Key Points
- To determine whether central endogenous opioid mechanisms and cardiac nerves drive the sudden decompensatory vasodilatation observed during severe blood loss.
- Simulated acute haemorrhage in 5 unanaesthetized rabbits by inflating an inferior vena cava balloon cuff to reduce cardiac output by 8.3% of baseline per minute.
- Assessed haemodynamic changes under sham conditions, graded intravenous (0.04–8 mg/kg) and intracisternal (0.2–69 µg/kg) naloxone, and intrapericardial procaine blockade.
- Sham treatment produced a biphasic response: an initial compensatory phase followed by abrupt decompensation at approximately 55% resting cardiac output, with steep rises in vascular conductance and precipitous arterial pressure drops.
- High-dose naloxone (intravenous 4–8 mg/kg; intracisternal 4–69 µg/kg) and cardiac nerve blockade abolished the second decompensatory phase, preserving arterial pressure and vascular constriction throughout simulated haemorrhage.
- Intracisternal naloxone blocked decompensation at doses 90 to 900 times lower than intravenous naloxone, whereas lower doses of either route exerted no protective effect.
Structured PICO
Does naloxone or cardiac nerve blockade prevent haemodynamic decompensation during simulated haemorrhage in awake rabbits?
PPopulationFive unanaesthetized rabbits
IInterventionGraded doses of intravenous (0.04-8 mg kg-1) and intracisternal (0.2-69 micrograms kg-1) naloxone, and cardiac nerve blockade with intrapericardial procaine prior to simulated haemorrhage
CComparatorSham treatment prior to simulated haemorrhage
OOutcomeHaemodynamic response (systemic vascular conductance, heart rate, and arterial pressure)surrogate
An endogenous opiate mechanism within the central nervous system, triggered by a signal from the heart, is responsible for haemodynamic decompensation during severe reduction in cardiac output.