Circulatory and respiratory effects of infused adenosine in conscious man.

Fuller, Richard W.; Maxwell, David; Conradson, T-B; Dixon, C. M. S.; Barnes, Peter J.

doi:10.1111/j.1365-2125.1987.tb03174.x

Cited by 65 publications

(35 citation statements)

References 33 publications

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“…We and others Torsell et al, 1985) have not observed any reflex tachycardia, which could be an advantage compared with agents such as sodium nitroprusside or prostacyclin (Sollevi, 1986;Bush et al, 1988). However, some workers have reported tachycardia in supine subjects (Fuller et al, 1987;Watt et al, 1987;Conradson et al, 1987) and with higher doses (0.14 mg kg-' min-) of adenosine (Sollevi, 1986). The differences may be related to posture, dose, or differences in individual sensitivity.…”

Section: Resultsmentioning

confidence: 95%

“…Inspection of these data revealed significant changes only for Qp.eff ( Figure 2) and SVR (Figure 3) at the highest dose of adenosine. Since tachycardia has been reported during adenosine infusion (Sollevi, 1986;Fuller et al, 1987;, the heart rate data are also plotted (Figure 4) Time (min) Figure 4 Change in heart rate (HR) in beats min-'.…”

Section: Resultsmentioning

confidence: 99%

“…It has a half-life in blood of less than 1 min (Klabunde, 1983), and is broken down by adenosine deaminase, adenosine kinase or Sadenylhomocysteinase to the inactive metabolites hypoxanthine and inosine (Fox & Kelley, 1978). Infused adenosine causes tachycardia and a rise in skin temperature without any change in blood pressure in normal volunteers (Fuller et al, 1987). It is also a coronary vasodilator (Watt et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

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

Bush

Busst

Clarke

et al. 1989

Brit J Clinical Pharma

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1 The purine nucleoside adenosine relaxes smooth muscle in vitro and is a vasodilator in animals, but its effects on cardiac output and systemic vascular resistance have not been measured in normal conscious human subjects. 2 We have studied the effects of infused adenosine in doses of 0.005, 0.03 and 0.07 mg kg-l min-' on pulmonary blood flow and systemic vascular resistance in eight healthy volunteers, using a non-invasive, inert gas method and mass spectrometry.3 At a dose of 0.07 mg kg-' min-', there was a rise in effective pulmonary blood flow (which is approximately equivalent to cardiac output) of 0.52 ± 0.081 min-' m-2 (mean ± s.e. mean) and a fall in estimated systemic vascular resistance of 357 ± 44 dyn s cm-5. Despite this marked systemic vasodilation, there was no significant change in mean heart rate. 4 The effects of this dose of adenosine were maximal 2 min after starting the infusion, and had disappeared within 5 min of stopping it. 5 Adenosine may be therapeutically useful in the reduction of left ventricular afterload, where the absence of reflex tachycardia may be advantageous. We suggest that adenosine in doses of 0.03 mg kg-' min-1 should be evaluated as a selective pulmonary vasodilator.

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Section: Resultsmentioning

confidence: 95%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Bush

Busst

Clarke

et al. 1989

Brit J Clinical Pharma

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“…theophylline (Hedner et al, 1982;Eldridge et al, 1985). On the other hand, adenosine stimulates breathing in conscious, unanesthetised humans (Fuller et al, 1987;Griffith et al, 1997). The depressant effect of adenosine on breathing in vivo is more potent during the time period around birth and/or is also more severe in anesthetised animals (Herlenius et al, 2002).…”

Section: Ballanyi K Atp Channels In Brain Hypoxiamentioning

confidence: 99%

Protective role of neuronal KATP channels in brain hypoxia

Ballanyi

2004

Journal of Experimental Biology

127

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SUMMARY During severe arterial hypoxia leading to brain anoxia, most mammalian neurons undergo a massive depolarisation terminating in cell death. However,some neurons of the adult brain and most immature nervous structures tolerate extended periods of hypoxia–anoxia. An understanding of the mechanisms underlying this tolerance to oxygen depletion is pivotal for developing strategies to protect the brain from consequences of hypoxic-ischemic insults. ATP-sensitive K+ (KATP) channels are good subjects for this study as they are activated by processes associated with energy deprivation and can counteract the terminal anoxic-ischemic neuronal depolarisation. This review summarises in vitro analyses on the role of KATP channels in hypoxia–anoxia in three distinct neuronal systems of rodents. In dorsal vagal neurons, blockade of KATPchannels with sulfonylureas abolishes the hypoxic-anoxic hyperpolarisation. However, this does not affect the extreme tolerance of these neurons to oxygen depletion as evidenced by a moderate and sustained increase of intracellular Ca2+ (Cai). By contrast, a sulfonylurea-induced block of KATP channels shortens the delay of occurrence of a major Cai rise in cerebellar Purkinje neurons. In neurons of the neonatal medullary respiratory network, KATP channel blockers reverse the anoxic hyperpolarisation associated with slowing of respiratory frequency. This may constitute an adaptive mechanism for energy preservation. These studies demonstrate that KATP channels are an ubiquituous feature of mammalian neurons and may, indeed, play a protective role in brain hypoxia.

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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: 98%

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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Circulatory and respiratory effects of infused adenosine in conscious man.

Cited by 65 publications

References 33 publications

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

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

Protective role of neuronal KATP channels in brain hypoxia

Adenosine for Reversal of Hemorrhagic Shock in Rabbits

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