Characteristics of emodin on modulating the contractility of jejunal smooth muscle

2012 ◽  
Vol 90 (4) ◽  
pp. 455-462 ◽  
Author(s):  
Dapeng Chen ◽  
Yongjian Xiong ◽  
Li Wang ◽  
Bochao Lv ◽  
Yuan Lin
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Inhibitory Effect ◽  
Intestinal Smooth Muscle ◽  
Low Doses ◽  
Contractile State ◽  
Myosin Phosphorylation ◽  
Bidirectional Regulation ◽  
The Central Nervous System ◽  
High Doses

Emodin is traditionally used as a laxative and is found to increase or decrease the contractility of intestinal smooth muscle in low doses and high doses, respectively. In this study, we propose that bidirectional regulation (BR) on the contractility of jejunal smooth muscle (CJSM) is inducible by emodin in the absence of control by the central nervous system. The results indicated that emodin-induced BR had the following characteristics. A stimulatory effect on CJSM was induced by emodin at 7 low contractile states, and an inhibitory effect was induced on CJSM at 7 high contractile states. Emodin-induced BR on myosin phosphorylation was also observed. BR was not observed in the presence of tetrodotoxin, suggesting that enteric nervous system is required for producing BR. The stimulatory effect of emodin on CJSM was abolished by atropine and diphenhydramine, respectively, suggesting that BR was correlated with cholinergic and histamine system while jejunal smooth muscle was at low contractile state. The inhibitory effect of emodin on CJSM was abolished by phentolamine, propranolol, and L-NG-nitroarginine (L-NNA), respectively, suggesting that BR was related to adrenergic hyperactivity and with a nitric oxide relaxing mechanism while jejunal smooth muscle was in a high contractile state. The exact mechanism, however, needs further investigation.

Some Aspects of the Psychopharmacological Activity of Maprotiline (Ludiomil®): Effects of Single and Repeated Treatments

1978 ◽  
Vol 6 (6) ◽  
pp. 421-429 ◽  
Author(s):  
A Delini-Stula ◽  
E Radeke ◽  
A Vassout
Keyword(s):  
Nervous System ◽  
Chronic Treatment ◽  
Conditioned Fear ◽  
Conditioned Avoidance ◽  
Repeated Treatment ◽  
Antidepressant Effects ◽  
The Central Nervous System ◽  
Pre Treatment ◽  
High Doses ◽  
Psychopharmacological Activity

Three different aspects of the psychopharmacological activity of the antidepressant maprotiline were investigated: its influence on serotoninergic functions the effects produced by chronic treatment its central nervous depressant and anxiolytic properties. Study of the effects of maprotiline on 5-HTP-induced head-twitch in mice pre-treated with pargyline or on hyperpyrexia in rats provided no evidence that the drug interferes with serotonin-mediated functions in the central nervous system even after quite high doses. These findings corroborate the results of extensive neurobiochemical investigations, which failed to demonstrate any influence of maprotiline on the metabolism of serotonin. Chronic studies showed that classical effects of maprotiline such as antagonism against reserpine-induced ptosis or tetrabenazine-induced catalepsy do not change in their intensity after daily administration of the drugs in a dose of 30 mg/kg p.o.for 11 days. A new component of the action of the compound, not detectable after one single dose, seems to appear, however, after repeated treatment (8 days). This effect is manifested in the restoration of conditioned avoidance behaviour after its suppression by pre-treatment with reserpine. The same effect is produced by imipramine. It is suggested that this restorative effect may be due to an additional activation of the dopaminergic nervous system and may have a bearing on the appearance of clinical antidepressant effects. Maprotiline was found to potentiate central nervous depressant effects of drugs like chlorpromazine, phenobarbitone and propranolol. This affords further confirmation that, in addition to its antidepressant qualities, it possesses sedative actions. An anxiolytic component was also demonstrated in rats in which maprotiline suppressed the conditioned, fear-induced rise in body-temperature.

Development of adrenomedullary function in suckling rats: Effects of high doses of thyroxine and cortisol

1990 ◽  
Vol 123 (1) ◽  
pp. 100-107
Author(s):  
L. Goya ◽  
C. Aláez ◽  
A. M. Pascual-Leone
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adrenal Glands ◽  
Normal Development ◽  
Insulin Administration ◽  
Newborn Rats ◽  
Short Intervals ◽  
Slowing Down ◽  
The Central Nervous System ◽  
High Doses

Abstract. The development of epinephrine, norephinephrine, and total catecholamine secretion in plasma and andrenal glands was studied in newborn rats at short intervals: at day 2, 4, 6, 8, 10, 12 and 23. The increase in the plasma level of epinephrine represents a maturation of the secretion of the adrenal medulla. The increase in plasma of epinephrine and norepinephrine and the content of catecholamines in the adrenal glands of both normal animals and those treated with either high doses of T4 or cortisol at birth suggest a slowing down of the normal development of epinephrine secretion. This was confirmed by inducing hypoglycemia in these three groups of animals by a 20-h fast or by insulin administration (0.1436 μmol/kg). We conclude that both high doses of T4 and cortisol administered at birth seem to retard the development of the autonomic nervous system similar to the effect on the central nervous system.

Primitive Neuroectodermal Tumor of Cerebrum With Adipose Tissue

2001 ◽  
Vol 125 (2) ◽  
pp. 264-266
Author(s):  
Satish Krishnamurthy ◽  
Stephen Kent Powers ◽  
Javad Towfighi
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Primitive Neuroectodermal Tumor ◽  
Primitive Neuroectodermal Tumors ◽  
Mature Adipose Tissue ◽  
Neuroectodermal Tumors ◽  
The Central Nervous System

Abstract Primitive neuroectodermal tumors (PNETs) of the central nervous system are uncommon embryonal neoplasms, rarely occurring in adults. Differentiation into specific mesenchymal tissues, such as cartilage, bone, skeletal muscle, smooth muscle, or adipose tissue, is rare. We report a case of a 51-year-old woman with a PNET of cerebrum that showed extensive mature adipose tissue differentiation. This is the second case, to our knowledge, of PNET of cerebrum with adipose tissue elements that has been described.

β-Neoendorphin inhibits thyrotrophin secretion in rats

1983 ◽  
Vol 104 (4) ◽  
pp. 437-442 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of β-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. β-neoendorphin (500 μg/kg) was injected iv, and the rats were decapitated serially. TRH, TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by means of a specific radioimmunoassay for each. Hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after β-neoendorphin injection, and plasma concentrations tended to decrease, but not significantly so. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min. Plasma T4 and T3 levels did not change after the injection. Plasma ir-TRH and TSH responses to cold were significantly inhibited by β-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of β-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of β-neoendorphin on TSH release was prevented, but not in the l-dopa- or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. These findings suggest that β-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

scholarly journals Mechanism of penile erection

2017 ◽  
Author(s):  
Selim Cellek
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Smooth Muscle ◽  
Erectile Function ◽  
Penile Erection ◽  
Muscle Tone ◽  
Main Determinant ◽  
Smooth Muscle Tone ◽  
Sexual Stimuli ◽  
The Central Nervous System

Sexual stimuli (tactile, visual, olfactory, and imaginative) are processed and integrated in the central nervous system which then activates certain autonomic and somatic pathways within the peripheral nervous system. This coordinated activation of the central and peripheral nervous systems leads to penile erection which is actually a result of relaxation of vascular and cavernosal smooth muscle in the penis. In the flaccid (detumescent) penis, the smooth muscle tone is heightened. Penile erection (tumescence) requires a decrease in the smooth muscle tone. The tone of the penile smooth muscle therefore is the main determinant of erectile function. In this chapter, the current information on the control of erectile function by this central-peripheral-smooth muscle axis will be reviewed.

scholarly journals High doses of cefotaxime in treatment of adult meningitis due to Streptococcus pneumoniae with decreased susceptibilities to broad-spectrum cephalosporins.

1996 ◽  
Vol 40 (1) ◽  
pp. 218-220 ◽  
Author(s):  
P F Viladrich ◽  
C Cabellos ◽  
R Pallares ◽  
F Tubau ◽  
J Martínez-Lacasa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Streptococcus Pneumoniae ◽  
Broad Spectrum ◽  
Adjunctive Therapy ◽  
Maximum Dose ◽  
Central Nervous System Infection ◽  
The Central Nervous System ◽  
High Doses

We treated nine patients (10 episodes) with meningitis caused by Streptococcus pneumoniae isolates with decreased susceptibilities to broad-spectrum cephalosporins with high doses of cefotaxime (300 mg/kg of body weight per day; maximum dose, 24 g/day). Early adjunctive therapy with dexamethasone was also administered. Cefotaxime MICs were 0.5 (three episodes), 1 (five episodes), and 2 (two episodes) micrograms/ml, and MBCs ranged from 1 to 4 micrograms/ml. Therapy was well tolerated, and all patients experienced prompt clinical improvement. One patient died 8 days after the end of therapy, the central nervous system infection had already been cured, and the remaining patients recovered without relapses.

CONTROL BY THE CENTRAL NERVOUS SYSTEM OF RECTAL SMOOTH MUSCLE

1939 ◽  
Vol 2 (4) ◽  
pp. 356-360 ◽  
Author(s):  
Orthello R. Langworthy ◽  
Seymour J. Rosenberg
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Smooth Muscle ◽  
The Central Nervous System
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