to amiloride (10 -100 micromol x L(-1)), the L-type and T-type calcium currents were depressed. Amiloride resulted in a concentration-dependent inhibition of peak (Ca,L), But amiloride did not change the shape of their I - V curves. It only decreased the amplitudes of the currents of the two types. When myocytes were incubated with 100 micromol x L(-1) amiloride, I(Kr) was slightly depressed and I(Ks) did not change. Amiloride (1 - 100 micromol x L(-10) depressed I(K1) in a concentration-dependent manner.</p><p><b>CONCLUSION</b>Amiloride depressed potassium and calcium currents, which may give support to its uses in some diseases of the cardiovascular system.</p>
Subject(s)
Animals , Female , Male , Amiloride , Pharmacology , Anti-Arrhythmia Agents , Pharmacology , Calcium Channels, L-Type , Calcium Channels, T-Type , Cell Separation , Guinea Pigs , Heart Ventricles , Cell Biology , Myocytes, Cardiac , Patch-Clamp Techniques , Potassium Channels, Inwardly Rectifying , Potassium Channels, Voltage-Gated , Sodium-Hydrogen ExchangersABSTRACT
<p><b>AIM</b>To observe the effects of ouabain on vascular smooth muscle (VSM) of the guinea pig and its interactions with Ca2+ and norepinephrine (NE).</p><p><b>METHODS</b>Using isolated thoracic aortic ring of the guinea pig, the degrees of contractile activity of drugs were recorded.</p><p><b>RESULTS</b>Ouabain showed a direct contractile effect in a concentration-dependent manner on thoracic aortic ring of guinea pig. Ouabain shifted the NE dose-response curve to the left without changing in the maxium response. Ouabain shifted the CaCl2 dose-response curve to the left and upward, increased the maximum response to Ca2+; In Ca(2+)-free medium, the ouabain induced contraction was abolished, an increase in extracellular Ca2+ restored the response; nifedipine and verapamil abolished the ouabain induced contraction.</p><p><b>CONCLUSION</b>The ouabain induced contraction is mainly dependent on the extracellular Ca2+ concentration, independent on the presence of endothelia of aorta, suggesting that Ca2+ antagonist may treat the hypertension induced by ouabain. Ouabain, NE and CaCl2 have synergetic contractile effects, suggesting that the synergetic contractile effects of ouabain and NE may contribute to the generation and development of hypertension.</p>