PubMed · 7827534
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K Long, R Long. 1994. Treating open-angle glaucoma.. https://pubmed.ncbi.nlm.nih.gov/7827534/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
The slow but constant modifications of the pharmacopeia and prescribing habits are at the origin of changes in the causes of intoxications by medications, which are reflected in the syndromes observed in daily practice. New syndromes have appeared: serotoninergic syndrome, adrenergic syndromes, toxic malignant hyperthermia, opioid toxic syndrome, intoxication by drugs with membrane-stabilizing effect. Recognizing these syndromes is not only useful to determine the possible causes of on intoxication, but also to direct appropriate, specific therapeutic interventions.
The aims of this study were to determine if neural pathways between the duodenum and sphincter of Oddi are intramural, activated by duodenal electrical field stimulation (EFS) in vitro, and contain capsaicin-sensitive primary afferents. The possible involvement of cholinergic (muscarinic and/or nicotinic) and adrenergic receptors in these pathways were also investigated. Duodenal EFS (5-60 Hz, 70 V, 0.5 ms duration, 10 s train) at sites 2 cm oral and 2 cm anal to the sphincter of Oddi-duodenal junction produced frequency-dependent excitatory responses in the sphincter of Oddi, measured by manometry (n = 3). Excitatory responses from duodenal circular muscle were also evident. Tetrodotoxin (1 microM; n = 7) pretreatment abolished both sphincter of Oddi and duodenal responses to duodenal EFS. Crushing the duodenum between the site of stimulation and the sphincter of Oddi-duodenal junction also abolished sphincter of Oddi response. The sphincter of Oddi responses to duodenal EFS at the oral and anal sites were reduced by pretreatment with (i) atropine (100 nM: n = 7) to 19 +/- 6% (P < 0.05) and 22 +/- 8% (P < 0.05) of control respectively. (ii) hexamethonium (100 microM: n = 9) to 10 +/- 2% (P < 0.01) and 6.0 + 2.5% (P < 0.01) of control respectively and (iii) guanethidine (1 microM; n = 6) to 75 +/- 6% (P < 0.05) and 78 +/- 10% (P < 0.05) of control, respectively. Combined pretreatment with phentolamine and propranolol (both 1 microM; n = 7) was without effect, as was capsaicin (1 microM; n = 12) pretreatment. Excitatory intramural pathways between the sphincter of Oddi and the duodenum are primarily cholinergic in nature and contain an adrenergic component. Capsaicin-sensitive primary afferents are not involved.
It is generally accepted that mechanical stress of cardiomyocytes increases RNA and protein synthesis of myosin heavy chain (MHC) quantitatively but it is still a matter of debate whether MHC gene expression is also changed qualitatively. We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)]. Relative distribution of MHC mRNA isoforms (alpha and beta) was studied by quantitative polymerase chain reaction. Expression of MHC isoenzymes was the same in contracting (34.5% beta-MHC) and arrested (40.5% and 33.0% beta-MHC in KCl and BDM, respectively) cardiomyocytes. However, treatment with phenylephrine for the same period increased significantly beta-MHC expression to 55%. We conclude that hormonal factors rather than Ca2+ or mechanical stress regulate qualitatively MHC gene expression.