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At least 127 records · Page 7Linked to original sources
PubMed1979

Regional blood flow determination in rats by the microsphere method during i.v. infusion of vasodilating agents.

The present experiments were performed to gain information on changes in various organ flow rates during i.v. infusion of vasodilating substances. The microsphere method with the reference sample technique was used in rats to measure simultaneously different organ flow rates. The detection of the spheres (non-radioactive) was performed by macerating the tissues and counting samples under the microscope. As only one microsphere-infection per animal was performed, an untreated experimental group served as a control. The cardiac output was measured in a separate series. The effects of isoproterenol, pentoxifylline, bencyclane, acetylcholine, and dihydroergotoxine (mixture of 3 compounds, Hydergin) consisted of flow increases in several organs while the flow in others remained nearly unchanged. Only during the action of sodium nitroprusside the flow values were found decreased or remained unchanged. This substance led to decreased cardiac output, whereas that in the other groups was unchanged or raised. The experiments point to quantitatively different reactions on cardiac output distribution during application of the vasodilating substances tested.

Animals↗
PubMed1993

[Vasodilator agents: the lesson from large clinical trials].

The results of trials of vasodilators in patients with chronic heart failure showed improved survival by adding ACE-inhibitors or a combination of isosorbide dinitrate and hydralazine to the usual therapy with digoxin and diuretics. However, the mean prolongation of life is unsatisfactory (10-17 months) and very small effects are observed on the various measures of quality of life. In patients with asymptomatic left ventricular dysfunction, the treatment with ACE-inhibitors reduces the progression to the clinical phase of heart failure but not in all patients. Therefore is attractive to evaluate new agents to improve the results of the present therapeutic strategies. The attempts to combine new vasodilators to regimens including ACE-inhibitors have been inconclusive or even deleterious. The identification of subgroups of patients with different clinical, hemodynamic and neurohormonal characteristics may allow a more appropriate use of the new therapeutic resources.

Clinical Trials as Topic↗
PubMed1989

[Vasodilator agents and the vascular endothelium].

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).

Endothelium, Vascular↗
PubMed1993

The effects of pertussis toxin on vasoconstrictor and vasodilator agents in the pithed rat may not be an indicator of G-protein receptor coupling.

1. In the present study, rats were treated with pertussis toxin (8.4 micrograms, i.v.) to determine whether pertussis toxin-sensitive G-proteins were linked to receptors that mediate effects in the cardiovascular system. 2. In the pithed rat the pressor responses to the alpha-adrenoceptor agonists noradrenaline and (to a lesser extent) methoxamine were attenuated by pertussis toxin treatment; the tachycardia produced by noradrenaline was unaffected. The pressor response to serotonin was also attenuated by pertussis toxin treatment. These observations are consistent with known effects of pertussis toxin on these receptors. 3. The vasodepressor responses to the muscarinic receptor agonist carbachol and to adenosine were reduced by pertussis toxin, suggesting that these events may have been mediated by pertussis toxin-sensitive G-proteins. However, the depressor responses to the beta 2-adrenoceptor agonist salbutamol and to the receptor-independent vasodilator drugs sodium nitroprusside and hydralazine were also reduced by pertussis toxin. These latter effects suggest that caution must be used in interpreting the effects of pertussis toxin since the mechanism of action of these drugs as elucidated in vitro is thought not to involve pertussis toxin-sensitive G-proteins.

Animals↗
PubMed2001

Effect of trapidil, an antiplatelet and vasodilator agent on gentamicin-induced nephrotoxicity in rats.

This study was carried out to evaluate the effect of trapidil, an antiplatelet and vasodilator drug, on the nephrotoxicity by an aminoglycoside, gentamicin, in rats. Forty female Wistar rats were divided into six different groups. One group served as a control group and the other groups were treated as follows: gentamicin (50 mg kg(-1) twice daily)-treated, gentamicin plus trapidil (4 or 20 mg kg(-1) daily)-treated and only trapidil-treated (4 or 20 mg kg(-1) daily) groups. Serum urea, creatinine and nitrite/nitrate levels were measured. Moreover, histopathological as well as electron microscopic examinations were performed. At a lower dose (4 mg kg(-1)) trapidil did not prevent the development of renal tubular damage by gentamicin. However, a higher dose of trapidil (20 mg kg(-1)) inhibited the ability of gentamicin to increase the levels of creatinine and urea. Furthermore, both light and electron microscopic evaluation confirmed the nephroprotective effect of the higher dose of trapidil. The level of the stable nitric oxide (NO) metabolite, nitrite, was also increased by trapidil. In conclusion, trapidil at a higher dose may protect against gentamicin nephrotoxicity. The mechanism underlying trapidil nephroprotection is not known, but may result from the antagonism of platelet-derived growth factor (PDGF), vasodilatation, inhibition of trombosit aggregation, and/or NO release.

Animals↗