Hemorrhagic shock is a major cause of death in modern societies. Some patients, when treated, fail to sustain normal cardiovascular parameters, requiring
fluid therapy and vasoactive drugs. Among drugs with cardiovascular profile other than
catecholamine,
vasopressin (VP) is emerging as an option. To better understand its effects during
hemorrhagic shock, we compared the effects of VP and
noradrenaline (NA), associated to
fluid therapy. In this work, hamsters were subjected to
shock by withdrawal of 40% of their blood volume and were then divided into five groups. One group was treated with
saline solution, and the remaining ones with VP (three groups) and NA (one group) combined to fluid
resuscitation. To assess receptor role, two more VP groups were pretreated with specific receptor blockers (anti-V1 or anti-V2, respectively) before its infusion. Microcirculatory parameters such as vessel diameter, red blood cell velocity, and functional capillary density were evaluated. In addition, blood gas analysis and
lactate levels were also determined. Measurements were performed at baseline, after
shock, and
after treatment. At the end, leukocyte-endothelium interaction was evaluated, and animals were followed up to determine survival time. Neither
saline solution nor NA recovered microcirculatory parameters, but VP treatment returned to near baseline values, except when
V2 receptors were blocked. Functional capillary density was higher in the VP group
after treatment, without statistical difference from baseline values. When
V2 receptors were blocked, recovery was not achieved
after treatment. The VP group also had a smaller number of adhering leukocytes and improved 72-h survival time compared with the NA one. This study suggests that, in
hemorrhagic shock, treatment with low-dose VP, in combination with
fluid therapy, improves tissue perfusion. This outcome is mediated mostly by
V2 receptors, eliciting vasodilatation and consequently blood flow redistribution through the microcirculation.