Skip header and navigation

Refine By

4 records – page 1 of 1.

[Content of fibroblasts, macrophages, granulocytes and lymphocytes in the connective tissue regenerate of the skin in wound healing as affected by noradrenaline, acetylcholine, propranolol and atropine]

https://arctichealth.org/en/permalink/ahliterature10608
Source
Morfologiia. 1999;116(4):41-5
Publication Type
Article
Date
1999
Author
A N Grabovoi
Author Affiliation
Department of Histology, A.A. Bogomolets National Medical University, Kiev, Ukraine.
Source
Morfologiia. 1999;116(4):41-5
Date
1999
Language
Russian
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Animals
Atropine - pharmacology
Cell Count - drug effects
Connective Tissue - drug effects
English Abstract
Fibroblasts - drug effects
Granulocytes - drug effects
Lymphocytes - drug effects
Macrophages - drug effects
Norepinephrine - pharmacology
Propranolol - pharmacology
Rats
Regeneration - drug effects
Skin Physiology - drug effects
Wound Healing - drug effects
Abstract
Effects of acetylcholine, noradrenaline, atropine and propranolol on cell number in connective tissue regenerates of the skin in wound healing were studied in white rats. Noradrenaline causes the decrease of inflammatory reaction, fibroblast content in regenerate and basophilia of their cytoplasm. Acetylcholine conversely increases cell reaction, but slows down the re-modelling of connective tissue regenerate. The definite dynamic balance between catecholamine and acetylcholine systems of reparation processes regulation in wound healing is noted. This balance could deviate under external influences. The expression of various cellular element reaction to the dermal regenerate on adreno- and cholinotropic influences tends to change during wound healing.
PubMed ID
10486809 View in PubMed
Less detail

[Effect of beta receptor blockaders on the status of the lysosomal system of peripheral blood neutrophils in rabbits with immobilization stress]

https://arctichealth.org/en/permalink/ahliterature11881
Source
Fiziol Zh. 1992 May-Jun;38(3):43-9
Publication Type
Article
Author
V V Lunina
S B Vovk
Source
Fiziol Zh. 1992 May-Jun;38(3):43-9
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Cell Count - drug effects
Cell Degranulation - drug effects - physiology
Depression, Chemical
Disease Models, Animal
English Abstract
Female
Lysosomes - drug effects - physiology
Male
Neutrophils - drug effects - pathology - ultrastructure
Propranolol - pharmacology
Rabbits
Restraint, Physical - psychology
Stress, Psychological - blood
Time Factors
Abstract
The investigation carried out on mature rabbits under conditions of beta-adrenoreceptors' blocking by obsidan has revealed that 12-hour immobilization caused neutrophilic leukocytosis in the peripheral blood, degranulation of neutrophils, increase of acid phosphatase activity. These changes occurred much earlier as compared with those in the control group were more pronounced and lasted for a less period of time. Consequently, beta-receptors are the necessary components in the formation of stress-syndrome under the influence of an +non-infectious stressor.
PubMed ID
1499761 View in PubMed
Less detail

The peripheral platelet count in response to adrenergic alpha-and beta-1-receptor stimulation.

https://arctichealth.org/en/permalink/ahliterature13096
Source
Scand J Haematol. 1978 Nov;21(5):427-32
Publication Type
Article
Date
Nov-1978
Author
K. Fredén
P. Lundborg
L. Vilén
J. Kutti
Source
Scand J Haematol. 1978 Nov;21(5):427-32
Date
Nov-1978
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Adult
Blood Cell Count
Blood Platelets
Blood Pressure - drug effects
Cell Count - drug effects
Epinephrine - pharmacology
Heart Rate - drug effects
Humans
Male
Propranolol - pharmacology
Abstract
The aim of the present work was to investigate the effect of adrenergic alpha- and beta-1-receptor stimulation on the peripheral platelet count. The experiments were carried out on 8 healthy male volunteers using radioisotopically labelled platelets. 3 subjects received i.v. infusions of adrenaline (0.09 microgram X kg-1 X min-1) before and after the ingestion of 40 mg propranolol. In response to the first infusion there was an instant increase in the venous platelet-bound radioactivity (PBR) which amounted to 12% over basal value. This effect of adrenaline seemed to be potentiated by propranolol pretreatment. 5 subjects received i.v. infusions of the highly selective beta-1-receptor agonist H 133/22 (prenalterol, Hässle, Sweden). In response to a cumulative dose of 4.75 mg prenalterol a slight but significant (P less than 0.05) decrease in PBR occurred. It is concluded that alpha-receptor stimulation causes a depletion of platelets from the exchangeable splenic platelet pool resulting in a concomitant increase in the peripheral platelet count. Beta-receptor stimulation has an opposite effect on the spleen. The trapping of platelets by the spleen is mediated both via beta-1- and beta-2-receptors, but the effect of beta-2-receptor stimulation seems to predominate.
PubMed ID
32612 View in PubMed
Less detail

Photoreceptor apoptosis induced by a single systemic administration of N-methyl-N-nitrosourea in the rat retina.

https://arctichealth.org/en/permalink/ahliterature51081
Source
Am J Pathol. 1996 Feb;148(2):631-41
Publication Type
Article
Date
Feb-1996
Author
M. Nakajima
K. Yuge
H. Senzaki
N. Shikata
H. Miki
M. Uyama
A. Tsubura
Author Affiliation
Department of Ophthalmology, Kansai Medical University, Osaka, Japan.
Source
Am J Pathol. 1996 Feb;148(2):631-41
Date
Feb-1996
Language
English
Publication Type
Article
Keywords
Animals
Apoptosis
Cell Count - drug effects
Cell Nucleus - drug effects
Female
Injections, Intraperitoneal
Methylnitrosourea - administration & dosage - toxicity
Microscopy, Electron
Photoreceptors - drug effects - pathology - ultrastructure
Pigment Epithelium of Eye - drug effects - ultrastructure
Proliferating Cell Nuclear Antigen - analysis
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Retina - drug effects - pathology
Retinal Degeneration - chemically induced - pathology
Vimentin - analysis
Abstract
Retinal degeneration was induced by a single intraperitoneal injection of N-methyl-N-nitrosourea in female Sprague-Dawley albino rats at 50 days of age by two dose regimens, which were observed sequentially at 24, 48, and 72 hours and 7, 21, and 35 days after the treatment. After a dose of 75 mg/kg, methylnitrosourea evoked progressive retinal degeneration in all treated rats whereas a dose of 50 mg/kg was less effective. The 75-mg/kg-treated rats showed selective destruction of the photoreceptor cells by an apoptotic mechanism, as confirmed morphologically and by the terminal dUTP nick end labeling method. Apoptosis had already started at 24 hours after the treatment and was completed by day 7. During the photoreceptor degeneration, proliferation of glial fibrillary acidic protein and vimentin-positive Müller cells as detected by proliferating cell nuclear antigen labeling appeared at 48 hours and was prominent 72 hours after the treatment, and macrophage infiltration within the retina as recognized by ED1 positivity was maximal 7 and 21 days after the treatment. Retinal degeneration was also induced in female Brown-Norway colored rats in a similar dose-dependent manner. Pigment epithelium was discontinuous above Bruch's membrane, and migration of the swollen pigment epithelium toward the inner nuclear layer was seen 7 days after the treatment. Therefore, as also confirmed electron microscopically, the most striking change was the destruction of photoreceptor cells by the apoptotic process, followed by Müller cell proliferation, pigment epithelium migration, and macrophage infiltration for cell debris phagocytosis, resulting in a thin remnant of retina with attenuated inner nuclear cells in direct contact with Bruch's membrane or with the pigment epithelium and/or with the Müller cells 35 days after the treatment.
PubMed ID
8579125 View in PubMed
Less detail