Evidence that some imidazoline derivatives inhibit peripherally the vasopressor sympathetic outflow in pithed rats.

Imidazoline derivatives (e.g. clonidine and moxonidine) and alpha(2)-adrenoceptor agonists (e.g. B-HT 933) have been shown to inhibit sympathetically-induced [(3)H]noradrenaline release in several isolated blood vessels. The present study has compared the potential capability of agonists at imidazoline I(1/2) receptors and/or alpha(1/2)-adrenoceptors to inhibit the sympathetically-induced vasopressor responses in pithed rats. For this purpose, male Wistar rats were pithed and prepared for measurement of diastolic blood pressure and heart rate. Then, the vasopressor responses induced by either selective electrical stimulation (2 ms, 60 V; 0.03, 0.1, 0.3, 1 and 3 Hz) of the vascular sympathetic outflow (T(7)-T(9)) or i.v. bolus injections of exogenous noradrenaline (0.03, 0.1, 0.3, 1 and 3 microg/kg) were determined before and during i.v. continuous infusions of the agonists B-HT 933 (alpha(2)), clonidine (alpha(2), I(1)), moxonidine (alpha(2), I(1)), cirazoline (alpha(1), I(2)), agmatine (putative endogenous ligand of imidazoline receptors) and methoxamine (alpha(1)), or equivalent volumes of physiological saline. Electrical sympathetic stimulation elicited frequency-dependent vasopressor responses which were significantly inhibited during the continuous infusions of B-HT 933, clonidine, moxonidine, cirazoline and agmatine, but not of physiological saline. Interestingly, the vasopressor responses to exogenous noradrenaline, which remained unaffected during the infusions of physiological saline, B-HT 933, moxonidine, cirazoline and agmatine, were significantly blocked during the infusions of clonidine or methoxamine. These results suggest that B-HT 933, moxonidine, cirazoline and agmatine induced a prejunctional inhibition of the vasopressor sympathetic outflow in pithed rats, whilst clonidine inhibited the vasopressor sympathetic outflow by both prejunctional and postjunctional mechanisms.

[Effect of position with respect to gravitational force on the hydrodynamics of an experimental model of saccular aneurysm]. / Influencia de la posición con respecto a la fuerza de gravedad sobre la hidrodinámica de un modelo experimental de aneurisma sacular.

We wish to confirm the hypothesis that the hydrodynamics of brain aneurysms depend partially on their position, with respect to the force of gravitation, and so developed an experimental model of latex aneurysms, which was subjected to a pulsatile flow. Four different registers were made with an injection of ink and radioisotopes. A physical model was designed which allowed a quantitative analysis of the results and which allows a mathematical analysis of the aneurysm's hydrodynamics. The results suggest that when an aneurysm is oriented against the force of gravity, it has a very low risk of thrombosis, and the scarce turbulence of the flow condition a lower risk of growth and rupture, in comparison with other conditions. The greatest flow turbulence against the wall is found in the aneurysm oriented downwards, that is parallel to the force of gravity. Due to its hydrodynamics, the downwards aneurysm has the highest probability of complication, since it has; a) higher risk of rupture due to the impact of the stream upon the wall and to the turbulence this impact produces, b) a higher risk of thrombosis produced by the circulatory stasis which has a dome. This combination of factors (rupture and thrombosis) allows these aneurysms to grow more than others.