Renal nerves are not involved in sodium and water retention during mechanical ventilation in awake dogs.
BACKGROUND
The role of renal nerves during positive end-expiratory pressure ventilation (PEEP) has only been investigated in surgically stressed, anesthetized, unilaterally denervated dogs. Anesthesia, sedation, and surgical stress, however, decrease urine volume and sodium excretion and increase renal sympathetic nerve activity independent of PEEP. This study investigated in awake dogs the participation of renal nerves in mediating volume and water retention during PEEP.


METHODS
Eight tracheotomized, trained, awake dogs were used. The protocol consisted of 60 min of spontaneous breathing at a continuous positive airway pressure of 4 cm H2O, followed by 120 min of controlled mechanical ventilation with a mean PEEP of 15-17 cm H2O (PEEP), and 60 min of continuous positive airway pressure. Two protocols were performed on intact dogs, in which volume expansion had (hypervolemic; electrolyte solution, 0.5 ml x kg(-1) x min(-1)) and had not (normovolemic) been instituted. This was repeated on the same dogs 2 or 3 weeks after bilateral renal denervation.


RESULTS
Hypervolemic dogs excreted more sodium and water than did normovolemic dogs. There was no difference between intact and renal-denervated dogs. Arterial pressure did not decrease when continuous positive airway pressure was switched to PEEP. Plasma renin activity, aldosterone, and antidiuretic hormone concentrations were greater in normovolemic dogs. The PEEP increased aldosterone and antidiuretic hormone concentrations only in normovolemic dogs.


CONCLUSIONS
In conscious dogs, renal nerves have no appreciable contribution to sodium and water retention during PEEP. Retention in normovolemic dogs seems to be primarily caused by an activation of the renin-angiotensin system and an increase in the antidiuretic hormone. Excretion rates depended on the volume status of the dogs.
Clinic of Anesthesiology and Operative Intensive Care Medicine, Campus Virchows-Clinics, Charité Medical Faculty of Humboldt University Berlin, Germany. willehad.boemke@charite.de
W
W
Boemke
M O
MO
Krebs
K
K
Djalali
H
H
Bünger
G
G
Kaczmarczyk
D000450:Aldosterone / Q000097:blood; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D004285:Dogs; D004837:Epinephrine / Q000097:blood; D005260:Female; D006400:Hematocrit; D006439:Hemodynamics / Q000502:physiology; D007668:Kidney / Q000294:innervation* / Q000502:physiology; D009638:Norepinephrine / Q000097:blood; D011175:Positive-Pressure Respiration; D011188:Potassium / Q000097:blood / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood / Q000652:urine*; D014667:Vasopressins / Q000097:blood; D014867:Water / Q000378:metabolism*
D014867:Water; D014667:Vasopressins; D002245:Carbon Dioxide; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D012083:Renin; D011188:Potassium; D009638:Norepinephrine; D004837:Epinephrine