Biomedical subjects

X X Luo

Publications and source records attributed to X X Luo.

At least 19 recordsLinked to original sources

PubMed2004

Effects of Chinese, Japanese and Western tea on hepatic P450 enzyme activities in rats.

Previous studies have reported that green tea effectively protects against cancers caused by various dietary carcinogens. As P450 enzymes are the major system responsible for the metabolism of many carcinogens, we hypothesise that tea consumption may alter the catalytic activities of P450 enzymes. We conducted this study to screen the effects of four different teas on the activities of P450 enzymes. Tea solutions (2.5%) were prepared by adding boiling water to tea leaves and filtering. Female Wistar rats were divided into five groups (n = 4 each); each had free access to tea solutions while the control group was supplied with water for 4 weeks. Animals were sacrificed and livers were removed for preparation of microsomes. Enzyme activities were determined by incubation of liver microsomes with the appropriate CYP substrate. The activity of CYP1A1 in livers from rats receiving Oolong (Chinese) tea (185 +/- 63 pmol/mg/min), Japanese green tea (197 +/- 22 pmol/mg/min) and Earl Grey tea (228 +/- 40 pmol/mg/min) was significantly higher (p < 0.05) than in the control group (94 +/- 34 pmol/mg/min), whereas no change was observed in the activity of CYP1A2 in any of tested animals. The hepatic activity of CYP2D6 was greater only in rats drinking Earl Grey tea compared to the controls (235 +/- 37 vs 161 +/- 41 pmol/mg/min, p < 0.05). There were also significant increases (p < 0.05) in the activity of CYP3A in livers of animals given Oolong tea (653 +/- 174 vs 382 +/- 114 pmol/mg/min) and Earl Grey tea (751 +/- 202 pmol/mg/min), while Jasmine and Japanese green tea had no significant effect. These results indicate that not all types of tea cause alterations in liver CYP enzymes as some elevated activities and some did not. Further studies are needed to determine whether there is a relationship between the effect of tea on CYP activities and anti-carcinogenesis.

Animals↗

PubMed1996

Significance of elevated cytochrome aa3 in a state of endotoxemia in dogs.

It is now possible to detect quantitative changes in cytochrome aa3 by means of near-infrared spectrophotometry. This technique is also suitable for determining oxidised hemoglobin (HbO2), reduced hemoglobin (Hb), cerebral blood volume, and the redox state of cytochrome aa3 (cyt aa3) in the tissues. The significance of elevated cyt aa3, measured by near-infrared spectrophotometry, is still unclear, so we investigated this question using both near-infrared spectrophotometry and oxygen saturation meters in endotoxemic dogs. Ten anaesthetised mongrel dogs were injected with endotoxin (E. coli 0111: B4 Difco 2 mg/kg i.v.) and the redox state of Hb and cyt aa3 was determined in real time by near-infrared spectrophotometry. The levels of arterial and cisternal venous oxygen saturation were recorded simultaneously by two Oximetrix 3 saturation meters to calculate the cerebral arterial and venous oxygen saturation difference (Sata-vO2D) in real time. HbO2 decreased along with the fall in mean arterial pressure and remained at a low level, while Hb increased and remained at a high level. The cerebral blood volume decreased in the endotoxic early stage and then returned gradually towards baseline. Cyt aa3 showed an increase following endotoxin injection and maintained an oxidised form. The cerebral Sata-vO2D rose to about three times the control level. From these observations, an increase of oxidised cytochrome aa3 after endotoxin administration seems to be a compensatory protective effect in response to the cerebral oxygen demand rather than over-oxygenation or hyperoxia.

Animals↗

PubMed1996

Direct evidence for histamine H3 receptor-mediated inhibition of norepinephrine release from sympathetic terminals of guinea pig myocardium.

AIM: To study the histamine H3 receptors mediated inhibition of norepinephrine (NE) release from cardiac sympathetic terminals of guinea pig isolated atria. METHODS: Release of NE induced by electric field stimulation (50 mA, 5 ms) in the bath solution was measured by HPLC-ECD. RESULTS: The release of NE caused by field stimulation was attenuated by (R)-alpha-methyl-histamine (alpha-MeHA, 0.1 nmol.L-1(-10) mumol.L-1) in a concentration-dependent manner. Thioperamide concentration-dependently antagonized the inhibition of alpha-MeHA. Blockade of H1, H2, alpha 2, beta 2-receptors failed to prevent the inhibitory effect of alpha-MeHA. Thioperamide (1 nmol.L-1(-10) mumol.L-1), when used alone, concentration-dependently facilitated the release of NE evoked by field stimulation. CONCLUSION: The presynaptic histamine H3-receptors inhibited the NE release from cardiac sympathetic terminals.

Adrenergic Fibers↗

PubMed1995

[Improvement of cerebral oxidative metabolism and cytochrome aa3 redox state by 7.5% hypertonic saline during hemorrhagic hypotension in dogs].

Our previous study reported that 20% (1.5 ml.kg-1 hypertonic saline could significantly improve the disturbances of cerebral oxidative metabolism induced by hemorrhagic hypotension in dogs. The aim of the present study is to evaluate if 7.5% hypertonic saline induces circulatory improvement. Ten dogs were randomly divided into two groups of 5 each resuscitated with either physiological saline as control or 7.5% hypertonic saline (4 ml.kg-1) after their mean arterial blood pressure decreased to 35 mmHg for 45 minutes by hemorrhage. The changes of cerebral tissue oxy- and deoxyhemoglobin, cerebral blood volume (total hemoglobin), and oxy-cytochrome aa3 were continuously monitored by near infrared spectroscopy throughout the experiment. The experimental result showed that oxy-hemoglobin, oxy-cytochrome aa3, and cerebral blood volume decreased but deoxyhemoglobin increased significantly 45 minutes after hemorrhage. Treatment with 7.5% hypertonic saline significantly restored these variables except for cerebral blood volume and all the animals survived to the end of experiment. But in the control group treated with the same dose of physiological saline, the above variables improved little compared with the baseline; and all the animals died before the end of 60 min experimental observation. Therefore we conclude that 7.5% hypertonic saline (4 ml.kg-1) can also effectively improve the disturbance of cerebral oxidative metabolism induced by hemorrhagic hypotension.

Animals↗

PubMed1995

[Presynaptic histamine H3-receptors exist on cardiac sympathetic terminals of guinea pig].

This is the first time to report the existence of new presynaptic inhibitory autoreceptors--histamine H3-receptors in guinea pig myocardium. We found that (R)-alpha-methylhistamine (alpha-MeHA), a selective histamine H3-receptor agonist, attenuates the sympathetic inotropic response of isolated guinea pig atria elicited by electrical field stimulation. This inhibition was associated with a marked reduction in endogenous norepinephrine release. The above phenomenon was antagonised by selective histamine H3-receptor antagonists, and inhibited by pretreatment with N ethylmeleimide. The cardiac sympathetic response could be attenuated or facilitated by increase or decrease of endogenous histamine. Our findings indicate that the endogenous histamine might be involved in the modulation of cardiac sympathetic neurotransmission by interacting with histamine H3-receptors and the receptors are probably coupled to a G(o)/Gi protein.

Animals↗

PubMed1994

Hypertonic saline improves cerebral oxidative metabolism and cytochrome aa3 redox state during hemorrhagic hypotension in dogs.

Hypertonic saline used in the treatment of hemorrhagic shock dramatically improves cardiovascular performance. In the present study, our focus was on whether it would improve disturbances of cerebral oxidative metabolism induced by hemorrhagic hypotension. Fourteen dogs were bled over a period of 15 min so that the mean arterial blood pressure of seven dogs (group H) fell to 65 mmHg and that of the other seven (group L), to 45 mmHg. These pressures were maintained for 30 min, and then 20% hypertonic saline (1.5 ml/kg body weight) was injected intravenously. Cerebral oxyhemoglobin, deoxyhemoglobin, cerebral blood volume, and oxidized cytochrome aa3 were continuously monitored by near-infrared spectroscopy throughout the experiment. The experimental results showed that 45 min of hemorrhagic hypotension led to decreases in cerebral oxyhemoglobin (from control level 0 to -25.5 +/- 7.5 microM/liter brain tissue in group H and to -32.3 +/- 7.5 microM/liter brain tissue in group L), in total hemoglobin (from control level 0 to -7.2 +/- 1.8 microM/liter brain tissue in group H and to -6.5 +/- 1.7 microM/liter brain tissue in group L), and in oxidized cytochrome aa3 in group L (from control level 0 to -0.8 +/- 0.4 microM/liter brain tissue), but to increases in deoxyhemoglobin (from control level 0 to 15.5 +/- 5.0 microM/liter brain tissue in group H and to 25.8 +/- 3.4 microM/liter brain tissue in group L) and in oxidized cytochrome aa3 in group H (from control level 0 to 0.6 +/- 0.3 microM/liter brain tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Comparison of effects of margarite extract and recombinant human superoxide dismutase on paraquat-induced superoxide anion radicals in rat lung.

The effects of medicinal margarite extract and recombinant human superoxide dismutase (r-h SOD) on acute paraquat intoxication were examined in the rat lung. Forty-eight Sprague-Dawley rats under pentobarbital anesthesia were randomly assigned to one of four groups receiving i.v. injection of physiological saline (control), i.v. injection of 70 mg/kg paraquat, or i.v. injection of either 50 mg/kg of margarite extract or 50,000 unit/kg of r-h SOD 10 minutes before and 1 and 2 hours after an equivalent paraquat administration. Examination of lung superoxide anion radicals (O2-.), lipid peroxides, and histopathological changes showed that paraquat significantly increased superoxide anion radicals (383% of control) reacted with CLA-phenyl. Both margarite extract and r-h SOD decreased superoxide anion radicals to 119% and 83% of control, respectively. Margarite extract, rather than r-h SOD, significantly alleviated the paraquat-induced infiltration of polymorphonuclear leukocytes and macrophages into the alveolar walls. There were no significant inter-group differences in lipid peroxides in the lung. Component analysis showed that margarite extract was rich in L- and D-arginine. The scavenging mechanism of margarite extract may be related to L-arginine but needs to be further verified in the future study.

Animals↗

PubMed1994

[Histopathological changes produced in organs by platelet activating factor].

This experiment was conducted to investigate the effect of platelet activating factor (PAF) on the pathological changes in organs using 10 mice (C3H/HeN). Ten mice were divided into two groups of acute and chronic experiment groups. In acute experiment, each mice received iv bolus injection of PAF 2.5 micrograms.kg-1 and in chronic experiment daily ip injection of PAF 7.5 micrograms.kg-1 for 7 days. Histopathology was observed with light microscopy after one hour or after 7 days by haematoxylin and eosin stain. In acute experiment, congestion of the lung, liver, kidney and spleen in all cases, right ventricular dilation in 2 cases and villous necrosis in the small intestine in 4 cases were observed. In chronic experiment, hyaline thrombus with congestion of the lung in 3 cases and congestion of the liver and kidney in all cases were observed. Splenomegaly with increased macrophage was observed, but no necrosis in the small intestine was observed. Marked findings were villous necrosis in the small intestine in acute experiment and hyaline thrombus in the lung as well as splenomegaly in chronic experiment.

Animals↗

PubMed1994

[Synthesis of N-(4-carbomethoxy-4-phthalimidobutanoyl)-N-substituted glycines, proline and pyroglutamic acid].

This paper reports the synthesis of eleven N-(4-carbomethoxy-4-phthalimidobutanoyl)-N-substituted glycines (VII1-9), proline (VII10) and pyroglutamic acid (VII11) expected to have inhibitory activity on angiotensin converting enzyme. All of the compounds mentioned above and the corresponding t-butyl esters of VII1-9 were not reported in the literature previously. The structures were confirmed through their IR, 1HNMR, MS spectra and elemental analysis. In preliminary test in rats, compounds VII8, VII9 and VII10 showed marked hypotensive activity.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

[Protective effect of tetramethylpyrazine on ischemic neuronal damage in the gerbil hippocampus].

The effect of tetramethylpyrazine on ischemic neuronal damage was studied in gerbil hippocampus in the terms of histopathological change and cerebral tissue lipid peroxides. Fifteen-five Mongolian gerbils were randomly assigned to one of three groups: sham-operated as control, subjected to 12 min global cerebral ischemia followed by 7 day spontaneous circulatory reperfusion, in which animals were treated with either ip. physiological saline or 60 mg/kg of tetramethylpyrazine 30 min before ischemia and daily thereafter for 7 days. The number of survival pyramidal neurons in the CA1 was counted: 263 +/- 8 (cell/mm) in the sham-operated group, 20 +/- 6 in the ischemia group, and 189 +/- 56 in the group treated with tetramethylpyrazine. Changes in lipid peroxides, expressed as malondialdehyde (MDA), was 134.5 +/- 5.0 nmol/g tissue in the sham-operated group, 193.5 +/- 5.1 in the ischemia group, and 137.6 +/- 10.8 in the group treated with tetramethylpyrazine. These results indicate that tetramethylpyrazine has a protective effect on the ischemic neuronal damage in hippocampus. Free radicals and free calcium may play an important role in pyramidal neuron necrosis in hippocampus following cerebral ischemia.

Animals↗

PubMed1994

Presynaptic histamine H1- and H3-receptors modulate sympathetic neurotransmission in isolated guinea pig vas deferens.

The action of (R)-alpha-methylhistamine (alpha-MeHA), a selective H3-receptor agonist, on field stimulation induced contraction of guinea pig vas deferens was composed of 2 components: the "inhibition" (0.1-100 nmon.L-1) and the "enhancement" (1-10 mumol.L-1). In the presence of histamine H1 antagonist, chlorpheniramine (1 mumol.L-1), alpha-MeHA (0.1 nmol.L-1-10 mumol.L-1) showed only a concentration-dependent inhibition. Selective histamine H3-receptor antagonist, thioperamide (1 nmol.L-1-10 mumol.L-1) antagonized the inhibitory effect of alpha-MeHA and increased the contractile amplitude of vas deferens elicited by field pulses when thioperamide was used alone. alpha-MeHA 10 mumol.L-1 enhanced the contractile amplitude, which was reversed by chlorpheniramine 1 mumol.L-1, but not by ranitidine (1 mumol.L-1). Pyridelethylamine, an H1-receptor agonist, facilitated concentration-dependently the contractile response of vas deferens. The effect was antagonized by chlorpheniramine, but not by ranitidine. Dimaprit, an H2-receptor agonist had no effect on the field stimulation induced sympathetic response. Both alpha-MeHA and pyridelethylamine failed to influence the contraction of vas deferens elicited by direct field stimulation in smooth muscle or by exogenously applied norepinephrine. It was concluded that histamine H1- and H3-receptors existed in sympathetic terminals of guinea pig vas deferens and facilitated or inhibited the sympathetic neurotransmission.

Animals↗

PubMed1994

Inhibition of sympathetic neurotransmission via NEM-sensitive H3-receptors in the guinea pig vas deferens.

The influence of N-ethylmaleimide (NEM) on sympathetic neurotransmission induced by field stimulation on the isolated guinea pig vas deferens was studied. Application of (R)-alpha-methylhistamine (0.1 mcmol/l) significantly inhibited the sympathetic response by 26.0%, while thioperamide facilitated the sympathetic contraction of vas deferens evoked by field pulses by 221.1%. Pretreatment of vas deferens with NEM (60 mcmol/l) for 15 min abolished both the inhibitory and facilitatory effects. Attenuation of thioperamide facilitatory effect by NEM was not significantly altered when the H3-receptors were occupied by thioperamide prior to and during NEM treatment. The results suggest that effects mediated by H3-receptors in the guinea pig vas deferens were NEM-sensitive and possibly transmitted by Gi or Go proteins.

Animals↗

PubMed1994

[Comparative study of 20% marine salt and 20% NaCl on circulatory dynamics during hemorrhagic shock in dogs].

This study was conducted to investigate the effect of 20% marine salt as compared with 20% NaCl solution, on the circulatory dynamics in hemorrhagic shock using mongrel dogs. Ten mongrel dogs were randomly divided into two groups. One treated with 20% marine salt, and the other treated with 20% NaCl. Modified Wigger's method was used to induce hemorrhagic shock. Hypotension was kept at 45 mmHg for 45 minutes and then 1.5 ml.kg-1 of 20% marine salt or 20% NaCl was injected intravenously in bolus. Twenty percent marine salt reduced total peripheral resistance and increased cardiac output with statistically significant difference compared with 20% NaCl. There were increases in MAP, PAP and PWP without statistic differences between the two groups. These results suggest that 20% marine salt, including various trace elements, is superior to 20% NaCl in improving cardiac output and TPR during hemorrhagic shock.

Animals↗

PubMed1993

Acute morphologic changes in orbicularis oculi muscle after doxorubicin injection into the eyelid.

This study attempts to gain a better understanding of the primary cause of doxorubicin myotoxicity to aid in the development of a protocol to increase its effectiveness in treating muscle spasm diseases. The time course of acute injury to the orbicularis oculi muscle after injection of doxorubicin into the eyelids of rabbits was examined. The effects of doxorubicin injection were immediate and dramatic. Within 5 minutes, the muscle cells in the eyelids showed signs of myofibrillar dissolution. This process continued for the first 24 hours, with a marked decrease in the total number of myofibers by 1 hour after drug treatment. By 4 days after doxorubicin injection, most of the treated muscle had a more normal morphology, although some ongoing myofibrillar dissolution was present. There was evidence for a limited amount of muscle regeneration. Three levels of injury were seen: a severe, irreversible injury in the majority of the myofibers; a mild, reversible injury in a subset of the fibers; and a group of myofibers apparently uninjured as a result of doxorubicin treatment. Doxorubicin toxicity in skeletal muscle is of rapid onset. Understanding the primary cause and acute changes in doxorubicin myotoxicity may accelerate the development of improved protocols to increase the effectiveness of doxorubicin in treating muscle spasm diseases.

Animals↗

PubMed1993

Effects of hypertonic saline solution (20%) on cardiodynamics during hemorrhagic shock.

The cardiodynamic effects of using hypertonic saline solution were analyzed in dogs after inducing hemorrhagic shock. Administration of 1.5 mL/kg 20% sodium chloride resulted in circulatory improvement: 200% increase in blood pressure, 260% increase in cardiac output, 60-70% increase in pulmonary arterial pressure, 66% increase in pulmonary wedge pressure, 200% increase in central venous pressure, 33% decrease in total peripheral resistance, and 40% decrease in pulmonary vascular resistance. The effects of sodium chloride on cardiodynamics probably resulted in elevation of preload and reduction of afterload.

Animals↗

PubMed1992

[The effects of 20% saline solution on the circulatory dynamics during the hemorrhagic shock state].

This experiment was performed to study the effects of administration of 20% saline solution 1.5 ml.kg-1 on the circulatory dynamics during the hemorrhagic shock state. Administration of 20% saline solution 1.5 ml.kg-1 during the hemorrhagic shock produced twofold increase of the mean arterial blood pressure for one hour, 2.5 fold increase of the cardiac output, increasing tendency in the mean pulmonary arterial pressure, central venous pressure, and the heart rate, accompanied by decrease in total peripheral resistance and the pulmonary blood vessel resistance. There were no improvements in acidosis and hematocrit. These data suggest that the circulatory improvements after the administration of 20% saline solution depend on an increase in cardiac output as the result of improvements in both pre- and after-load, but not of plasma volume expansion. The results also suggest that the administration of 20% saline solution 1.5 ml.kg-1 is useful for an emergency case with acute circulatory insufficiency or for emergency resuscitation.

Animals↗

PubMed1991

Histamine H3-receptors inhibit sympathetic neurotransmission in guinea pig myocardium.

The histamine H3 agonist, (R)-alpha-methylhistamine (alpha-MeHA, 10(-10) to 10(-5) M), caused a concentration-dependent inhibition of the sympathetic contractile response to electrical field stimulation of guinea pig isolated atria, but alpha-MeHA did not alter the basal tension or the contraction induced by exogenously applied norepinephrine. Blockade of H1 and H2 histamine receptors, and alpha- and beta-adrenoceptors failed to prevent the inhibitory effect of alpha-MeHA, whereas the specific H3 receptor antagonist, thioperamide, concentration dependently reversed the inhibitory effect of alpha-MeHA. At the concentration of 10(-7) M, which was effective for antagonizing the action of alpha-MeHA, thioperamide did not modify the sympathetic responses facilitated by the beta 2-adrenoceptor agonist, clenbuterol, or attenuated by the alpha 2-adrenoceptor agonist, clonidine. Our results suggest that H3 receptors exist on the cardiac sympathetic terminals, which may modulate adrenergic neurotransmission in guinea pig myocardium.

Animals↗

PubMed1990

[Effects of ranitidine and cimetidine on automaticity in isolated myocardium of guinea pig].

At 0.1-30 mumols/L, neither ranitidine (Ran) nor cimetidine (Cim) inhibited the rate of spontaneous contraction in isolated right atria of guinea pig. When the concentration was higher than 100 mumols/L, both Ran and Cim exhibited weak negative chronotropic effects with IC50 of 109 +/- 3 and 436.5 +/- 1.9 mumols/L, respectively. However, the positive chronotropic effects of histamine (H) were markedly antagonized by Ran and Cim with IC50 of 0.40 +/- 0.29 and 1.8 +/- 0.6 mumols/L respectively. Ran (0.1 mumols/L) and Cim (1 mumols/L) competitively antagonized the concentration-dependent response of positive chronotropic effect mediated by H and had no influence on that induced by isoproterenol in right atria of guinea pig. Ran (10 mumols/L) and Cim (50 mumols/L) prevented the abnormal automaticity elicited by H and H (0.12 +/- 0.09 mumols/L) + Oua (0.04 +/- 0.02 mumols/L) which acted synergically. The abnormal automaticity induced by Oua (1.5 +/- 2.3 mumols/L) was antagonized by Ran (10 mumols/L) and not by Cim (50 mumols/L). Our results suggest that these effects of Ran and Cim are mainly attributed to cardiac H2 receptor blockade.

Animals↗