Anaphylatoxin‐induced shock and two patterns of anaphylactic shock: Hemodynamics and mediators*

Pávek, K; Piper, Priscilla J.; Smedegård, G.

doi:10.1111/j.1748-1716.1979.tb00103.x

Cited by 47 publications

(20 citation statements)

References 16 publications

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“…However, this communication illustrates by one intensely studied example with one clinically used histamine releaser (experiments in animals and human subjects for more than /0 years [29-32, 34, 39, 40, 44, 54] that the classical symptoms of anaphylaxis are rare in histamine-release responses in general and only more common ("classical") in grade III reactions. Increasing experience, however, in animals [6,25,42,49,50,60] and in man [61] is forming the suggestion that even this may not be true: Clinical pictures of severe heart attack or arrhythmias may be caused by histaminerelease responses which clearly have to be classified as grade III reactions.…”

Section: Discussionmentioning

confidence: 99%

Definition and classification of the histamine-release response to drugs in anaesthesia and surgery: Studies in the conscious human subject

Doenicke²,

et al. 1982

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Summary. In 2 clinical studies in 40 conscious human volunteers and 164 orthopedic patients histamine-release responses were diagnosed, defined and classified. Polygeline (Haemaccel) in its now outdated formulation [40] was chosen as a clinical histamine releaser. The main interest was not concentrated on the extreme, the "classical" anaphylactic response, but on the average histamine-release response found in clinical experiments with so many drugs in the last 10 years.In human volunteers 600 ng/kg histamine was i.v. injected. Indicants for a systemic anaphylactoid reaction with the highest incidence ratio were tachycardia, plasma histamine levels > t ng/ml, "metallic taste", flush, congestion of head, "wet eyes" and tears, hypertension and headache. Following polygeline none of these subjects developed a life-threatening reaction, but 12 showed a systemic response, 11 a cutaneous reaction and 17 were non-responders. Indieants for a systemic anaphylactoid reaction with the highest incidence ratio were plasma histamine levels > 1 ng/ml, tachycardia, wheals, sensation of heat, narrowness of throat, hypertension, headache and wet eyes or tears.In a prolective, cohort study in the orthopedic patients 3 subjects with life-threatening reactions, 27 with systemic response, 96 with cutaneous reaction and 38 non-responders were included. Indicants with the highest incidence ratio were tachycardia, plasma histamine levels > 1 ng/ml, erythema and wheals, cough, flush, stuffy nose and facial oedema. With this trial the indicants for diagnosing a systemic histamine release response in volunteers were validated in patients to a large extent.Thus the average histamine-release response was defined by clinical signs such as tachycardia and mild hypertension, scattered hives such as spots of erythema and wheals, respiratory symptoms in the laryngeal and nasal region, such as cough, narrowness in the throat, stuff), nose and sneezing and by pathological plasma histamine levels (> 1 ng/ml), in addition histamine-release responses were differentiated as cutaneous responses, systemic responses and life-threatening responses by clinical and operational criteria and by plasma histamine levels. Using clinical trials and medical * Dedicated to Professor Otto Lindenschmidtt ** Supported by grant of Deutsche Forschungsgemeinschafl (Lo 199/10 and Lo 199/13-6) Offprint requests to: Professor Dr. W. Lorenz (address see above) decision making procedures the incidence of systemic histamine-release responses in patients higher by two orders of magnitude than in other studies reported hitherto.

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Section: Discussionmentioning

confidence: 99%

Definition and classification of the histamine-release response to drugs in anaesthesia and surgery: Studies in the conscious human subject

Doenicke²,

et al. 1982

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“…Evidence also exists that, during sepsis, extensive activation of the complement system occurs resulting in loss of homeostasis, which may in some manner compromise survival. Intravenous infusion of C5a into dogs generated a shock syndrome characterized by portal blood pooling and an associated decrease in venous return, cardiac output, and arterial pressure (20). In experimental sepsis caused by massive i.v.…”

Section: Discussionmentioning

confidence: 99%

Role of C5a in Multiorgan Failure During Sepsis

Huber‐Lang

Sarma

et al. 2001

The Journal of Immunology

205

178

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In humans with sepsis, the onset of multiorgan failure (MOF), especially involving liver, lungs, and kidneys, is a well known complication that is associated with a high mortality rate. Our previous studies with the cecal ligation/puncture (CLP) model of sepsis in rats have revealed a C5a-induced defect in the respiratory burst of neutrophils. In the current CLP studies, MOF occurred during the first 48 h with development of liver dysfunction and pulmonary dysfunction (falling arterial partial pressure of O2, rising partial pressure of CO2). In this model an early respiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactate. During these events, blood neutrophils lost their chemotactic responsiveness both to C5a and to the bacterial chemotaxin, fMLP. Neutrophil dysfunction was associated with virtually complete loss in binding of C5a, but binding of fMLP remained normal. If CLP animals were treated with anti-C5a, indicators of MOF and lactate acidosis were greatly attenuated. Under the same conditions, C5a binding to blood neutrophils remained intact; in tandem, in vitro chemotactic responses to C5a and fMLP were retained. These data suggest that, in the CLP model of sepsis, treatment with anti-C5a prevents development of MOF and the accompanying onset of blood neutrophil dysfunction. This may explain the protective effects of anti-C5a in the CLP model of sepsis.

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“…The perfusion pressure of the guinea-pig lung was variably increased by C5adesArg (Pavek et al, 1979). Regal (1982) and Marceau & Hugli, (1984) have described a vasoconstrictor effect of CSa on guineapig isolated blood vessels.…”

Section: Introductionmentioning

confidence: 99%

“…Vasoconstriction was apparently mediated by a combined effect of histamine and cyclo-oxygenase products. Furthermore, histamine and prostaglandins, but no slow reacting substance ofanaphylaxis (SRS-A) activity, were detected by bioassay in the effluent of C5a-perfused lung tissue (Pavek et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

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Effects of the C5a anaphylatoxin and its relationship to cyclo‐oxygenase metabolites in rabbit vascular strips

Hugli

Marceau

1985

British J Pharmacology

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Strips of rabbit blood vessels were suspended in vitro and responses to complement peptides C3a and C5a were recorded isotonically. Human C3a (up to 1.5 μm) was inactive on rabbit vascular strips. Human C5a (2.9–59 nm) decreased spontaneous activity of the rabbit portal vein under resting baseline tension. The C5a relaxed strips of portal vein and pulmonary artery that were precontracted with noradrenaline (NA, 200 nm). On the portal vein, C5a‐induced relaxation was preceded by a transient contractile phase which decreased with repeated applications of C5a. The magnitude of C5a‐induced relaxation of both vessels increased with repeated stimulation by C5a. Maximal levels of relaxation for the third application of C5a at 59 nm averaged 44% and 17% of the NA‐induced contraction plateau in portal vein and pulmonary artery, respectively. Strips of rabbit aorta responded minimally to C5a. Indomethacin (5.6 μm) significantly inhibited C5a‐induced relaxation of the portal vein and pulmonary artery but had no effect on the early contractile response of the portal vein. Mepyramine (10 μm) failed to modify the C5a response from either vessel, but it reduced the contractile phase of the C5a response on the portal vein when applied in conjunction with indomethacin. The drug SKF 88046, an end organ antagonist of thromboxane (TX) A2 and some contractile prostaglandins, reduced the contractile phase and increased relaxation of the portal vein to C5a but did not modify the response of the pulmonary artery. Radioimmunoassays for 6‐keto‐prostaglandin F1α (6‐keto‐PGF1α) and TXB2 were performed on the fluid bathing rabbit isolated blood vessels. C5a promoted release of 6‐keto‐PGF1α over the basal release rate in rabbit tissues. Only trace quantities of TXB2 were produced by rabbit vessels exposed to C5a. It is concluded that the mechanical response of blood vessels to C5a is mainly determined by the type of cyclo‐oxygenase products released and by the sensitivity of each blood vessel to these active lipids. Tissue histamine release is also responsible for a component of the response of rabbit portal vein to C5a. The relaxant effect of C5a on rabbit blood vessels may be a phenomenon related to the previously reported hypotensive action of classical anaphylatoxins in vivo.

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Anaphylatoxin‐induced shock and two patterns of anaphylactic shock: Hemodynamics and mediators*

Cited by 47 publications

References 16 publications

Definition and classification of the histamine-release response to drugs in anaesthesia and surgery: Studies in the conscious human subject

Definition and classification of the histamine-release response to drugs in anaesthesia and surgery: Studies in the conscious human subject

Role of C5a in Multiorgan Failure During Sepsis

Effects of the C5a anaphylatoxin and its relationship to cyclo‐oxygenase metabolites in rabbit vascular strips

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