RESUMO
Different vasoactive factors can modulate cardiovascular adaptation to hemorrhagic shock including Nitric Oxide [NO]. In this study we investigated the effect of the NO synthase inhibitor for treatment of decompensated hemorrhagic shock in normotensive and hypertensive rats. Twenty four male Wistar rats were divided into two groups: The normotensive and hypertensive groups. Hypertension was induced by the DOCA Salt method for eight weeks. Then, the animals were given hemorrhagic shock by continuously withdrawing blood until the mean arterial pressure [MAP] reached to 40 mmHg. The animals were maintained in the shock state for 120 minutes. Subsequently, they were randomly assigned to L-NAME-treated and non treated groups and monitored for 60 minutes. The survival time was recorded. Blood samples were taken before and after the shock and 60 minutes after L NAME administration. Infusion of L-NAME caused a significant increase in MAP in normotensive animals, however, slightly increased MAP in hypertensive animals. The heart rate did not significantly alter. Hemorrhage caused a marked increase in serum nitrite levels in both groups [P<0.05]. L NAME treatment significantly reduced the serum nitrite concentration in the normotensive group [P<0.05], without any change in the hypertensive group. All animals who received L-NAME treatment survived at the end of experiment. Fifty percent of the hypertensive animals died four hours after the experiment. The 72 hour survival rate was similar in the L-NAME treated groups. L-NAME infusion during decompensated hemorrhagic shock plays a protective role in the improvement of hemodynamic responses and short term survival rate in normotensive animals
RESUMO
Background and aim: ventral tegmental area [VTA] is located in the mesencephalon and it is one of the main nuclei that play a major role in drug abuse or addiction. In this study we investigated the effect of electrical stimulation of the VTA on addiction to morphine
Methods: intravenous self-administration was used to quantify the level of drug-dependence. Twenty-four Wistar rats were divided into three groups: 1] Sham or saline group that had surgery and received saline by self-administration. 2] Control or morphine group that had surgery and received morphine by self-administration. 3] Case or morphine + stimulation [25 [micro]A 100 Hz 0.14 ms period for 10 minutes] group that had surgery and received electrical stimulation 15 minutes before morphine self-administration
Results: addiction was seen only in the morphine group, and electrical stimulation of the VTA prevented the addiction
Conclusion: electrical current stimulates all type of the neurons in the VTA. Since dopaminergic neurons comprise two-third of its neurons, VTA stimulation may cause the release of dopamine in the nucleus accumbence and produce rewards so that the animal needs no further rewards from morphine