A Comparison of Sodium Bicarbonate and Sodium Lactate Infusion in the Induction of Panic Attacks

Gorman, Jack M.; Battista, David; Goetz, Raymond R.; Dillon, Donald J.; Liebowitz, Michael R.; Fyer, Abby J.; Kahn, Jeffrey P.; Sandberg, Diana; Klein, Donald F.

doi:10.1001/archpsyc.1989.01810020047008

Cited by 59 publications

(23 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Unlike other mental disorders, PD is relatively unique as its pathognomonic feature, the PA, can be experimentally-induced in PD patients, but rarely in healthy individuals, by exposure to a rapidly expanding list of putative panicogenic agents with diverse pharmacological profiles, including sodium lactate (Pitts, Jr. and McClure, Jr., 1967), carbon dioxide (CO 2 ; Gorman et al, 1984), cholecystokinin tetrapeptide (CCK-4; Bradwejn et al, 1991;Bradwejn et al, 1992), yohimbine (α 2 -receptor antagonist)(Charney et al, 1987), sodium bicarbonate (Gorman et al, 1989a), caffeine (Charney et al, 1985), isoproterenol hydrochloride (Nesse et al, 1984;Rainey, Jr. et al, 1984), meta-chlorophenylpiperazine (van der Wee et al, 2004;m-CPP, 5-HT2C agonist; van Veen et al, 2007), and fenfluramine (a serotonin-releasing agent; Targum and Marshall, 1989). At the very least, a well-validated panicogenic agent should fulfill the following criteria: 1) the agent should be safe for use in humans; 2) the agent should specifically and reliably induce PAs in PD patients, but not healthy individuals; 3) the induced PA should be transient and reversible; 4) the PA should be blocked by therapeutics known to be effective in treating naturally occurring PAs in PD (e.g., selective-serotonin reuptake inhibitors, SSRIs); and 5) the induced PA should share the symptomatology of naturally occurring PAs (Griez and Schruers, 1998;Guttmacher et al, 1983;Kellner, 2011).…”

Section: Introduction To Panic Disordermentioning

confidence: 99%

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

Paul

Johnson

Shekhar

et al. 2014

Neuroscience & Biobehavioral Reviews

View full text Add to dashboard Cite

The Deakin/Graeff hypothesis proposes that different subpopulations of serotonergic neurons through topographically organized projections to forebrain and brainstem structures modulate the response to acute and chronic stressors, and that dysfunction of these neurons increases vulnerability to affective and anxiety disorders, including Panic Disorder. We outline evidence supporting the existence of a serotonergic system originally discussed by Deakin/Graeff that is implicated in the inhibition of panic-like behavioral and physiological responses. Evidence supporting this panic inhibition system comes from the following observations: 1) serotonergic neurons located in the ‘ventrolateral dorsal raphe nucleus (DRVL) as well as the ventrolateral periaqueductal gray (VLPAG) inhibit dorsal periaqueductal gray-elicited panic-like responses; 2) chronic, but not acute, antidepressant treatment potentiates serotonin’s panicolytic effect; 3) contextual fear activates a central nucleus of the amygdala-DRVL/VLPAG circuit implicated in mediating freezing and inhibiting panic-like escape behaviors; 4) DRVL/VLPAG serotonergic neurons are central chemoreceptors and modulate the behavioral and cardiorespiratory response to panicogenic agents such as sodium lactate and CO2. Implications of the panic inhibition system are discussed.

show abstract

Section: Introduction To Panic Disordermentioning

confidence: 99%

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

Paul

Johnson

Shekhar

et al. 2014

Neuroscience & Biobehavioral Reviews

View full text Add to dashboard Cite

show abstract

“…Alguns estudos revelaram que pacientes com TP apresentam ataques de pânico após procedimentos em que há exposição a agentes como lactato de sódio, 1 cafeína, 2 isoproterenol 3 e dióxido de carbono. 4,5 Entre os modelos experimentais de ansiedade, os testes de indução de ataques de pânico com dióxido de carbono (CO 2 ) a 35% têm algumas características de interesse especial: é um método seguro, não invasivo e utiliza uma técnica simples, provocando nos indivíduos responsivos um aumento intenso de ansiedade, semelhante aos ataques espontâneos de pânico.…”

Section: Introductionunclassified

Ataques de pânico provocados pelo dióxido de carbono: estudo clínico-fenomenológico

Valença

Nardi

Nascimento

et al. 2001

Rev. Bras. Psiquiatr.

View full text Add to dashboard Cite

Objetivos: Verificar a sensibilidade de pacientes com transtorno de pânico (TP) ao teste de indução de ataques de pânico com dióxido de carbono (CO 2 ) a 35% e analisar a intensidade, a duração e a sintomatologia dos ataques de pânico produzidos por esse agente em laboratório, comparando-os com os ataques de pânico espontâneos nesses pacientes. Métodos: Foram selecionados 31 pacientes com TP com ou sem agorafobia (DSM-IV). Após uma semana sem medicação, os pacientes realizavam duas inalações de capacidade vital: uma de mistura carbogênica (CO 2 35% e O 2 65%) e outra de ar atmosférico comprimido ("placebo"), ordenadas ao acaso e separadas por um intervalo de 20 minutos. Essas inalações eram repetidas após duas semanas. Nesse período, os pacientes não recebiam nenhuma medicação psicotrópica. Resultados: Dos pacientes, 22 (71,0%) apresentaram ataque de pânico em pelo menos um dos testes com CO 2 . Os sintomas relatados por eles com maior freqüência foram: dificuldade de respirar (n=20, 91,0%), sensação de sufocação/asfixia (n=18, 81,8%), tontura (n=18, 81,8%), estremecimento (n=14, 63,6%), palpitações (n=13, 59,0%) e medo de enlouquecer (n=12, 54,5%). Desse grupo, 11 pacientes (50,0%) consideraram os ataques de pânico experimentados no laboratório mais intensos, comparados aos ataques de pânico espontâneos, quatro (18,2%) consideraram haver a mesma intensidade entre os dois, e sete (31,8%) consideraram o ataque de pânico no laboratório mais leve. Conclusão: Pacientes com TP têm elevada sensibilidade ao CO 2 . A inalação de mistura gasosa com 35% de CO 2 produz sintomas semelhantes aos ataques de pânico espontâneos, em pacientes com TP. Esse teste pode ser considerado um bom modelo laboratorial para o TP.Ansiedade. Transtorno de pânico. Ataque de pânico. Dióxido de carbono. Objectives:To verify the sensibility of panic disorder patients to carbon dioxide challenge test and the intensity, duration and symptoms of panic attacks produced by the gas in these patients, comparing these data with those from spontaneous panic attacks. Methods: Thirty-one patients with panic disorder with or without agoraphobia (DSM-IV) were selected. After one week without receiving any medication, these patients were asked to perform two full inhalations (vital capacity): one with a carbonic mixture (35% CO 2 , 65% O 2 ) and the other with compressed atmospheric air (placebo), assigned randomly and separated by a 20-minute interval. These inhalations were repeated after 2 weeks. During this period no participants in the study received any kind of psychotropic drug. Results: Twenty-two patients (71.0%) had a panic attack in at least one of the tests where the CO 2 mixture was used. Among them (n=22), the most frequently reported symptoms were: shortness of breath (n=20, 91.0%), a feeling of suffocation or asphyxia (n=18, 81.8%), dizziness (n=18, 81.8%), trembling (n=14, 63.6%), palpitations (n=13, 59.0%), and fear of losing one's mind (n=12, 54.5%). Eleven patients (50.0%) thought the laboratoryinduced panic attacks were more intense than ...

show abstract

“…Additionally NaLac and hypertonic NaCl both increased arginine vasopressin, but hypertonic (3%) NaCl caused a greater increase. Sodium bicarbonate (Gorman et al, 1989) provoked equivalent panic-associated responses in Panic Disorder patients. Furthermore, 11 of 20 PD subjects (65%) were more likely to experience a PA in response to lactate dissolved in 0.9%NaCl versus lactate dissolved in 5%dextrose, which induced a PA in 4 of 20 PD subjects (20%) (George et al, 1995).…”

Section: Section 4 – Panic Attacks Triggers: Laboratory and Potentialmentioning

confidence: 99%

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

Johnson

Federici

Shekhar

2014

Neuroscience & Biobehavioral Reviews

View full text Add to dashboard Cite

Panic disorder (PD) is a severe anxiety disorder that is characterized by recurrent panic attacks (PA), which can be unexpected (uPA, i.e., no clear identifiable trigger) or expected (ePA). Panic typically involves an abrupt feeling of catastrophic fear or distress accompanied by physiological symptoms such as palpitations, racing heart, thermal sensations, and sweating. Recurrent uPA and ePA can also lead to agoraphobia, where subjects with PD avoid situations that were associated with PA. Here we will review recent developments in our understanding of PD, which includes discussions on: symptoms and signs associated with uPA and ePAs; Diagnosis of PD and the new DSM-V; biological etiology such as heritability and gene x environment and gene x hormonal development interactions; comparisons between laboratory and naturally occurring uPAs and ePAs; neurochemical systems that are associated with clinical PAs (e.g. gene associations; targets for triggering or treating PAs), adaptive fear and panic response concepts in the context of new NIH RDoc approach; and finally strengths and weaknesses of translational animal models of adaptive and pathological panic states.

show abstract

A Comparison of Sodium Bicarbonate and Sodium Lactate Infusion in the Induction of Panic Attacks

Cited by 59 publications

References 19 publications

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic

Ataques de pânico provocados pelo dióxido de carbono: estudo clínico-fenomenológico

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

Contact Info

Product

Resources

About