Morphine-Induced Redistribution of Cardiac Output in the Unanesthetized Monkey

Miller, Robert; Rp, Forsyth; Kl, Melmon

doi:10.1159/000136283

Cited by 16 publications

(13 citation statements)

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“…enkephalins elicit a pressure response in conscious, but a decrease in blood pressure in anaesthetized animals (see Lang et al, 1982). It has also been shown that morphine can cause an increase in cerebral blood flow in conscious animals (Miller et al, 1972;Koskinen & Bill, 1983) whereas under anaesthesia a decrease was seen (Takeshita et al, 1972;Buchweitz et al, 1984). The effects of various pharmacological agents on the single unit activity in the CNS is also affected by the consciousness of the animal (Trulson, 1984).…”

Section: Discussionmentioning

confidence: 99%

Effect of low intravenous doses of TRH, acid‐TRH and cyclo(His‐Pro) on cerebral and peripheral blood flows

Koskinen

1986

British J Pharmacology

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Local cerebral and peripheral blood flow in conscious and anaesthetized rabbits were investigated with the microsphere method, before and after the i.v. administration of 25 or 50 gpg kg'-thyrotropinreleasing hormone (TRH). Before the experiment, the cervical sympathetic chain was sectioned on one side in order to evaluate the possible effect of the sympathetic nerves on cranial and extracranial blood flows. 2 Blood flow was also determined in anaesthetized rabbits before and after the administration of the TRH metabolites cyclo(His-Pro) and acid-TRH and after subsequent administration of 50 pg kg-' TRH. 3 TRH caused an increase in mean arterial blood pressure (MAP) of about I to 2 kPa whereas cyclo(His-Pro) and acid-TRH had no effect on MAP.4 In the anaesthetized animal an increase in total cerebral blood flow (CBFtO), from 71 ± 7 to 107 ± 12 g min'-100g-1 (P < 0.05) was observed on the sympathetic intact side after 25 fig kg'-TRH and a further increase to 130 ± 9 g min' 100gI (P < 0.01) after 50 Ag kg-' TRH. A similar effect was observed on the sympathotomized side.5 An effect on CBF in the conscious animal was not detected. The control CBFO. (104 ± 8 g min' 100g-') was higher in these animals than in the anaesthetized animals (P <0.02).6 Neither cyclo(His-Pro) nor acid-TRH mimicked the effect of TRH on CBF. 7 In several peripheral tissues, e.g. skin, pancreas and gastric mucosa, a reduction in blood flow was noted after the administration of TRH in both anaesthetized and conscious rabbits.8 It was concluded that TRH can induce cerebral vasodilatation in animals with a depressed CBF, whereas the vasoconstrictor effect of TRH in peripheral organs is not markedly affected by the state of consciousness.

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Section: Discussionmentioning

confidence: 99%

Effect of low intravenous doses of TRH, acid‐TRH and cyclo(His‐Pro) on cerebral and peripheral blood flows

Koskinen

1986

British J Pharmacology

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“…Aspirin and aspirin-like nonsteroid antiinflammatory drugs (NSAID) still belong to the most widely distributed and most frequently used drugs [1]. However, even today, in spite of tremendeous research efforts their mode(s) of action in inflammation remains abscure or at least controversial [2].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

Brune¹,

Gräf²,

Glatt³

1976

Agents and Actions

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A variety of acidic and non-acidic compounds are potent inhibitors of prostaglandin (PG) synthesis in vitro. However, only a few, namely the acidic nonsteroid anti-inflammatory drugs (NSAID) are useful anti-inflammatory analgesics in the clinic. Since inhibition of PG-synthesis is believed to be the main target of NSAID in inflammation this superiority of acidic compounds remains unexplained. We have considered that one explanation could be that only acidic NSAID appear in high concentrations in inflamed tissue to inhibit PG-synthesis sufficiently. To test this hypothesis the following experiments were carried out: (A) PG-synthesis and its inhibition by acidic and non-acidic NSAID was measured in vivo at the site of inflammation. It was found that in therapeutic doses only acidic NSAID were capable to reduce PG-synthesis significantly. (B) Measurement of drug concentration in inflamed tissue showed that only acidic NSAID were found in significantly higher concentrations in inflamed than in control tissue. From these observations it is concluded that a specific pharmacokinetic behaviour of acidic NSAID leading to high concentrations in inflamed tissue is a decisive aspect of their anti-inflammatory action.

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“…Despite its prevalent use, the effects of morphine on the heart and coronary vessels are poorly understood. Morphine is thought to have little effect on systemic hemodynamics (1,3,4), although both a transient decrease (5), or no change (1,3,4) in systemic vascular resistance as well as reduced (6)(7)(8) and enhanced (9) myocardial contractility have been observed. Despite its frequent use in patients with myocardial ischemia, little is known about the effects of morphine on the coronary vascular bed.…”

Section: Introductionmentioning

confidence: 99%

“…Despite its frequent use in patients with myocardial ischemia, little is known about the effects of morphine on the coronary vascular bed. Earlier studies concluded that it had little effect (8) or that it dilated the coronary bed (3,(10)(11)(12)(13). However, only one of these studies was conducted in the intact animal (3), and none measured coronary blood flow continuously or took into account changes in cardiac 1 Abbreviations used in this paper: dP/dt, rate of change of pressure; LV, left ventricular; MS, morphine sulfate.…”

Section: Introductionmentioning

confidence: 99%

Effects of morphine on coronary and left ventricular dynamics in conscious dogs.

Vatner¹,

Marsh²,

Swain³

1975

J. Clin. Invest.

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A B S T R A C T We studied the effects of i.v. 2 mg/kg morphine sulfate (MS) on coronary blood flow and resistance, left ventricular (LV) diameter and pressure (P), rate of change of pressure (dP/dt), and dP/dt/P in conscious dogs. An initial transient reduction in coronary vascular resistance, associated with increases in heart rate, dP/dt, dP/dt/P, and reductions in LV enddiastolic and end-systolic size were observed. This was followed by a prolonged increase in mean coronary vascular resistance, lasting from 5 to 30 min, while heart rate, arterial pressure, and LV end-diastolic diameter returned to control levels and dP/dt/P remained slightly but significantly above control. At 10 min, late diastolic coronary flow had fallen from 44+3 ml/min to a minimum level of 25±3 ml/min, while late diastolic coronary resistance had risen from 1.68±0.10 to 3.04±0.28 mm Hg/ml/min. Morphine also induced substantial coronary vasoconstriction when heart rate was held constant. Neither the MS-induced coronary vasoconstriction nor the positive inotropic response was abolished by bilateral adrenalectomy. The positive inotropic response of MS was reversed after beta blockade, but not the coronary vasoconstriction. Alpha receptor blockade abolished the late coronary vasoconstrictor effects of morphine, and only dilatation occurred. In anesthetized dogs MS failed to produce late coronary vasoconstriction. Coronary vasoconstriction was not observed in conscious dogs after a respiratory-depressant dose of morphine, 10 mg/kg i.v. Smaller doses of MS, 0.25 mg/kg every 15 min, produced significant coronary vasoconstriction after a total dose of 0.75 mg/kg in the conscious dogs.

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Morphine-Induced Redistribution of Cardiac Output in the Unanesthetized Monkey

Cited by 16 publications

References 0 publications

Effect of low intravenous doses of TRH, acid‐TRH and cyclo(His‐Pro) on cerebral and peripheral blood flows

Effect of low intravenous doses of TRH, acid‐TRH and cyclo(His‐Pro) on cerebral and peripheral blood flows

Inhibition of prostaglandin synthesis in vivo by nonsteroid anti-inflammatory drugs: Evidence for the importance of pharmacokinetics

Effects of morphine on coronary and left ventricular dynamics in conscious dogs.

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