Reversal by Vasopressin of Intractable Hypotension in the Late Phase of Hemorrhagic Shock

Abstract

Vasopressin is a uniquely effective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and catecholamine vasopressors. Vasopressin deficiency may contribute to the pathogenesis of this condition.

Vasopressor Therapy Using Vasopressin Prior to Crystalloid Resuscitation in Irreversible Hemorrhagic Shock under Isoflurane Anesthesia in Dogs

“…The exact reason for the increased CO in the V-C group is unknown but can be explained based on the assumption that vasopressin administration cause peripheral vasoconstriction in the state of hypovolemic shock. This is mediated by vasopressin via V 1 receptors located on the vascular endothelium, and this enables vasopressin to maintain vasopressor activity during hypoxia and acidosis, which result from prolonged shock state [13]. By virtue of this characteristic, vasopressin can be administered before fluid resuscitation in irreversible hypovolemic shock.…”

“…Vasopressin, an endogenous neurohypophysial hormone, has recently been recognized to be an effective vasopressor that successfully restores circulation when it is unresponsive to fluid resuscitation and catecholamine [13]. Vasopressin differs from other catecholamines because it acts on V 1 receptors.…”

Physiology of Vasopressin Relevant to Management of Septic Shock

“…29,44,53 However, during prolonged hemorrhagic shock in dogs, an initial increase in plasma vasopressin levels to 319 pg/mL was followed by a decrease to 29 pg/mL. 45,46 Similarly, acute endotoxin-induced shock results in extremely high levels of vasopressin (Ͼ 500 pg/mL in dogs and Ͼ 300 pg/mL in baboons). 54 Importantly, vasopressin levels in established septic shock and vasodilatory shock are low ( Table 2).…”

Sustained stimulation of vasopressin and oxytocin release by ATP and phenylephrine requires recruitment of desensitization-resistant P2X purinergic receptors

“…Postural changes induce acute elevations in plasma VP (21), while prolonged decreases in blood pressure and/or volume can elicit increases in plasma VP/OT that are sustained for hours to days (3,15,29). The absence of these sustained elevations in plasma VP leads to cardiovascular collapse in hemorrhagic and septic shock (24,27,30).Simultaneous exposure of explants of the hypothalamoneurohypophyseal system (HNS) to ATP and phenylephrine [(PE) to mimic noradrenergic activation of ␣1-receptors (␣1-AR)] results in conversion of the small, transient response elicited by either agent alone to a larger and sustained elevation in VP/OT release (20). This synergistic effect of ATP and PE may be responsible for the sustained increase in VP secretion that occurs during chronic hypotension and/or hypovolemia.…”

“…Postural changes induce acute elevations in plasma VP (21), while prolonged decreases in blood pressure and/or volume can elicit increases in plasma VP/OT that are sustained for hours to days (3,15,29). The absence of these sustained elevations in plasma VP leads to cardiovascular collapse in hemorrhagic and septic shock (24,27,30).…”