Vasopressin and renin-angiotensin maintain arterial pressure during PEEP in nonexpanded, conscious dogs.
Increases of plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP) induce positive fluid balances by decreasing renal excretion. We investigated whether elevated levels of AVP and/or PRA maintain mean arterial pressure (MAP) during PEEP under conditions where plasma volume is not expanded. Six conscious chronically tracheotomized beagle dogs, kept under standardized conditions, were investigated in four protocols. They were 1) control: 1 h spontaneous breathing with a continuous positive airway pressure of 4 cmH2O (CPAP 4) followed by 2 h CMV with PEEP, resulting in a mean airway pressure of approximately 20 cmH2O (CMV 20 referred to as "PEEP"); 2) vasopressin blockade: 1 h CPAP 4, 2 h PEEP after intravenous application of an AVP V1-receptor antagonist (AVPA); 3) converting enzyme inhibition: 1 h CPAP 4, 2 h PEEP plus angiotensin-converting enzyme inhibition (ACEI); and 4) combined blockade: 1 h CPAP 4, 2 h PEEP plus AVPA + ACEI. In AVPA + ACEI, MAP decreased during PEEP from 101 +/- 4 to 75 +/- 10 mmHg, glomerular filtration rate (GFR) decreased from 3.6 +/- 0.3 to 1.7 +/- 0.7 ml.min-1.kg body wt-1, heart rate increased from 95 +/- 10 to 122 +/- 7 beats/min, plasma aldosterone increased from 62 +/- 26 to 353 +/- 63 pg/ml, plasma epinephrine increased from 81 +/- 15 to 352 +/- 89 pg/ml (all changes P < 0.05), and plasma norepinephrine did not change. Neither MAP nor GFR changed during PEEP in control experiments in which both PRA and AVP increased, in AVPA experiments in which PRA increased, or in ACEI experiments in which AVP increased. We conclude that both AVP and angiotensin II contribute to the maintenance of MAP and GFR during PEEP. When both hormones are inhibited, no immediate compensation exists to prevent an acute fall in MAP and GFR.
Kaczmarczyk
G
G
Arbeitsgruppe Experimentelle Anästhesie, Virchow-Klinikum, Humboldt-Universität zu Berlin, Germany.
Vogel
S
S
Krebs
M
M
Bünger
H
H
Scholz
A
A
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000097:blood* / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006727:Hormone Antagonists / Q000494:pharmacology; D006728:Hormones / Q000097:blood; D007668:Kidney / Q000502:physiology; D011175:Positive-Pressure Respiration; D012084:Renin-Angiotensin System / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D065092:Antidiuretic Hormone Receptor Antagonists; D006727:Hormone Antagonists; D006728:Hormones; D001127:Arginine Vasopressin; C025043:vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(O- methyl-L-tyrosine)-8-L-arginine-