Anaphylactic shock decreases cerebral blood flow more than what would be expected from severe arterial hypotension.
The effects of acute reduction in arterial blood pressure in severe anaphylactic shock (AS) on cerebral blood flow are of paramount importance to be investigated. We studied cerebral circulation and oxygenation in a model of severe AS and compared it with a pharmacologically induced arterial hypotension of similar magnitude. Anaphylactic shock was induced by 1 mg intravenous ovalbumin (OVA) in sensitized rats. Rats were randomized to three groups: (i) no resuscitation (OVA; n = 10) (ii) intravenous volume expansion (10 mL in 10 min after OVA injection) (OVA + VE; n = 10); (iii) control hypotension (100 μg of nicardipine followed by continuous infusion of 1 mg · 100 g · h intravenously; NICAR; n = 10). Mean arterial pressure (MAP), carotid blood flow (CBF), cardiac output, cerebral cortical blood flow (CCBF; estimated by laser Doppler technique), and cerebral tissue oxygen pressure (PtiO2) were recorded over the 15 min following AS induction in all three groups. Results are expressed as mean (SD). One minute after OVA or nicardipine injection, there was a rapid and significant 50% decrease in MAP from basal values. In the OVA group, AS severely altered systemic and cerebral hemodynamics in 5 min: 93% (SD, 4%) decrease in CBF, 66% (SD, 8%) in CCBF, and 44% (SD, 8%) in PtiO2; the decrease in CBF was significantly (P < 0.05) attenuated in the OVA + VE group; however, CCBF and PtiO2 were not statistically different in the OVA versus OVA + VE groups. On the contrary, nicardipine-induced hypotension had only a limited impact on CBF, cardiac output, CCBF, and PtiO2 for a similar MAP decrease. There was a linear relation between CCBF and blood pressure in the OVA (regression slope: 0.87 [SD, 0.06]; median r = 0.81) but not in the NICAR group (regression slope: 0.23 [SD, 0.32]; median r = 0.33). Anaphylactic shock resulted in severe impairment of cerebral blood flow and oxygenation, beyond what could be expected from the level of arterial hypotension.
Groupe Choc, Contrat AVENIR INSERM U 961, Faculté de Médecine, Université de Lorraine, Vandoeuvre-lès-Nancy, France.
Julien
J
Davidson
Feng
F
Zheng
Keiko
K
Tajima
Grégoire
G
Barthel
Ionel
I
Alb
Adriana
A
Tabarna
Simon N
SN
Thornton
Maud
M
Lambert
Dan
D
Longrois
Gérard
G
Audibert
Jean-Marc
JM
Malinovsky
Paul-Michel
PM
Mertes
D000707:Anaphylaxis / Q000139:chemically induced / Q000150:complications / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D019585:Intracranial Hypotension / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009529:Nicardipine / Q000009:adverse effects / Q000494:pharmacology; D051381:Rats; D012151:Resuscitation / Q000379:methods; D014665:Vasodilator Agents / Q000009:adverse effects / Q000494:pharmacology
D014665:Vasodilator Agents; D009529:Nicardipine