Search PubMed⌕ Search

Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 127 records · Page 7Linked to original sources

Increase of locomotor activity by acupuncture on Bai-Hui point in rats.

The effect of acupuncture on locomotor activity was investigated in rats. Stimulation with acupuncture inserted in Bai-Hui point, which is located at the vertex of the head, increased the spontaneous locomotor activity of rats measured in ANIMEX meter. This effect was obtained in rats which received acupuncture significantly at 60 min later as compared with sham-treated control. The sleeping time induced by hexobarbital was also reduced markedly in rats receiving acupuncture. An activation of the central nervous system by acupuncture at Bai-Hui point can thus be considered. This action was unrelated to opioids because naloxone failed to modify it. Increase in locomotor activity was abolished by an intraperitoneal (i.p.) injection of alpha-methyl-p-tyrosine (200 mg/kg) at 2 h before insertion of acupuncture. Deprenyl at the dose sufficient to elevate monoamine enhanced this action of acupuncture. Mediation of cerebral monoamines can also be considered. This view was supported by the dose-dependent inhibition of chlorpromazine. Action of acupuncture was not observed in apomorphine (0.5 mg/kg, i.p.)-treated rats, probably due to an activated receptor of dopamine. Otherwise, action of acupuncture was enhanced by para-chlorophenylalanine, the depleter of endogenous 5-hydroxytryptamine (5-HT), and eliminated by 5-hydroxytryptophan, the precursor of 5-HT, in the initial stage of insertion. Participation of 5-HT can be considered as an initial way in rats that received acupuncture at Bai-Hui point. These results suggested that stimulation of Bai-Hui point with acupuncture can activate central neurotransmission of monoamines to increase the spontaneous locomotor activity in rats.

Acupuncture Points↗

Isolation of synaptosomes from the rat urinary bladder.

Synaptosomes are nerve-end particles (NEP) isolated by using the technique of differential centrifugation. The synaptosome offers a good model for biochemical and pharmacological studies of the nerve endings. No report has been made on synaptosome isolation from the urinary bladder. The purpose of our work was to develop the use of synaptosome in the research of neurophysiology and neuropharmacology of the urinary bladder. Synaptosome-rich fraction was prepared from tissue homogenate of male Wistar rat urinary bladder by differential centrifugation (1000, 17,000 and 100,000 g) with discontinuous sucrose gradient. Electron microscopy showed synaptosomes as thin-walled bags containing a large number of synaptic vesicles. Two types of synaptosomes were easily discerned: those containing small agranular vesicles, and those containing dense-cored vesicles. The acetylcholine, norepinephrine, epinephrine and dopamine contents in the preparation were measured by the method of high-performance liquid chromatography. The respective concentrations were 300.4 +/- 30.1, 962.8 +/- 58.5, 617.3 +/- 59.8 and 1354.8 +/- 144.2 pmol/mg synaptosomal protein. In conclusion, it has been demonstrated that synaptosome-rich fractions can be prepared from the rat urinary bladder. Thus it is possible to apply this methodology for the investigation of the neurobiology of urinary bladders.

Animals↗

Alterations in urinary bladder synaptosomal neurotransmitter concentrations in two-week streptozotocin-induced diabetic rats.

Three-month-old male Wistar rats were rendered diabetic with a single intravenous injection of streptozotocin (60 mg/kg body weight). Two weeks after induction of diabetes, synaptosome-rich fractions were prepared from urinary bladder tissue homogenate of the diabetic rats and control rats by differential centrifugation (1000 x g, 17,000 x g and 100,000 x g) with discontinuous sucrose gradient. Synaptosomal acetylcholine, norepinephrine, epinephrine and dopamine were measured by the method of high-performance liquid chromatography. The respective neurotransmitter concentrations for the diabetic rats were 1537.8 +/- 65.3, 4757.7 +/- 361.9, 3720.7 +/- 276.1, and 2447.8 +/- 196.8 pmol/mg synaptosomal protein, respectively; those for the control rats were 338.1 +/- 25.0, 1009.0 +/- 54.6, 645.3 +/- 52.2, and 1426.1 +/- 123.9 pmol/mg protein, respectively. Thus, the synaptosomal concentrations for all the measured neurotransmitters were significantly higher in the diabetic rats (P < 0.05 for each comparison). In conclusion, it has been demonstrated that the vesicle-bound acetylcholine and catecholamines in the synaptosome-rich fraction of the urinary bladder were significantly increased in 2-week diabetic rats. This finding would suggest impaired neurotransmitter release from both the bladder sympathetic and parasympathetic efferent nerve endings in early streptozotocin-induced diabetes.

Acetylcholine↗

Comparisons of neurotransmitter concentrations in the synaptosomal preparation of the normotensive and hypertensive rat urinary bladder.

Synaptosome-rich fractions were prepared from tissue homogenate of the urinary bladder of the spontaneously hypertensive rat and normotensive Wistar-Kyoto rat by differential centrifugation (1000 x g, 17 000 x g and 100 000 x g) with discontinuous sucrose gradient. Synaptosomal acetylcholine, norepinephrine, epinephrine and dopamine were measured by the method of high-performance liquid chromatography. The respective neurotransmitter concentrations for the normotensive rats were 300.4 +/- 30.1, 962.8 +/- 58.5, 617.3 +/- 59.8, and 1354.8 +/- 144.2 pmol/mg synaptosomal protein. For the hypertensive rats, the acetylcholine concentration (203.8 +/- 23.0 pmol/mg protein) was significantly lower (P < 0.05), while the norepinephrine, epinephrine and dopamine concentrations (1459.0 +/- 180.3, 971.3 +/- 62.2, and 2161.0 +/- 243.4 pmol/mg protein, respectively) were significantly higher (P < 0.05 for all) than those of the normotensive rats. In conclusion, it has been demonstrated that the vesicle-bound catecholamines in the synaptosome-rich fraction of the urinary bladder were significantly increased in hypertensive rats. On the contrary, the synaptosomal acetylcholine concentration was significantly decreased. These findings are suggestive of increased sympathetic innervation and decreased parasympathetic innervation in the urinary bladder of the spontaneously hypertensive rat.

Acetylcholine↗

The norepinephrine tissue concentration and neuropeptide Y immunoreactivity in genitourinary organs of the spontaneously hypertensive rat.

Tissue concentration of norepinephrine and neuropeptide-Y immunoreactivity (NPY-IR) were measured in the urinary bladder, urethra, prostate and corpus cavernosum of the spontaneously hypertensive rat, as well as the normotensive Wistar-Kyoto rat. The results showed significantly increased tissue norepinephrine concentrations in the urinary bladder, urethra and prostate of the spontaneously hypertensive rat when compared to those of the normotensive rat (hypertensive, n = 18: 18.3 +/- 2.1, 14.9 +/- 1.7, 22.6 +/- 2.3 vs. normotensive, n = 18: 11.2 +/- 1.9, 10.4 +/- 1.3, 16.7 +/- 2.4 nmol/g tissue, respectively, P < 0.05 in each case). No difference was noted in the cavernosal tissue (hypertensive, n = 18: 11.3 +/- 1.6 vs. normotensive, n = 18: 10.1 +/- 1.8 nmol/g tissue, P > 0.01). Correspondingly, tissue NPY-IR was significantly increased in the bladder, urethra and prostate tissue of the spontaneously hypertensive rat (hypertensive, n = 18: 39.7 +/- 5.6, 25.3 +/- 3.4, 31.5 +/- 2.8 vs. normotensive, n = 18: 27.4 +/- 3.1, 18.6 +/- 2.7, 24.2 +/- 3.2 pmol/g tissue, respectively, P < 0.05 in each case). Again, no significant difference was observed in the cavernosal tissue (hypertensive, n = 18: 15.9 +/- 2.2 vs. normotensive, n = 18: 14.8 +/- 2.6 pmol/g tissue, P > 0.01). It is therefore concluded that increased tissue concentration of norepinephrine and NPY-IR were present in the urinary bladder, urethra and prostate of the spontaneously hypertensive rat. The significance of such biochemical findings needs further investigation but may suggest increased sympathetic innervation or activity. On the contrary, no corresponding changes were observed in the corpus cavernosum of the hypertensive rat.

Animals↗

Characterization of subtypes of gamma-aminobutyric acid receptors in an Ascaris muscle preparation by binding assay and binding of PF1022A, a new anthelmintic, on the receptors.

We examined the effect of PF1022A, one of the gabergic anthelmintics newly developed in Japan, on gamma-aminobutyric acid (GABA) receptors using a radioligand binding technique in isolated membrane preparations of the nematode Ascaris suum. Membrane protein was prepared from the homogenate of somatic muscle cells after ultracentrifugation. In addition to the basic binding of [2,3-3H-(N)]-GABA, the radioligand [methyl-3H]-bicuculline is used to identify the GABAA receptor, whereas [butyl-4-3H]-baclofen is employed for GABAB receptor sites. The dissociation constants (Kd values) and the maximal numbers of binding sites (Bmax values) from Scatchard plotting for GABA receptors are close to those obtained in mammalian brain. PF1022A displaced in a concentration-dependent way the binding of [2,3-3H(N)]-GABA and [methyl-3H]-bicuculline as did other specific gabergic agents. In addition, PF1022A decreased the binding of [butyl-4-3H]-baclofen at a higher concentration, although this binding did not represent GABAB sites. In a comparison of the inhibition constants (Ki values) of PF1022A with those of other agents, it is conclusive that PF1022A bound with GABA receptors. A direct effect of PF1022A on GABA receptors can thus be postulated.

Animals↗

6-Hydroxydopamine induces thymocyte apoptosis in mice.

6-Hydroxydopamine (6-OHDA) induces degeneration of noradrenergic nerves and has been shown to alter the immune responses. In this study, intraperitoneal administration of 6-OHDA induces mouse thymus atrophy. The lowest levels of thymus weight and cell number were reached at days 3 and 5 in mice receiving 6-OHDA treatment; they gradually recovered thereafter. On flow cytometry analysis, the most substantial reductions were recorded for CD4+CD8+ thymocytes, although the numbers of other subpopulations, i.e. CD4+CD8-, CD4-CD8+ and CD4-CD8- cells were also reduced. DNA fragmentation, a characteristic of apoptosis, was detected in the thymocytes following 6-OHDA injection. Pretreatment with desipramine greatly blocked the reduction in thymus size and thymocyte number, the changes in thymocyte subpopulations, the percentage of subdiploid (apoptotic) cells and the appearance of DNA fragmented bands. Furthermore, 6-OHDA-induced thymocyte apoptosis could also be detected in vitro, and was blocked by desipramine treatment. These results indicate that 6-OHDA induces mouse thymocytes to undergo apoptosis both in vivo and in vitro, and this effect is inhibited by catecholamine uptake blocker.

Animals↗

The in vitro antioxidant activity of trilinolein and other lipid-related natural substances as measured by enhanced chemiluminescence.

There is abundant evidence for the premise that oxygen-derived free radicals (OFR) mediate ischemia/reperfusion injury to the myocardium. OFR scavengers such as superoxide dismutase can effectively reduce damage through lipid peroxidation during ischemia/reperfusion. Enhanced chemiluminescence, which has been used to measure OFR, was used to measure the antioxidant activity of fatty acids (palmitic and linoleic acid) and triglycerides (triolein, tristearin) and natural plant antioxidants (magnolol, catechin, trilinolein). Trilinolein, which has recently been isolated from natural products, as well as the well-known water soluble analogue of vitamin E-Trolox, were used as control. During pretreatment with chemicals, at concentrations of 10(-9) to 10(-7) M, enhanced chemiluminescence of linoleic acid (C 18:2) showed a dose-responsive reduction of OFR with a maximal mean reduction of -31.9% when compared to baseline. A saturated fatty acid such as palmitic acid (C 16:0) showed only relatively weak antioxidant activity at concentrations of 10(-7) to 10(-6) M with a maximum reduction of OFR of- 15.2% only. control chemicals such as trilinolein and Trolox showed significant antioxidant activity. At concentrations between 10(-10) and 10(-6) M and trilinolein has the most potent antioxidant activity with a maximal mean reduction of OFR of -48.0%, whereas Trolox showed only -39.2%. As for the natural plant antioxidants, only catechin showed potent antioxidant activity (-40%). Polyunsaturated triglycerides such as triolein (oleic acid, C 18:1) also possess significant OFR scavenging effect (-31.9%) whilst saturated triglycerides such as tristearin (stearic acid, C 18:0) had only relatively weak antioxidant activity (-15.2%). Generally, the antioxidant activity of unsaturated compounds is stronger than saturated compounds; double-bond existence may partially explain this phenomenon.

Antioxidants↗

Changes of neuropeptide Y messenger RNA and peptide by drugs influencing endogenous norepinephrine content in cerebrocortex of the rat.

Cotransmission of classic transmitters at the synapse has been mentioned for both the CNS and the PNS. Neuropeptide Y (NPY) is a cotransmitter in noradrenergic neurotransmission. In an attempt to understand the heteroregulation of norepinephrine (NE) and NPY biosynthesis, the present study was performed using radioimmunoassay of NPY and northern blotting of cDNA probes for characterization of NPY mRNA. Values of NPY-like immunoreactivity (NPY-ir) were elevated in the cerebrocortex from rats that received treatment with fusaric acid, an inhibitor of dopamine-beta-hydroxylase, with a parallel decrease in NE. Similar results were also observed in rats treated with DSP-4, an alkylator of vesicles in noradrenergic nerve terminals. Moreover, cerebrocortical NPY-ir was reduced in rats receiving treatment with pargyline, an inhibitor of monoamine oxidase, with an elevation of catecholamine in parallel. Activity of NPY mRNA was modified by these drugs in a similar way. However, values of NPY-ir and NE in the cerebrocortex were not influenced by treatment with sodium nitroprusside or guanethidine at a dose producing hypotensive effect. Mediation of hypotensive reflex can thus be ruled out. The data obtained suggest that in vivo decrease of NE by drugs increases biosynthesis of NPY in the cerebrocortex of rats.

Animals↗

In vitro inhibitory effects of chebulinic acid on the contractile responses of cardiovascular muscles.

1. The effects of chebulinic acid, which has been shown to elicit blood pressure lowering effect in rats, on aortic vascular contraction as well as cardiac contraction were studied in rats. 2. Chebulinic acid had no effect on KCl-induced aortic contraction, but irreversibly inhibited the contractile responses to phenylephrine in an apparently non-competitive manner. Chebulinic acid also inhibited contractile responses of rat aorta to 5-hydroxytryptamine and angiotensin II. 3. Chebulinic acid inhibited the binding of [3H]-prazosin to dog aortic microsomal membranes in a concentration-dependent manner with an IC50 value of 0.34 mmol/L. Results of saturation binding experiments suggest a mixed mode of inhibition by chebulinic acid (i.e. a decrease in both the maximal number of binding sites and the affinity for prazosin). 4. Chebulinic acid concentration-dependently and reversibly inhibited the maximal left ventricular pressure of rat heart in a Langendorff preparation with 50% inhibition occurring at a concentration of 0.3 nmol/L. 5. We conclude that chebulinic acid exerts non-specific inhibitory actions in vascular preparations. Its inhibitory effect on cardiac contraction was reversible and three orders of magnitude more potent than that on vascular contraction. We suggest that the hypotensive effect of chebulinic acid is probably mediated via the decrease in cardiac output resulting from reduced left ventricular contraction.

Adrenergic alpha-Antagonists↗

Inhibitory effect of propofol on sympathetic neurotransmission results in changes of plasma neuropeptide Y in rats.

1. The effects of propofol on sympathetic neurotransmission and changes of plasma level of neuropeptide Y-like immunoreactivity (NPY-ir) were investigated in rats. 2. Intraperitoneal injection of propofol into rats lowered the systemic blood pressure and plasma NPY-ir in a dose-dependent manner. 3. Decrease of plasma NPY-ir induced by propofol was not modified in adrenalectomized rats. In the activation of adrenergic neurotransmission by a ganglionic nicotinic agonist, elevation of plasma NPY-ir was also reduced by propofol indicating the direct effect on peripheral adrenergic nerve terminals. 4. Plasma level of NPY-ir reversed in parallel with the recovery of anaesthesia induced by propofol. After an intracerebroventricular injection of propofol into the rats, both the lowering of plasma NPY-ir and the induction of anaesthesia were observed. Thus, a central nervous system effect of propofol can also be considered in its effect on plasma NPY-ir. 5. The data suggest that propofol has the ability to lower plasma NPY-ir in rats through an inhibition of adrenergic neurotransmission via central nervous pathway and/or peripheral nerve terminal blockade.

Adrenalectomy↗

Trilinolein preserves mitochondria ultrastructure in isolated rat heart subjected to global ischemia through antioxidant activity as measured by chemiluminescence.

Oxygen-derived free radicals (OFR) have been proposed as the cause of myocardial damage through lipid peroxidation during ischemia and reperfusion. Antioxidants can effectively ameliorate the damage induced by lipid peroxidation. Trilinolein is a triacylglycerol recently purified from the well known traditional Chinese herb Panax pseudoginseng, which has been used in treating circulatory disorders among Chinese for hundreds of years; it has linoleate as the only fatty acid residue in all three esterified positions of glycerol. This chemical has recently been demonstrated to have antioxidant activity by enhanced chemiluminescence. The addition of phorbol myristic acetate (PMA) to medium containing leukocytes produces OFR; this phenomenon was measured by chemiluminescence. Addition of trilinolein to medium containing leukocytes preceding the addition of PMA suppressed the production of OFR. The control value of chemiluminescence of a medium containing leukocytes with addition of PMA was 9.23 +/- 1.19 x 10(3) mV. The most effective concentration of trilinolein was 10(-7) mol/l which decreased the signals to 4.59 +/- 0.02 x 10(3) mV (p < 0.001). The antioxidant effect had a concentration-response curve similar to alpha-tocopherol. After pretreatment for 15 min with trilinolein at a concentration of 10(-7) mol/l in isolated perfused rat heart which had been subjected to 60 min of global ischemia, the integrity of the rat heart mitochondria was preserved as examined under the electron microscope. No swelling of mitochondria occurred and there was good alignment of cristae and absence of amorphous density. Previous experiments have shown that trilinolein can also improve erythrocyte deformability in vitro. Infarct size reduction of about 50% was also demonstrated in in vivo rat heart subjected to 4 h coronary occlusion. The mechanism of myocardial protection, in addition to the antioxidant effect, is suggested as maintaining the membrane fluidity of cardiomyocytes.

Animals↗

Dark-cycle video surveillance of sexual performances of normal and diabetic rats.

Clinically, a 59% prevalence of impotence was reported among diabetic male patients. Neurological, vascular, endocrinologic and psychological factors are probably involved. Previous reports with the rat model found deterioration of sexual behavior and reproductive function caused by streptozotocin (STZ)-induced diabetes. The purpose of the present study was to develop the dark-cycle video recording methodology for the observation of rat sexual activities and to study the effect of STZ-induced diabetes on sexual performances of the rat. Adult male Wistar rats were rendered diabetic with intraperitoneal injection of STZ (60 mg/kg body weight). In the 4th week a diabetic rat or a control rat was caged with an adult ovariectomized female rat during the dark cycle. The female had been brought into behavioral estrus with intramuscular injection of 0.1 mg estradiol benzoate 3 days before and 1.0 mg progesterone 3 h before testing. Infrared-light-illuminated video recording was performed to evaluate the sexual performances. The mounting latency and frequency, intromission latency and frequency, the hit rate as well as the post-ejaculatory period of the diabetic rats were significantly deteriorated when compared with the controls (p < 0.05). However, the ejaculatory latency showed no significant difference between the two groups (p > 0.05). In conclusion, it has been demonstrated that with this methodology, behavioral studies on nocturnal animals like the rat can be carried out conveniently. It was shown that the sexual arousal mechanism and copulation-ejaculatory mechanism were both depressed in STZ-induced diabetic rats. The same study model can be used for further pathophysiological and pharmacological researches on the sexual behaviors of diabetic rats.

Animals↗

Treatment effect of "ryu-wei-ti-huang-wan" (a Chinese herbal prescription) on the sexual performance of male rats with streptozotocin-induced diabetes.

The treatment effect of "ryu-wei-ti-huang-wan', a Chinese prescription composed of extracts from six plants, on diabetic impotence was evaluated in the present study. Adult male Wistar rats were divided into three groups: (1) rats rendered diabetic with a single intraperitoneal injection of streptozotocin (60 mg/kg body weight); (2) rats with streptozotocin-induced diabetes treated with a ryu-wei-ti-huang-wan powder preparation at a dose of 30 mg powder/kg body weight twice a day, and (3) control rats. A male rat was caged with an adult ovariectomized female rat during the dark cycle. Infra-red-light-illuminated video recording was utilized to evaluate the sexual performance. The diabetic rats exhibited depressed mounting activity and no intromission or ejaculation. After ryu-wei-ti-huang-wan treatment either for 1 day or 2 weeks, the diabetic rats showed significant improvement in mounting performance with preservation of intromission and ejaculation. No significant difference in the blood sugar level was noted between the treatment and non-treatment groups. In conclusion, the diabetic rats showed impairment in sexual arousal, erectile as well as ejaculatory functions. Ryu-wei-ti-huang-wan was effective in preserving these functions with a rapid onset. It is evident that the extracts exert the therapeutic effects not through a lowering of blood sugar. These substances are potentially useful in the clinical treatment of male diabetic impotence.

Animals↗

Evidence of nonadrenergic, noncholinergic contraction in rat urinary bladder by 1,1-dimethylphenylpiperazinium stimulation in vivo.

Nonadrenergic, noncholinergic (NANC) contraction has been demonstrated in animal urinary bladder. However, the exact nature of the NANC innervation is still unclear. 1,1-Dimethylphenylpiperazinium (DMPP), which generates action potentials in the cell body of the postganglionic neuron and causes neurotransmitter release (both acetylcholine and noradrenaline), was given intravenously (0.1-0.7 mg/kg) to 3-month-old female Wistar rats under anesthesia (n = 20). Intravesical pressure, heart rate and blood pressure of the rats were monitored on Gould polygraph. Monophasic dose-dependent contractile response was observed upon administration of DMPP in 12 of 20 rats. After total adrenergic and cholinergic blockade with atropine, guanethidine, phentolamine and propranolol, the contractile response was reduced, not completely, in the animals. At the dose of 0.7 mg/kg, the contraction was reduced to about 48% of the original response. The study provides in vivo evidence for NANC contraction in the rat urinary bladder, moreover, the neurotransmitter is released from the postganglionic neurons.

Action Potentials↗

Clinical evidence of genetic anticipation in adult-onset idiopathic dystonia.

Idiopathic dystonia occurs in both hereditary and sporadic forms. In this report, we studied the age of onset and family history of 260 patients (probands) with idiopathic adult-onset dystonia (IAD), cranial or cervical. The mean age at onset of these patients was (45.71 +/- 15.85) years. Forty-nine probands had a positive family history of dystonia or tremor in first- and second-degree relatives, and 7 had affected siblings only. The significance of tremor as a part of clinical manifestation of dystonia was evidenced by a high frequency of postural or action tremor in patients and relatives. Retrospectively, we examined the age of onset of dystonia (cervical or cranial) on successive generations in 49 families. Age of onset of clinical symptoms was earlier, by an average of 21.25 years, in the second generation than in the first generation. The mean age at onset of affected family members differed significantly between successive generations in these 49 families (p = 1.11 x 10(-8)). Our results suggest a tendency for earlier onset of dystonia and worsening of disease phenotype in succeeding generations in the same family. These findings are most compatible with genetic anticipation and suggest that an unstable trinucleotide repeat is most likely involved in adult-onset primary cranial or cervical dystonia. In addition, tremor as an integral part of dystonia needs further evaluation by molecular genetic studies.

Adult↗

Effect of oral L-carnitine on serum myoglobin in hemodialysis patients.

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.

Administration, Oral↗

Decrease of anesthetics activity by electroacupuncture on Jen-Chung point in rabbits.

The effect of acupuncture at life-saving point on the central nervous depressive action of anesthetics was investigated in rabbits. Stimulation with electroacupuncture (EA) inserted in Jen-Chung point, which is located at the mid-point on the upper lip, decreased the sleeping time induced by pentobarbital or propofol. However, this action of acupuncture was not modified by naloxone at the doses sufficient to block opiate receptors. Plasma beta-endorphin detected by radioimmunoassay was also not markedly changed in rabbits which received similar electrostimulation. Moreover, pretreatment with para-chlorophenylalanine at a dose sufficient to deplete endogenous 5-hydroxytryptamine (5-HT) failed to influence the action of EA. Mediation of endogenous opioids and/or 5-HT in this action of EA was then ruled out. Prazosin reversed the sleeping time decreasing action of acupuncture in a dose-dependent manner. Also, the action of acupuncture was eliminated in rabbits which received intracerebroventricular injection of guanethidine at a dose which could block noradrenergic nerve terminals. It is suggested that stimulation of Jen-Chung point through EA can activate noradrenergic neurotransmission in the brain, which in turn reduces the central nervous depressive activity of anesthetics.

Acupuncture Analgesia↗