The Cardiovascular Effects of Morphine THE PERIPHERAL CAPACITANCE AND RESISTANCE VESSELS IN HUMAN SUBJECTS

Zelis, Robert; Mansour, Edward; Capone, Robert J.; Mason, Dean T.

doi:10.1172/jci107869

Cited by 142 publications

(34 citation statements)

References 42 publications

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“…This vasodilatation occurs 8-15 min after injection of morphine. However, the immediate effect of intravenous morphine on the isolated hand is a venoconstriction for 1-2 min followed by dilatation (Zelis, Mansour, Capone & Mason, 1974). Intra-arterial injection of morphine produces an immediate and large increase in forearm blood flow which is predominantly muscle flow (Samuel & Dundee, 1975) but no effect is seen in hand blood flow which is predominantly skin flow (Zelis et al 1974).…”

Section: Discussionmentioning

confidence: 99%

“…However, the immediate effect of intravenous morphine on the isolated hand is a venoconstriction for 1-2 min followed by dilatation (Zelis, Mansour, Capone & Mason, 1974). Intra-arterial injection of morphine produces an immediate and large increase in forearm blood flow which is predominantly muscle flow (Samuel & Dundee, 1975) but no effect is seen in hand blood flow which is predominantly skin flow (Zelis et al 1974). The initial vessel constriction observed by Zelis et al (1974) after the agonist morphine, may be of relevance to the rapid vasodilatation we have observed after the antagonist naloxone.…”

Section: Discussionmentioning

confidence: 99%

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Naloxone increases blood flow in the human hand.

Archer¹,

Benroubi²,

Pyke³

et al. 1985

The Journal of Physiology

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SUMMARY1. Intravenous injection of 2 mg naloxone produced a rapid and pronounced rise of blood flow (63 + 5-0 to 670 +151 ml min-1 100 ml-1) and skin temperature (28&3 + 3-0 to 32-4 + 1-2 'C) in the finger and hand of seven of ten normal volunteers. In the other three there was only a small response. Skin temperature did not change in either the face or the foot. Three responding subjects who were retested with 0 4 mg naloxone showed a smaller and briefer response.2. To exclude a local effect of naloxone on skin blood flow due to release of histamine, responders and non-responders were tested with naloxone and morphine pricked into the skin of the hand and forearm. All showed a weal and flare reaction to morphine which was not abolished by mixture with naloxone; none showed any reaction to naloxone alone.3. These results suggest that, in some subjects at least, skin blood flow in the hand may be under endogenous opioid control and they raise the possibility that opioid antagonists might have value in the treatment of disorders of skin blood flow such as Raynaud's disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Naloxone increases blood flow in the human hand.

Archer¹,

Benroubi²,

Pyke³

et al. 1985

The Journal of Physiology

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“…It decreased left ventricular ejection fraction. These workers again commented on the commonly held belief that morphine was a peripheral veno-dilator and referred to other publications of the group in which they had concluded a central sympatholytic role for morphine (Zelis et al, 1974;Mansour et al, 1970).…”

Section: Editorialmentioning

confidence: 95%

Haemodynamic Effects of Morphine

1976

Inpharma

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EDITORIALThe haemodynamic effects of morphine Morphine is often assumed to be a peripheral veno-dilator and a reduction in venous return to be the reason for its efficacy in acute pulmonary oedema. A group of allied workers investigated this hypothesis and were able to draw some definite conclusions. Vismara et al. (1976) studied the effects of venous tone in the forearms of patients with pulmonary oedema. They concluded that 'since the drug morphine sulfate (sic) does not cause a major pooling of blood in the limbs, the favourable effect of narcotics in patients with pulmonary edema (sic) must be caused by other mechanisms such as splanchnic pooling, afterload reduction or reduced breathing effort.' In the same year, Lee et al. (1976) compared the effects of morphine, meperidine and pentazocine on the haemodynamic status of patients with acute myocardial infarction. They could demonstrate no significant haemodynamic effect (including any change in pulmonary capillary wedge pressure) of either morphine or meperidine. Pentazocine, however, increased systemic and arterial pressures, left ventricular filling pressure and systemic vascular resistance. It decreased left ventricular ejection fraction. These workers again commented on the commonly held belief that morphine was a peripheral veno-dilator and referred to other publications of the group in which they had concluded a central sympatholytic role for morphine (Zelis et al., 1974;Mansour et al., 1970).There is no doubt that morphine is the analgesic of choice in severe, ischaemic chest pain (Newland, 1986). It is also extremely effective in relieving the dyspnoea associated with acute left ventricular failure and pulmonary oedema. However, the concept of a 'medical phlebotomy' has not been proven and the benefits of morphine are likely to lie more in its central sympatholytic and anxiolytic properties.

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“…24 -M The vasodilator effect of PTH in dogs is evident at doses that are too small (0.01 U/kg) to cause hypercalcemia. Chemical manipulations of the H -Asp -Arg -Val -Tyr -He -His -Pro -Phe -His -Leu -OH H -Asp -Arg -Val -Tyr -He -His -Pro -Phe -OH H -Arg -Pro -Pro -Gly -Phe -Ser -Pro -Phe -Arg -OH H -Arg -Pro -Lys -Pro -Gin -Gin -Phe -Phe -Gly -Leu -Met -NH 2 pyroGlu -Leu -Tyr -Glu -Asn -Lys -Pro -Arg -Arg -Pro -Tyr -He -Leu -OH H -A I a -G r y -C y s -L y s -A s n -P h e -P h e -T r p -L y s -T h r -P h e -T h r -S e rCys -OH pyroGln -Arg -Leu -Gly -Asn -Gin -Trp -Ala -Val -Gly -His -Leu -Met -OH pyroGlu -His -Pro -NH 2 H -Cys -Tyr -He -G|n -Asn -Cys -Pro -Leu -Gly -NH 2 H -Cys -Tyr -Phe -Gin -Asn -Cys -Pro -Arg -Gly -NH 2 VASOACTIVE PEPTlDES/Sa/rf [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] PTH molecule show that distinct and different parts of the sequence are responsible for the hypercalcemic and vasoactive properties. 25 The occurrence of basic amino acids in adjacent positions may be important to the vasodilator activity of PTH."…”

Section: Parathyroid Hormone (Pth)mentioning

confidence: 99%

Vasoactive peptides. State-of-the-art review.

Said¹

1983

Hypertension

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SUMMARY At least 16 naturally occurring peptides either constrict or dilate blood vessels. Many of these peptides are present in nerve cells and nerve terminals supplying systemic and pulmonary blood vessels and the heart. Such neuropeptides are released locally as neurotransmitters, and can influence vascular tone, local and regional blood flow, arterial blood pressure, and cardiac function. There is evidence for the participation of at least some vasoactive peptides in the regulation of these functions and in the mediation or modulation of systemic shock and arterial hypertension. The investigation of vasoactive peptides in relation to cardiovascular function and dysfunction is at a promising threshold. There is a growing conviction that these peptides participate in the regulation of many organ functions. Neuroscientists, endocrinologists, and gastroenterologists have led other groups in recognizing the likely physiological and clinical significance of these peptides, most of which are found in the brain and gut.1 " 1 Since many biologically active peptides are capable of influencing vascular smooth muscle, and thus blood flow and blood pressure, peptides with these vasoactive properties are reviewed here. Emphasis is placed on the cardiovascular effects of the more recently identified peptides, with special reference to their possible roles in the regulation of blood pressure in normal and abnormal states. Bradykinin and angiotensins, which are extensively reviewed elsewhere, are only briefly mentioned here. Biological Activity of PeptidesWhich Peptides are Vasoactive?Peptides with vasoactive properties are given in the accompanying list (see box), which is not meant to be complete. For some of these peptides (e.g., angiotensin II, bradykinin), vasoactivity is a dominant feature of their biological actions; for others (e.g., prolactin, parathyroid hormone), the pressor or vasodepressor activity has generally been overshadowed by other actions of the peptide.As will become apparent in the following para : graphs, the ability to induce either vasodilation or vasoconstriction is shared by a variety of apparently unrelated peptides. It is possible in some instances, however, t o ' recognize certain structural features among these peptides that correlate with their vasodilator or vasoconstrictor activity. Such features will be noted. AngiotensinsAngiotensin II (table 1) is one of the most potent systemic vasopressors known. Its formation from angiotensin I through the action of angiotensin-converting enzyme, the localization and properties of this enzyme, and the physiology, pathophysiology, and pharmacology of the renin-angiotensin systems in the body are topics of recent comprehensive reviews.5 "" Bombesin A 14-residue peptide (table 1) isolated from the skin of the frog Bombina bombina, bombesin has spasmogenic activity on a variety of vascular and non-vascular smooth muscle structures.12 It induces vasoconstriction and systemic hypertension in most animal species, hypotension in monkeys, but neither in humans...

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The Cardiovascular Effects of Morphine THE PERIPHERAL CAPACITANCE AND RESISTANCE VESSELS IN HUMAN SUBJECTS

Cited by 142 publications

References 42 publications

Naloxone increases blood flow in the human hand.

Naloxone increases blood flow in the human hand.

Haemodynamic Effects of Morphine

Vasoactive peptides. State-of-the-art review.

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