ANAPHYLACTIC SHOCK DECREASES CEREBRAL BLOOD FLOW MORE THAN WHAT WOULD BE EXPECTED FROM SEVERE ARTERIAL HYPOTENSION

被引:29
|
作者
Davidson, Julien [2 ]
Zheng, Feng [2 ]
Tajima, Keiko [2 ]
Barthel, Gregoire [2 ]
Alb, Ionel [2 ,4 ]
Tabarna, Adriana [2 ,4 ]
Thornton, Simon N. [3 ]
Lambert, Maud [2 ]
Longrois, Dan [5 ]
Audibert, Gerard [2 ,4 ]
Malinovsky, Jean-Marc [2 ,6 ]
Mertes, Paul-Michel [1 ,2 ]
机构
[1] Hop Univ Strasbourg, SAMU, Strasbourg, France
[2] Univ Lorraine, Fac Med, Contrat AVENIR INSERM U 961, Grp Choc, Vandoeuvre Les Nancy, France
[3] Univ Lorraine, Fac Med, Lab U961, Vandoeuvre Les Nancy, France
[4] CHU Cent, Dept Anesthesie Reanimat Chirurg, Nancy, France
[5] Univ Paris Diderot, Unite INSERM U698, Hop Bichat Claude Bernard, Dept Anesthesie Reanimat Chirurg, Paris, France
[6] CHU Reims, Dept Anesthesie Reanimat Chirurg, Reims, France
来源
SHOCK | 2012年 / 38卷 / 04期
关键词
Shock; anaphylaxis; cerebrovascular circulation; autoregulation; BROWN-NORWAY RATS; RECEPTOR BLOCKADE IMPROVES; PLATELET-ACTIVATING-FACTOR; NITRIC-OXIDE SYNTHASE; ARGININE-VASOPRESSIN; MODEL; MICROCIRCULATION; AUTOREGULATION; EPINEPHRINE; INHIBITION;
D O I
10.1097/SHK.0b013e3182690897
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
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 mu g of nicardipine followed by continuous infusion of 1 mg . 100 g(-1) . h(-1) 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 (PtiO(2)) 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 PtiO(2); the decrease in CBF was significantly (P < 0.05) attenuated in the OVA + VE group; however, CCBF and PtiO(2) 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 PtiO(2) 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(2) = 0.81) but not in the NICAR group (regression slope: 0.23 [SD, 0.32]; median r(2) = 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.
引用
收藏
页码:429 / 435
页数:7
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