Morphine blocks the bradycardia associated with severe hemorrhage in the anesthetized rat

Ohnishi, Mitsuo; Kirkman, Emrys; Marshall, Hazel; Little, R. A.

doi:10.1016/s0006-8993(97)00379-x

Cited by 20 publications

(11 citation statements)

References 30 publications

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“…It would not be possible to determine whether any difference in pattern of response to blood loss was due to, or resulted from, the difference in profile of blood pressure change during hemorrhage. This investigation was therefore conducted in line with previously published work in this area using a controlled fixed-volume hemorrhage model (8,11,(27)(28)(29)(30). Our results confirm that our model reflects the sequential activation of these reflexes as illustrated by the responses observed in the sham injury group.…”

Section: Experimental Modelsupporting

confidence: 89%

Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

McMahon

Kenny

Bennett

et al. 2008

Critical Care Medicine

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Section: Experimental Modelsupporting

confidence: 89%

Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

McMahon

Kenny

Bennett

et al. 2008

Critical Care Medicine

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“…Morphine modified the cardiovascular response to haemorrhage after blast, resulting in an initial maintenance of arterial pressure and a tachycardia, with abolition of the bradycardia normally associated with haemorrhage. It has previously been shown that morphine and other m opioid receptor agonists attenuate the depressor reflex associated with severe haemorrhage (Evans et al 1989;Evans & Ludbrook, 1990, 1991Ohnishi et al 1997). Therefore, the most likely explanation is that the response to blast augmented the depressor reflex associated with severe haemorrhage, which overrode the baroreflex, leading to an early fall in blood pressure and bradycardia.…”

Section: Discussionmentioning

confidence: 99%

“…Data are mean ± S.E.M. depressor response to haemorrhage (Evans et al 1989;Evans & Ludbrook, 1990, 1991Ohnishi et al 1997). However, it is unlikely that morphine is acting within the spinal cord to block the depressor response to severe haemorrhage since it is blockade, rather than activation, of m receptors at this site that attenuates the depressor response to blood loss (Ang et al 1999).…”

Section: Figurementioning

confidence: 99%

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The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

Sawdon

Ohnishi

Watkins

et al. 2002

Experimental Physiology

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Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea mediated in part via a vagal reflex. Blast casualties may also suffer blood loss, and the response to progressive simple haemorrhage is biphasic: an initial tachycardia followed by a vagally mediated reflex bradycardia which can be attenuated by μ opioid agonists. The aims of this study were to determine the effects of thoracic blast injury on the response to subsequent haemorrhage, and the effects of morphine, administered after blast, on the response to blood loss. Male Wistar rats, terminally anaesthetised with alphadolone‐alphaxolone (19‐21 mg kg−1 h−1 I.V.), were allocated randomly to one of three groups: Group I, sham blast; Group II, thoracic blast; Group III, thoracic blast plus morphine (0.5 mg kg−1 I.V. given 5 min after blast). Blast (Groups II and III) resulted in significant (P < 0.05, ANOVA) bradycardia, hypotension and apnoea. Sham blast (Group I) had no effect. Ten minutes later, haemorrhage (40% of the estimated total blood volume (BV)) in Group I produced a biphasic response comprising a tachycardia followed by a peak bradycardia after the loss of 33% BV. Arterial blood pressure did not fall significantly until the loss of 13.3% BV. In Group II the haemorrhage‐induced tachycardia was absent and the bradycardia was augmented: peak bradycardia was seen after the loss of 23% BV. Mean arterial blood pressure (MBP) began to fall as soon as haemorrhage commenced and was significant after the loss of 10% BV. Morphine (Group III) prevented the haemorrhage‐induced bradycardia and delayed the significant fall in MBP until the loss of 30% BV. It is concluded that the response to thoracic blast injury augments the depressor response to haemorrhage while morphine attenuates this response.

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“…One such condition might be hypotensive hemorrhage. Hypotensive hemorrhage is associated with a paradoxical decrease in sympathetic tone and heart rate and could be mediated in part through CNS opioid receptors (Olson et al, 1996;Ohnishi et al, 1997). Acupuncture may be another circumstance that leads to the release of opioids in the RVL (Chao et al, 1999).…”

Section: Functional Implicationsmentioning

confidence: 99%

μ‐opioid receptors are present in functionally identified sympathoexcitatory neurons in the rat rostral ventrolateral medulla

Aicher

Schreihofer

Kraus

et al. 2001

J of Comparative Neurology

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Agonists of the mu-opioid receptor (MOR) produce profound hypotension and sympathoinhibition when microinjected into the rostral ventrolateral medulla (RVL). These effects are likely to be mediated by the inhibition of adrenergic and other presympathetic vasomotor neurons located in the RVL. The present ultrastructural studies were designed to determine whether these vasomotor neurons, or their afferents, contain MORs. RVL bulbospinal barosensitive neurons were recorded in anesthetized rats and filled individually with biotinamide by using a juxtacellular labeling method. Biotinamide was visualized by using a peroxidase method and MOR was identified by using immunogold localization of an antipeptide antibody that recognizes the cloned MOR, MOR1. The subcellular relationship of MOR1 to RVL neurons with fast- or slow-conducting spinal axons was examined by electron microscopy. Fast- and slow-conducting cells were not morphologically distinguishable. Immunogold-labeling for MOR1 was found in all RVL bulbospinal barosensitive neurons examined (9 of 9). MOR1 was present in 52% of the dendrites from both types of cells and in approximately half of these dendrites the MOR1 was at nonsynaptic plasmalemmal sites. A smaller portion of biotinamide-labeled dendrites (16%) from both types of cells were contacted by MOR1-containing axons or axon terminals. Together, these results suggest that MOR agonists can directly influence the activity of all types of RVL sympathoexcitatory neurons and that MOR agonists may also influence the activity of afferent inputs to these cells. The heterogenous distribution of MORs within individual RVL neurons indicates that the receptor is selectively targeted to specific pre- and postsynaptic sites.

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Morphine blocks the bradycardia associated with severe hemorrhage in the anesthetized rat

Cited by 20 publications

References 30 publications

Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

μ‐opioid receptors are present in functionally identified sympathoexcitatory neurons in the rat rostral ventrolateral medulla

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