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.
- SourceAvailable from: Nicholas G KounisForensic science international 07/2013; · 2.10 Impact Factor
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ABSTRACT: Experiments have shown that anaphylaxis decreases cardiac output; increases left ventricular end diastolic pressure; induces severe early acute increase in respiratory resistance with pulmonary interstitial edema; and decreases splanchnic, cerebral, and myocardial blood flow more than what would be expected from severe arterial dilation and hypotension. This is attributed to the constrictive action of inflammatory mediators released during anaphylactic shock. Inflammatory mediators such as histamine, neutral proteases, arachidonic acid products, platelet-activating factor (PAF), and a variety of cytokines and chemokines constitute the pathophysiologic basis of Kounis hypersensitivity-associated acute coronary syndrome. Although the mechanisms of anaphylactic shock still remain to be elucidated, myocardial involvement due to vasospasm-induced coronary blood flow reduction manifesting as Kounis syndrome should be always considered. Searching current experimental and clinical literature on anaphylactic shock pathophysiology, causality, clinical appearance, and treatment via PubMed showed that differentiating global hypoperfusion from primary tissue suppression due to mast cell mediator constrictive action on systemic arterial vasculature is a challenging procedure. Combined tissue suppression from arterial involvement and peripheral vasodilatation, perhaps, occur simultaneously. In cases of anaphylactic shock treatment targeting the primary cause of anaphylaxis together with protection of coronary vasculature and subsequently the cardiac tissue seems to be of paramount importance.North American journal of medical sciences. 11/2013; 5(11):631-636.
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ABSTRACT: Anaphylactic shock is a real and life threatening medical emergency which is encountered in every field of medicine. The coronary arteries seem to be the primary target of anaphylaxis resulting in the development of Kounis syndrome. Kounis syndrome is a pan-arterial anaphylaxis -associated syndrome affecting patients of any age, involving numerous and continuously increasing causes, with broadening clinical manifestations and covering a wide spectrum of mast cell activation disorders. Recently, Kounis-like syndrome affecting the cerebral arteries was found to be associated with mast cell activation disorders. In anaphylactic shock, the decrease of cerebral blood flow is more than what would be expected from severe arterial hypotension. This is attributed to the early and direct action of anaphylactic mediators on cerebral vessels. While adrenaline is a life saving agent in the treatment of anaphylactic shock, it contains sodium betabisulfite as preservative and should be avoided in sulfite allergic patients. Potential allergens encountered in endodotic practice include formocresol, zinc compounds thiurams, sodium dimethyldithiocarbamade, and mercaptobenzothiazole that might have synergistic action. All these agents together with analgesics, antibiotics, antiseptics, formaldehyde, latex, local anaesthetics and metals used in dental practice, in general, can induce anaphylactic shock. Practitioners should be aware of these consequences. A careful history of previous atopy and reactions is of paramount importance for safe and effective management.International Endodontic Journal 06/2013; · 2.05 Impact Factor