Epinephrine but not vasopressin attenuates the airway response to anaphylactic shock in rats

Zheng, Feng; Copotoiu, Ruxandra; Tacquard, Charles; Demoulin, Bruno; Malinovsky, J. M.; Lévy, Bruno; Longrois, Dan; Barthel, Grégoire; Mertès, Paul-Michel; Marchal, François; Demoulin‐Alexikova, Silvia; Collange, Olivier

doi:10.1080/01902148.2017.1323981

Cited by 11 publications

(6 citation statements)

References 39 publications

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“…Furthermore, AVP acting on V1aRs depolarizes and increases firing rate of these preganglionic neurons ( Yan et al, 2017 ), which is suggestive of the broncho-constrictive and secretory effect of AVP. Nonetheless, available evidence points to limited effects of AVP on bronchoconstriction in laboratory animals ( Bhoola et al, 1962 ; Zheng et al, 2017 ) and humans ( Knox et al, 1989 ).…”

Section: The Respiratory Effects Of Vasopressinmentioning

confidence: 99%

Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

et al. 2021

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Vasopressin (AVP) is a key neurohormone involved in the regulation of body functions. Due to its urine-concentrating effect in the kidneys, it is often referred to as antidiuretic hormone. Besides its antidiuretic renal effects, AVP is a potent neurohormone involved in the regulation of arterial blood pressure, sympathetic activity, baroreflex sensitivity, glucose homeostasis, release of glucocorticoids and catecholamines, stress response, anxiety, memory, and behavior. Vasopressin is synthesized in the paraventricular (PVN) and supraoptic nuclei (SON) of the hypothalamus and released into the circulation from the posterior lobe of the pituitary gland together with a C-terminal fragment of pro-vasopressin, known as copeptin. Additionally, vasopressinergic neurons project from the hypothalamus to the brainstem nuclei. Increased release of AVP into the circulation and elevated levels of its surrogate marker copeptin are found in pulmonary diseases, arterial hypertension, heart failure, obstructive sleep apnoea, severe infections, COVID-19 due to SARS-CoV-2 infection, and brain injuries. All these conditions are usually accompanied by respiratory disturbances. The main stimuli that trigger AVP release include hyperosmolality, hypovolemia, hypotension, hypoxia, hypoglycemia, strenuous exercise, and angiotensin II (Ang II) and the same stimuli are known to affect pulmonary ventilation. In this light, we hypothesize that increased AVP release and changes in ventilation are not coincidental, but that the neurohormone contributes to the regulation of the respiratory system by fine-tuning of breathing in order to restore homeostasis. We discuss evidence in support of this presumption. Specifically, vasopressinergic neurons innervate the brainstem nuclei involved in the control of respiration. Moreover, vasopressin V1a receptors (V1aRs) are expressed on neurons in the respiratory centers of the brainstem, in the circumventricular organs (CVOs) that lack a blood-brain barrier, and on the chemosensitive type I cells in the carotid bodies. Finally, peripheral and central administrations of AVP or antagonists of V1aRs increase/decrease phrenic nerve activity and pulmonary ventilation in a site-specific manner. Altogether, the findings discussed in this review strongly argue for the hypothesis that vasopressin affects ventilation both as a blood-borne neurohormone and as a neurotransmitter within the central nervous system.

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Section: The Respiratory Effects Of Vasopressinmentioning

confidence: 99%

Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

et al. 2021

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“…Although the bronchodilatory actions of sevoflurance [sevoflurane], through lung resistance and decreased elastance, have been well documented, there are still conflicting results on the effects of desflurane on airway resistance 37 . Persistence of increased airway pressure in the presence of sevoflurane/desflurane might be because of bronchial oedema and/or pulmonary oedema, as described in animal models of anaphylactic shock 38 . In this case, epinephrine by continuous infusion is the drug of choice.…”

Section: Case Scenariosmentioning

confidence: 99%

“…37 Persistence of increased airway pressure in the presence of sevoflurane/desflurane might be because of bronchial oedema and/or pulmonary oedema, as described in animal models of anaphylactic shock. 38 In this case, epinephrine by continuous infusion is the drug of choice. Persistence of no capnogram/no flow/high pressure despite intravenous and inhaled bronchodilators and inhaled anaesthetics should lead to reconsideration of the diagnosis, such as a tension pneumothorax mimicking the whole clinical presentation and becoming progressively worse, or ventilation difficulties in patients with severe lung diseases.…”

Section: Case Scenariosmentioning

confidence: 99%

Clinical reasoning in anaphylactic shock: addressing the challenges faced by anaesthesiologists in real time

Gouél‐Cheron

Neukirch

Kantor

et al. 2021

European Journal of Anaesthesiology

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Acute hypersensitivity reactions to drugs occur infrequently during anaesthesia and the peri-operative period. When clinical presentation includes the classical triad, erythema, cardiovascular abnormalities and increased airway pressure, the diagnosis is evident and the challenge is to prescribe a therapeutic regimen according to guidelines and to manage refractory signs in a timely manner. In many situations, however, the initial clinical signs are isolated, such as increased airway pressure or arterial hypotension. Rendering a differential diagnosis with causes and mechanisms other than acute hypersensitivity reactions (AHRs) is difficult, delaying treatment with possible worsening of the clinical signs, and even death, in previously healthy individuals. In these difficult diagnostic situations, clinical reasoning is mandatory, and guidelines do not explicitly explain the elements on which clinical reasoning can be built. In this article, based on clinical evidence whenever available, experimental data and pathophysiology, we propose algorithms that have been evaluated by experts. The goal of these algorithms is to provide explicit elements on which the differential diagnosis of AHRs can be made, accelerating the implementation of adequate therapy.

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“…In ovalbumin-sensitised rats, anaphylaxis is associated with an almost immediate decrease in pulmonary compliance as a result of massive tracheal, bronchial, and intrapulmonary microvascular leakage, causing bronchospasm. 90 In human patients, pulmonary artery and pulmonary capillary wedge pressures are reduced, although it is possible that pulmonary arteriolar dilatation, pulmonary venous constriction, or both could still result in raised pulmonary capillary hydrostatic pressures. In some instances of anaphylaxis, fulminant pulmonary oedema with a high fluid protein content (>70% fluid/serum protein concentration) has been described, and this membrane oedema may occur with normal or low pulmonary capillary hydrostatic pressures, and in the presence of high mean positive airway pressures (with positive pressure invasive ventilation).…”

Section: Pulmonary Oedemamentioning

confidence: 99%

Molecular mechanisms and pathophysiology of perioperative hypersensitivity and anaphylaxis: a narrative review

Ebo

Clarke

Mertès

et al. 2019

British Journal of Anaesthesia

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Perioperative hypersensitivity reactions (POH) constitute a clinical and diagnostic challenge, a consequence of heterogeneous clinical presentations, and multiple underlying pathomechanisms. POH do not necessarily involve an allergen-specific immune response with cross-linking of specific immunoglobulin E (sIgE) antibodies on mast cells and basophils. POH can also result from alternative specific and non-specific effector cell activation/degranulation such as complement-derived anaphylatoxins and off-target occupancy of mast cell, basophil, or both surface receptors. Moreover, POH and anaphylaxis can occur independent from mast cell and basophil degranulation.The manifestations of POH primarily affect the cardiovascular, respiratory, and integumentary systems. POH present within the context of surgical or procedural pathology and the effects of surgical and anaesthetic techniques on pre-existing physiological reserve. The majority of cases of appropriately-treated intraoperative anaphylaxis can be considered a compensated cardiovascular anaphylaxis. With increasing severity of anaphylaxis, maldistribution and hypovolaemia lead to reduced venous return and circulatory failure. Treatment with a combination of epinephrine and i.v. fluid is critical for successful resuscitation, although the excessive use of epinephrine without adequate volume expansion may be deleterious. Neural control of the airways is important in the pathophysiology of bronchospasm. Anticholinergic drug premedication is beneficial in patients with hyperreactive airways. Pulmonary oedema can result from a combination of pulmonary capillary hypertension, incompetence of the alveolocapillary membrane, or both. Angioedema can be distinguished mechanistically into histaminergic and non-histaminergic (e.g. bradykinin-mediated). An understanding of the molecular mechanisms and pathophysiology of POH are essential for the immediate management and subsequent investigation of these cases.

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Epinephrine but not vasopressin attenuates the airway response to anaphylactic shock in rats

Abstract: Epinephrine was superior to AVP for alleviating the airway response in a rat model of AS. When bronchospasm and severe arterial hypotension are present during AS, epinephrine should be the drug of choice.

Cited by 11 publications

References 39 publications

Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

Vasopressin and Breathing: Review of Evidence for Respiratory Effects of the Antidiuretic Hormone

Clinical reasoning in anaphylactic shock: addressing the challenges faced by anaesthesiologists in real time

Molecular mechanisms and pathophysiology of perioperative hypersensitivity and anaphylaxis: a narrative review

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