Responses to propofol in the pulmonary vascular bed of the rat

Ad, Kaye; Anwar, Muhammad; Re, Banister; Cj, Feng; K, Turner; Pj, Kadowitz; Bd, Nossaman

doi:10.1034/j.1399-6576.1999.430411.x

Cited by 10 publications

(6 citation statements)

References 21 publications

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“…In addition, propofol has been shown to have significant vasodilator activity in the pulmonary vasculature in rats. 15 These mechanisms may contribute to the development of pulmonary edema.…”

Section: Discussionmentioning

confidence: 99%

Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

Waheed¹,

Oud²

2014

WestJEM

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Propofol is frequently used in the emergency department to provide procedural sedation for patients undergoing various procedures and is considered to be safe when administered by trained personnel. Pulmonary edema after administration of propofol has rarely been reported. We report a case of a 23-year-old healthy male who developed acute cough, hemoptysis and hypoxia following administration of propofol for splinting of a foot fracture. Chest radiography showed bilateral patchy infiltrates. The patient was treated successfully with supportive care. This report emphasizes the importance of this potentially fatal propofol-associated complication and discusses possible underlying mechanisms and related literature.

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Section: Discussionmentioning

confidence: 99%

Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

Waheed¹,

Oud²

2014

WestJEM

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“…However, nitric oxide or prostacyclin do not appear to mediate this endothelium-dependent response, because inhibiting their respective synthetic pathways had no effect on propofol-induced vasodilation. 6,7 There are conflicting reports concerning the role of adenosine triphosphate-sensitive K ϩ channel activation in mediating propofol-induced pulmonary vasodilation. 6,7 Adenosine triphosphate-sensitive K ϩ channel inhibition attenuated 7 or had no effect 6 on the pulmonary vasodilator response to propofol.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Vascular Effects of Propofol at Baseline, during Elevated Vasomotor Tone, and in Response to Sympathetic α- and β-Adrenoreceptor Activation

Kondo

Kim²,

Nakayama³

et al. 2001

Anesthesiology

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“…Propofol inhibited endothelium-dependent vascular relaxation induced by acetylcholine (Ach) and sodium nitroprusside by interfering at least partly with nitric oxide function (Miyawaki et al 1995). However, nitric oxide and prostacyclin did not mediate the vasodilator activity of propofol in the isolated blood-perfused rat lung (Kaye et al 1999).…”

Section: Pulmonary Circulationmentioning

confidence: 99%

“…More recent work however showed that propofol potentiated hypoxic pulmonary vasoconstriction, an effect caused by inhibition of K + ATP-mediated pulmonary vasodilatation (Nakayama and Murray 1999). Others questioned the role of K + ATP channel activation (Kaye et al 1999).…”

Section: Pulmonary Circulationmentioning

confidence: 99%

Propofol

Vanlersberghe¹,

Camu²

Handbook of Experimental Pharmacology

125

123

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The hypnotic agent propofol has pharmacokinetic characteristics that allow for rapid onset and offset of drug effect and fast elimination from the body. Elderly patients show a greater sensitivity to the hypnotic effect of propofol. The drug is extensively metabolized in the liver through the cytochrome P450 system and glucuronidation, with potential for drug interaction. Propofol does not cause significant inotropic depression at clinically relevant concentrations. But in vitro, propofol impairs isotonic relaxation of the heart and decreases free cytosolic Ca(2+) concentrations in myocardial cells. In animal models, the cardioprotective effects of propofol derive in part from its antioxidant and free radical scavenging properties. Propofol decreases cerebral blood flow and cerebral metabolic rate dose-dependently. The neuroprotective effect of propofol in animal models is attributed to its antioxidant property, the potentiation of gamma-aminobutyric acid type A (GABA(A))-mediated inhibition of synaptic transmission, and the inhibition of glutamate release. Subhypnotic doses of propofol induce sedative, amnestic, and anxiolytic effects in a dose-dependent fashion. Propofol impairs ventilation with a considerable effect on the control of ventilation and central chemoreceptor sensitivity. Propofol reduces the ventilatory response to hypercapnia and the ventilatory adaptation to hypoxia, even at subanesthetic doses. The drug potentiates hypoxic pulmonary vasoconstriction, an effect caused by inhibition of K(+) (ATP)-mediated pulmonary vasodilatation. Most of the pharmacological actions of propofol result from interaction with the GABA(A) receptor or with calcium channels. Propofol prolongs inhibitory postsynaptic currents mediated by GABA(A) receptors, indicating that its effects are associated with enhanced inhibitory synaptic transmission, but propofol also influences presynaptic mechanisms of GABAergic transmission. Propofol modulates various aspects of the host's inflammatory response. It decreases secretion of proinflammatory cytokines, alters the expression of nitric oxide, impairs monocyte and neutrophil functions, and has potent, dose-dependent radical scavenging activity similar to the endogenous antioxidant vitamin E.

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Responses to propofol in the pulmonary vascular bed of the rat

Abstract: Propofol has significant vasodilator activity in the pulmonary vascular bed of the rat but responses to propofol are not mediated or modulated by the release of nitric oxide, opening of K + ATP channels, or the release of vasodilator cyclooxygenase products.

Cited by 10 publications

References 21 publications

Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

Pulmonary Vascular Effects of Propofol at Baseline, during Elevated Vasomotor Tone, and in Response to Sympathetic α- and β-Adrenoreceptor Activation

Propofol

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