Pancuronium Bromide: An Indirect Sympathomimetic Agent

Domènech, Josep Mestres i; Garcia, Rita; Sasiain, J. M. Rodriguez; Loyola, A. Quintana; Oroz, José

doi:10.1093/bja/48.12.1143

Cited by 86 publications

(19 citation statements)

References 10 publications

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“…d-Tubocurarine is known to cause histamine release and sympathetic ganglion blockade (4). As opposed to these effects, pancuronium has been shown to induce adrenergic transmitter release from the postganglionic nerve endings (2). Furthermore, at least under thiamyal anesthe-sia, pancuronium induces a significant rise in free epinephrine concentration (17).…”

Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow and Metabolism following Pancuronium Bromide in Newborn Lambs

Belik

Delivoria‐Papadopoulos

1984

Pediatr Res

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ABSTRACT. The purpose of this study was to evaluate ture of newborn animal models has not been studied, it has been cerebral blood flow and metabolism following pancuronium shown in adult rats that there is an increase in cerebral blood bromide paralysis in healthy newborn lambs. Cerebral flow and cerebral oxygen consumption following paralysis (1). blood flow and cerebral metabolic rate for O2 and glucose The purpose of this study, therefore, was to evaluate the cerebral were measured along with blood pressure and blood gases blood flow and metabolism following pancuronium bromide before and again at 15 and 60 min following pancuronium paralysis in healthy newborn lambs. paralysis in seven newborn lambs. Pancuronium bromide paralysis had no effect on any of these parameters either at 15 or 60 min of paralysis. Total cerebral blood flow, MATERIALS AND METHODScerebral metabolic rate for 0 2 , and cerebral metabolic rate for glucose were 87 2 6 ml/min/100 g, 258 + 10 pmolOz/ min/100 g, and 53 f 10 mmol glucose/min/lOO g, respectively. Neither was any change in regional cerebral blood flow noted. In spite of being connected immediately to the ventilator, however, some animals experienced a transient Neuromuscular blocking agents are used in infants in neonatal intensive care units to induce respiratory muscle paralysis. Among the nondepolarizing muscle relaxants, pancuronium bromide is the most commonly used agent, based on fewer side effects following its administration. A recent study, however, in preterm infants reported an increase in cerebral blood velocity measured by Doppler technique following paralysis with curare or pancuronium bromide (Pavulotl) (9). Inasmuch as derangement of cerebral blood flow appears to be linked to the pathogenesis of intracranial hemorrhage encountered in the human premature brain (8), there is reason to postulate a relationship between cerebral blood flow changes following the use of skeletal muscle relaxants and intracranial hemorrhage in neonates.While the effect of muscle relaxants upon the cerebrovascula- Animal preparation. Studies were performed on newborn lambs less than 1 wk of age. Two to 3 days prior to the experiment, ketamine HCl, 10 mg/kg, was administered intramuscularly and additional 10-mg doses were given as necessary during the surgical procedure. Following subcutaneous infiltration with lidocaine HCl (I%), polyvinyl catheters (No. 5 French) were placed into the inferior vena cava for the administration of fluid and drugs, into the left brachial and femoral arteries for monitoring blood pressure and withdrawal of reference blood samples, and directly into the left cardiac ventricle through the femoral artery for injection of microspheres. Sagittal sinuses were chronicall; catheterized with a 2Sgauge stahless steel cannula with an over-the-needle Teflon catheter.Experimental protocol. On the day of the study, the animals were fed as usual. The larynx was visualized with the aid of a laryngdscope and an endotracheal tube was advanced and secured with tape to the mo...

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Section: Discussionmentioning

confidence: 99%

Cerebral Blood Flow and Metabolism following Pancuronium Bromide in Newborn Lambs

Belik

Delivoria‐Papadopoulos

1984

Pediatr Res

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“…The latter study and the present investigation also demonstrated that pancuronium alone, at concentrations up to 5 x 10-M, elicited no contractile activity in the vas, a preparation which responds to indirect sympathomimetic amines. Thus the noradrenaline-releasing effect of pancuronium, seen in the dog in vivo by Domenech et al (1976) was not evident in the rat tissues studied in vitro.…”

Section: Interactions Between Pancuronium and Cocainementioning

confidence: 78%

“…It is possible that pancuronium does exhibit weakly some properties of 17 fl-oestradiol because this would explain the depression of the response of the vas to St 91 seen after pancuronium and the depression of the response to NA seen on administration of pancuronium after cocaine (see Figures lb and 2a). The NA supersensitivity of vascular smooth muscle caused by pancuronium is probably of greater significance to the anaesthetist than the extensively studied effects on the heart (Saxena & Bonta, 1970;Ivankovich et al, 1975;Domenech et al, 1976). Fuzzey & Edwards (1971) examined the effect of pancuronium on heart rate, arterial blood pressure and calf muscle blood flow in anaesthetized patients with peripheral vascular disease.…”

Section: Interactions Between Pancuronium and Cocainementioning

confidence: 99%

“…This effect has been variously ascribed to blockade of muscarinic receptors leading to a reduction in vagal tone (Saxena & Bonta, 1970), blockade of neuronal uptake of noradrenaline (NA) (Ivankovich, Miletich, Albrecht & Zahed, 1975) and an indirect sympathomimetic effect (Domenech, Garcia, Sasiain, Loyola & Oroz, 1976). This study was designed to examine the second two postulates by investigating the action of pancuronium bromide on noradrenergically innervated tissues in vitro.…”

Section: Introductionmentioning

confidence: 99%

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On the Mechanism of Pancuronium‐induced Super‐sensitivityto Noradrenaline in Rat Smooth Muscle

Tomlinson

1979

British J Pharmacology

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Pancuronium bromide (5 × 10−5m) caused super‐sensitivityto noradrenaline in the rat isolated vas deferens and hepatic portal vein. This super‐sensitivitywas manifest as a parallel leftward shift of the dose‐response curve for noradrenaline with no alteration of the maximum response to the agonist. Pancuronium did not potentiate the response of the vas and portal vein to St 91, anα‐adrenocep‐tor agonist which is not a substrate for Uptake x. Pancuronium did not potentiate the response of the vas to CaCl2. In vasa deferentia made supersensitive to noradrenaline by treatment with cocaine (1 × 10−5m) pancuronium induced no further potentiation of the response to noradrenaline. However, the super‐sensitivityto noradrenaline induced by pancuronium alone was augmented by the addition of cocaine. Histofluorescence studies showed that pancuronium inhibited neuronal uptake of α‐methyl noradrenaline in various noradrenergically‐innervated tissues from reserpine‐treated rats. This study, with support from the literature, suggests that pancuronium induces noradrenaline super‐sensitivityby blockade of Uptake!.

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“…Recent evidence suggests that potentiation of the cardiac sympathetic component might also be involved (Ivankovitch, Militech, Albrecht & Zahed, 1975;Domenech, Garcia, Sasiain, Loyola & Oroz, 1976;Docherty & McGrath, 1977;1978). If so, this might provide a more satisfactory explanation than has, so far, been available for the clinical observations since vagal inhibition, alone, should not produce any considerable tachycardia without the presence of a sympathetic component and since tachycardia to pancuronium can still occur after atropine (Stoelting, 1972).…”

Section: Introductionmentioning

confidence: 99%

A Comparison of the Effects of Pancuronium Bromide and Its Monoquaternary Analogue, Org Nc 45, on Autonomic and Somatic Neurotransmission in the Rat

Docherty

McGrath

1980

British J Pharmacology

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IPotentiation by pancuronium of the effects of adrenergic nerve stimulation. previously shown in cardiovascular tissues, was also found in rat anococcygeus and vas deferens, in vitro or in vivo. 2 In the pithed rat, in the presence of pancuronium, pre-junctional ax-adrenoceptor-mediated feedback inhibition of cardiac sympathetic transmission was uncovered at relatively low stimulation frequencies by phentolamine or yohimbine. 3 The effects of pancuronium and its mono-quaternary analogue Org NC 45 on autonomic and somatic neuromuscular transmission were compared, in the pithed rat. Org NC 45 was less potent than pancuronium at blocking somatic neuromuscular transmission by a factor of 2.1, at blocking cardiac, parasympathetic transmission by a factor of 538 and at potentiating sympathetic transmission by a factor of 33.

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Pancuronium Bromide: An Indirect Sympathomimetic Agent

Cited by 86 publications

References 10 publications

Cerebral Blood Flow and Metabolism following Pancuronium Bromide in Newborn Lambs

Cerebral Blood Flow and Metabolism following Pancuronium Bromide in Newborn Lambs

On the Mechanism of Pancuronium‐induced Super‐sensitivityto Noradrenaline in Rat Smooth Muscle

A Comparison of the Effects of Pancuronium Bromide and Its Monoquaternary Analogue, Org Nc 45, on Autonomic and Somatic Neurotransmission in the Rat

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