Why the study?
Does adrenomedullectomy alter the haemodynamic response to hypertonic saline resuscitation during haemorrhagic hypotension in conscious rats?
Does adrenomedullectomy alter the haemodynamic response to hypertonic saline resuscitation during haemorrhagic hypotension in conscious rats?
The adrenal medulla is not essential for the cardiovascular resuscitative effects of hypertonic saline during haemorrhagic shock in rats.
Adrenal medulla dispensable for HTS resuscitation in rat hemorrhage; leaves open mechanism and translational relevance to humans.
The aim of this study was to determine if the adrenal medulla plays a role in mediating haemodynamic effects of hypertonic saline (HTS) resuscitation during haemorrhagic hypotension in conscious rats. Wistar-Kyoto rats were either adrenomedullectomized (ADMX, n = 11) or sham-operated (SHAM, n = 10) and implanted with intravascular catheters. Pre-haemorrhage resting mean arterial pressure (MAP) was lower in the ADMX than in the SHAM group. Haemorrhage was performed by withdrawal of blood through the venous catheter, and a MAP of 50 mmHg was maintained for 1 h by further withdrawal when necessary. Both groups responded to haemorrhage with marked bradycardia. Plasma adrenaline (A) rose 10-fold in response to hypotension in the SHAM group, while remaining at pre-haemorrhage levels in the ADMX group, indicating successful adrenal demedullation. Infusion of 2.0 ml kg-1 HTS (NaCl 8.0 mg ml-1 i.v.) produced an immediate increase in MAP and heart rate (HR) in both groups, to pre-haemorrhage values or higher. Plasma noradrenaline (NA) increased in both groups after HTS, while the high levels of A in the SHAM group slowly returned toward baseline. Plasma glucose and rate of haemodilution was higher in the SHAM group during and after hypotension. The maintenance of MAP above 60 mmHg was less effective in the SHAM group during the first 2 h after HTS, but after 24 h, prehaemorrhage MAP was established in both groups. In conclusion, the adrenal medulla does not play a major role in the response to HTS resuscitation.
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Elgjo et al. (1994) studied this question.
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