Effect of infused adenosine on cardiac output and systemic resistance in normal subjects.

Bush, Andrew; Busst, C M; Clarke, B. F.; Barnes, Peter J.

doi:10.1111/j.1365-2125.1989.tb05347.x

Cited by 41 publications

(13 citation statements)

References 21 publications

(32 reference statements)

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“…Dose-dependent decreases in SVR and increases in cardiac output have been observed in conscious subjects (Bush et al, 1989), but reflexlymediated increases in heart rate occur, and at higher doses, subjective symptoms such as nausea and pain, may limit the clinical utility of adenosine (Edlund et al, 1989). Clinical evaluations of AMP have not been reported.…”

Section: Resultsmentioning

confidence: 99%

Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Finegan

Clanachan

1991

British J Pharmacology

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1The haemodynamic effects of adenosine 5'-monophosphate (AMP) and sodium nitroprusside (SNP) were compared in anaesthetized dogs following the induction of acute left ventricular (LV) dysfunction. 2 LV dysfunction was induced by the intracoronary administration of glass microbeads until left ventricular end diastolic pressure (LVEDP) was increased from 5 to 15 mmHg. This was associated with a decrease in LV dP/dt and cardiac index (CI) of 30% and 27%, respectively, and an increase in systemic vascular resistance index (SVRI) of 37%. 3 Graded doses of AMP (100 to lOOOgkg-1 min-1) or SNP (ito 10ugkg-1 min-1) reduced SVRI and increased CI in a dose-related manner. Heart rate was not altered by either agent. At doses that caused similar reductions in SVRI, CI was increased more by AMP than by SNP. 4 The mechanisms responsible for the greater elevation of CI by AMP relative to SNP may be related to its more selective arterial vasodilator activity. SNP reduced cardiac preload that limited the expected increase in CI. 5 The haemodynamic profile of AMP suggests that it may be useful in the pharmacological management of acute cardiac failure, either when used alone or in combination with positive inotropic agents and/or selective venodilators.

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Section: Resultsmentioning

confidence: 99%

Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Finegan

Clanachan

1991

British J Pharmacology

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“…Current pharmacological data do not support the involvement of A 2 receptors in anxiety [277], or either receptor isoform in psychosis, but blockade of adenosine clearance produced antipsychotic effects in rats [278]. Adenosine agonists cannot be used as treatments, as they reduce cardiac output [170]. This effect was not observed when CBD was administered to either humans or animals; therefore, it is likely that CBD causes an indirect elevation of adenosine release as opposed to receptor activation.…”

Section: Cbd Receptor Targets In Psychosismentioning

confidence: 98%

“…Ttype VGCC α1G (CACNA1G) subunit expression is significantly increased in Purkinje cells in rodent models of ataxia, which results in the abnormal regulation of motor function [168]. Numerous studies on rodent models have also shown that palatal, Parkinsonian, and essential tremors are all dependent on T-type VGCC conductance [169,170]. Tremors were abolished upon channel blockade by zonisamide, a selective T-type VGCC antagonist [171].…”

Section: Cbd Ion Channel Targets In Movement Disordersmentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

447

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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“…In contrast to these observations, it has been found that adenosine increases contractility of the isolated rabbit heart (33) and ventricular preparations from the guinea pig heart (32). Adenosine infusion was also found to increase the cardiac output in normal subjects and in patients with coronary disease (25,26,34). On the other hand, it has been shown that adenosine produced no inotropic effect in isolated guinea pig ventricles (35).…”

Section: Statistical Analyses Of Resultsmentioning

confidence: 97%

“…It was found to dilate the isolated coronary arteries of various species (19)(20)(21) and to increase the coronary blood flow several fold (22). A number of studies have also shown that the continuous intravenous infusion of adenosine markedly reduced the systemic vascular resistance and mean arterial blood pressure in experimental animals (23,24) and in humans (25,26). Furthermore, adenosine has been shown to cause vasodilatation in canine (27), porcine (28), bovine (20) and human (29) isolated vascular smooth muscle strips.…”

Section: Statistical Analyses Of Resultsmentioning

confidence: 99%

Adenosine for Reversal of Hemorrhagic Shock in Rabbits

Abdel-Zaher

Abdel-Aal

Aly

et al. 1996

Japanese Journal of Pharmacology

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ABSTRACT-The potential use of adenosine in the treatment of hemorrhagic shock was evaluated in rabbits. Hemorrhagic shock was induced by bleeding the animals to a mean arterial blood pressure of 30-35 mmHg that was maintained for 2 hr. The intravenous infusion of 300 pg/kg/min adenosine for 1 hr, after reinfusion of the shed blood, was found to be capable of increasing the survival rate of rabbits subjected to hemorrhagic shock. In shocked rabbits, adenosine profoundly improved the postreinfusion depressed contractility of the heart, but it produced a decrease in the mean arterial blood pressure and heart rate. In the same animals, the plasma concentrations of glucose, lactate and inorganic phosphate, which were markedly elevated during shock, were returned back toward normal levels by the intravenous infusion of adenosine. Similarly the alteration that occurred in the plasma sodium, potassium and calcium levels during shock was corrected by adenosine. It is consequently concluded that the use of adenosine after shock improves tissue perfusion and enhances the functional recovery of cells by restoring their metabolic machinery and thereby improves the survival rate.

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Effect of infused adenosine on cardiac output and systemic resistance in normal subjects.

Cited by 41 publications

References 21 publications

Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Comparison of the haemodynamic effects of adenosine monophosphate with sodium nitroprusside in a canine model of acute global left ventricular dysfunction

Molecular Targets of Cannabidiol in Neurological Disorders

Adenosine for Reversal of Hemorrhagic Shock in Rabbits

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