Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation

Hashiba, Eiji; Hirota, Kazuyoshi; Suzuki, Kazuyuki; Matsuki, Akitomo

doi:10.1034/j.1399-6576.2003.00228.x

Cited by 14 publications

(15 citation statements)

References 23 publications

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“…Propofol can inhibit g-aminobutyric acid-mediated neurotransmission and activate the vagus nerve (Wang et al, 2004). Propofol also has vagolytic effects on the airway which can produce a degree of bronchoprotection (Hashiba, Hirota, Suzuki, & Matsuki, 2003). In this study, we found that propofol can decrease serum TNF-a production after HS in SHRs.…”

Section: Discussionmentioning

confidence: 88%

Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

Lee

Subeq

et al. 2009

Biological Research For Nursing

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Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-alpha and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-alpha, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-alpha level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs.

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Section: Discussionmentioning

confidence: 88%

Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

Lee

Subeq

et al. 2009

Biological Research For Nursing

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“…It usually occurs with lead impedance testing during VNS device placement, necessitating preparation for cardiac resuscitation. Although anesthetic technique (propofol, fentanyl, droperidol, and rocuronium) was reported in only one case and deemed noncontributory [27], propofolinduced VNS bradycardia has been reported in animals [28].…”

Section: Intraoperative Complicationsmentioning

confidence: 99%

Intraoperative and perioperative complications with a vagus nerve stimulation device

Fahy

2010

Journal of Clinical Anesthesia

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“…The mechanism involves direct or vagally mediated relaxation of airway smooth muscle [136][137][138][139][140]. Barbiturates, as compared to propofol, produce weaker inhibition of airway contraction [141,142], and when used alone, may actually induce airway smooth muscle contraction [9].…”

Section: Intravenous Anestheticsmentioning

confidence: 99%

Guideline-oriented perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease

2008

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Increased airway hyperresponsiveness is a major concern in the perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease. Guidelines using evidence-based medicine are continually being updated and published regarding the diagnosis, treatment, and prevention of these respiratory disorders. Perioperative management in these patients involves: (1) adequate control of airway hyperresponsiveness, including detection of purulent sputum and infection before surgery; (2) evidence-based control of anesthesia; and (3) the aggressive use of beta-2 adrenergic stimulants and the systemic administration of steroids for the treatment of acute attacks. Good preoperative control, including the use of leukotriene antagonists, can reduce the incidence of life-threatening perioperative complications. Awareness of recent guidelines is thus important in the management of patients with airway hyperresponsiveness. This review covers the most recent guidelines for the perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease.

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Effects of propofol on bronchoconstriction and bradycardia induced by vagal nerve stimulation

Abstract: Propofol has vagolytic effects on the airway but does not worsen bradycardia produced by parasympathetic stimulation.

Cited by 14 publications

References 23 publications

Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

Propofol Protects Against Hemorrhagic Shock-Induced Organ Damage in Conscious Spontaneously Hypertensive Rats

Intraoperative and perioperative complications with a vagus nerve stimulation device

Guideline-oriented perioperative management of patients with bronchial asthma and chronic obstructive pulmonary disease

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