Anaphylactic Shock Decreases Cerebral Blood Flow More Than What Would Be Expected From Severe Arterial Hypotension

Abstract

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.

Management of anaphylactic shock in the operating room

“…Doses reported were very different in those studies, from 2 IU IV to 40 IU plus infusion. In animal models, vasopressin has similar systemic effects than epinephrine but delays restoration of cerebral tissue oxygen pressure as compared to epinephrine [27,28]. The clinical consequences of these results are not known but underline the importance of taking into consideration regional circulations when assessing the efficacy of vasoconstrictors used in the resuscitation of AS.…”

“…Whereas cerebral blood flow is conserved during pharmacologically-induced arterial hypotension, one study showed a linear relationship between cerebral cortical blood flow and blood pressure during hypotension in AS in a rat model [27]. AS resulted in severe impairment of cerebral blood flow and oxygenation, beyond what could be expected from the level of arterial hypotension.…”

Kounis syndrome: A primary cause for the anaphylactic shock

“…The authors of this experiment definitely excluded peripheral vasodilatation as a cause of the registered anaphylactic cardiac damage [5]. Similarly, in a recent study [6], it was found that anaphylactic shock decreases cerebral blood flow more than what would be expected from severe arterial hypotension. This was attributed to direct action of anaphylactic mediators on the cerebral arterial system and not solely due to arterial hypotension.…”

The more allergens an atopic patient is exposed to, the easier and quicker anaphylactic shock and Kounis syndrome appear: Clinical and therapeutic paradoxes

“…In the clinical setting,[31] there are current reports according to which patients with anaphylactic cardiac shock do not respond to fluid replacement but recover with current acute myocardial infarction protocol and antiallergic treatment thus denoting that the heart is primarily affected. Furthermore, other recent experiments[32] have shown that anaphylactic shock decreases cerebral blood flow more than what would be expected from severe arterial hypotension. This was attributed to the early and direct action of anaphylactic mediators on cerebral vessels.…”