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Type 2 diabetes mellitus in the Goto-Kakizaki rat impairs microvascular function and contributes to premature skeletal muscle fatigue.
J Appl Physiol (1985)
March 2019
Department of Physiology, Michigan State University, East Lansing, Michigan.
Despite extensive investigation into the impact of metabolic disease on vascular function and, by extension, tissue perfusion and organ function, interpreting results for specific risk factors can be complicated by the additional risks present in most models. To specifically determine the impact of type 2 diabetes without obesity on skeletal muscle microvascular structure/function and on active hyperemia with elevated metabolic demand, we used 17-wk-old Goto-Kakizaki (GK) rats to study microvascular function at multiple levels of resolution. Gracilis muscle arterioles demonstrated blunted dilation to acetylcholine (both ex vivo proximal and in situ distal arterioles) and elevated shear (distal arterioles only).
View Article and Find Full Text PDFElectrical injuries. Biological values measurements as a prediction factor of local evolution in electrocutions lesions.
J Med Life
June 2014
"Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania Plastic Surgery and Reconstructive Microsurgery Department, Clinical Emergency Hospital, Bucharest, Romania.
Rationale: Taking into account the incidence and the severity of electrocutions, we consider it extremely necessary to find effective, appropriate and particularized therapeutic solutions aimed at improving the survival, decreasing the mortality, ensuring a superior functional and aesthetic effect and facilitating the social reintegration. Given the severity of the general condition of the electrically injured patient and the fact that any worsening of the lesions has a systemic echo, the selection of the timing for re-excision is very important. The postponement of the surgical timing can break the precarious metabolic equilibrium and can hasten the installation of the multisystem organ failure (MSOF).
View Article and Find Full Text PDFTwo pharmacological phases in antigen-induced immediate airway response in rats.
Biol Pharm Bull
December 2008
Central Pharmaceutical Research Institute, Japan Tobacco, Inc., Takatsuki, Osaka 569-1125, Japan.
The pharmacological profiles of antigen-induced immediate airway response (IAR) in rats are not fully understood. In this study, we established an ovalbumin (OVA)-induced IAR model using noninvasive measurement in rats, and evaluated the effects of commonly used and effective antiasthmatic drugs, i.e.
View Article and Find Full Text PDFTP receptor as a therapeutic target in atherosclerosis and related cardiovascular diseases.
Recent Pat Cardiovasc Drug Discov
November 2006
Department of Pharmacology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511, Japan.
It had already showed that several thromboxane A(2) receptor (TP receptor) antagonists might be utilized in the treatment of cardiovascular diseases. In addition, recent reports suggested that TP receptor antagonism may be able to restrict vascular inflammation in atherosclerotic vessels. In particular, S18886 has been developed as a non-prostanoid TP receptor antagonist derived from sulotroban that is characterized by a tetrahydronaphthalene ring as a spacer between the 4-cholophenylsulfonamide group and carboxylic acid.
View Article and Find Full Text PDFEvaluation of the effects of anti-thromboxane agents in platelet-vessel wall interaction.
Eur J Pharmacol
May 2002
Department of Pharmacological Sciences, University of Milan, via Balzaretti 9, 20133, Milan, Italy.
We evaluated the capacity of anti-aggregating agents to influence thromboxane A(2) and prostacyclin formation, arachidonic acid-endoperoxide redirection, platelet aggregation and vessel tone, in isolated rabbit aorta incubated with homologous platelets. Picotamide (N,N'bis(3-pyridinylmethyl)-4-methoxy-isophthalamide), the only dual thromboxane A(2)-synthase inhibitor/receptor antagonist in clinical use, inhibited arachidonic acid-induced platelet aggregation with low potency, increased 180-fold by aorta presence. It inhibited thromboxane A(2) formation in platelets and, in aorta presence, increased prostacyclin formation.
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