Document Detail

Intravenous hypertonic NaCl acts via cerebral sodium-sensitive and angiotensinergic mechanisms to improve cardiac function in haemorrhaged conscious sheep.
MedLine Citation:
PMID:  17640936     Owner:  NLM     Status:  MEDLINE    
Acute NaCl loading as resuscitation in haemorrhagic hypovolaemia is known to induce rapid cardiovascular recovery. Besides an osmotically induced increase in plasma volume the physiological mechanisms of action are unknown. We hypothesized that a CNS mechanism, elicited by increased periventricular [Na(+)] and mediated by angiotensin II type 1 receptors (AT(1)), is obligatory for the full effect of hypertonic NaCl. To test this we investigated the cardiovascular responses to haemorrhage and subsequent hypertonic NaCl infusion (7.5% NaCl, 4 ml (kg BW)(-1)) in six conscious sheep subjected to intracerebroventricular (i.c.v.) infusion of artificial cerebrospinal fluid (aCSF; control), mannitol solution (Man; 75 mmol l(-1) [Na(+)], total osmolality 295 mosmol kg(-1)) or losartan (Los; 1 mg ml(-1), AT(1) receptor antagonist) at three different occasions. Man normalized (144 +/- 6 mmol l(-1), mean +/- s.d.) the increase in i.c.v. [Na(+)] seen after aCSF (161 +/- 2 mmol l(-1)). Compared with control, both Man and Los significantly (P < 0.05) attenuated the improvement in mean arterial blood pressure (MAP), cardiac index and mesenteric blood flow (SMBF) in response to intravenous hypertonic NaCl: MAP, rapid response +45 mmHg versus +38 mmHg (Man) and +35 mmHg (Los); after 180 min, +32 mmHg versus +21 mmHg (Man) and +19 mmHg (Los); cardiac index after 180 min, +1.9 l min(-1) (m(2))(-1) versus +0.9 l min(-1) (m(2))(-1) (Man) and +0.9 l min(-1) (m(2))(-1) (Los); SMBF rapid response, +981 ml min(-1) versus +719 ml min(-1) (Man) and +744 ml min(-1) (Los); after 180 min, +602 ml min(-1) versus +372 ml min(-1) (Man) and +314 ml min(-1) (Los). The results suggest that increased periventricular [Na(+)] and cerebral AT(1) receptors contribute, together with plasma volume expansion, to improve systemic haemodynamics after treatment with hypertonic NaCl in haemorrhagic hypovolaemia.
Robert Frithiof; Stefan Eriksson; Frida Bayard; Tor Svensson; Mats Rundgren
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-07-19
Journal Detail:
Title:  The Journal of physiology     Volume:  583     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-20     Completed Date:  2007-12-06     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1129-43     Citation Subset:  IM    
Department of Physiology and Pharmacology, Karolinska Institutet, S-17177, Stockholm, Sweden.
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MeSH Terms
Angiotensin II / blood
Angiotensin II Type 1 Receptor Blockers / pharmacology
Blood Pressure / drug effects
Cardiovascular System / drug effects*
Diuretics, Osmotic / pharmacology
Hemorrhage / metabolism,  physiopathology*,  therapy*
Hypovolemia / metabolism,  physiopathology,  therapy
Infusions, Intravenous
Injections, Intraventricular
Losartan / pharmacology
Mannitol / pharmacology
Osmolar Concentration
Receptor, Angiotensin, Type 1 / metabolism*
Resuscitation / methods
Saline Solution, Hypertonic / pharmacology*
Sodium / cerebrospinal fluid*,  pharmacology
Vascular Resistance / drug effects
Vasopressins / blood
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Diuretics, Osmotic; 0/Receptor, Angiotensin, Type 1; 0/Saline Solution, Hypertonic; 11000-17-2/Vasopressins; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 69-65-8/Mannitol; 7440-23-5/Sodium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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