Effect of Intravenous Aminophylline upon the Incremental Exercise Performance of Healthy Men

Cg, Elliott; Rm, Nietrzeba; Td, Adams; Ro, Crapo; Rl, Jensen; Fg, Yanowitz

doi:10.1159/000194781

Cited by 9 publications

(12 citation statements)

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“…In agreement with the results of Elliott et al [23], we did not find any changes in Vqj, Ve and Wmax after A infusion; but at variance with that investigation, in which during effort HR was always significantly greater and R always unchanged, we found an increase of HR and R only at maximum work load. HRmax and VC02max were previously reported to be greater af ter theophylline than after placebo in 12 COPD patients during a progressive incre mental exercise on the bicycle ergometer [19].…”

Section: Discussionsupporting

confidence: 92%

“…However, only few studies have shown significant ameliorations in the absence of bronchodilatation [18,19]. Other studies in COPD patients [22,41] and healthy sub jects [23] did not find any changes in exer cise variables or the observed modifica tions were associated with bronchodilata tion [17],…”

Section: Discussionmentioning

confidence: 98%

“…[T-Agonists [2,15,25] and A [23] are able to elicit im provement of the twitch response predom inantly in fast-contracting muscles. How ever, most previous studies showing pot entiation of the contractility of respiratory muscles have been carried out in the dog which has more fast-twitch fibers in the di aphragm than man [39,40].…”

Section: Discussionmentioning

confidence: 99%

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Failure of Aminophylline and Salbutamol to Improve Respiratory Muscle Function and Exercise Tolerance in Healthy Humans

Violante¹,

Pellegrino²,

Vinay³

et al. 1989

Respiration

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We investigated the effects of intravenously administered aminophylline (A; 6 mg/kg over 20 min, followed by 0.9 mg/kg/h), salbutamol (S; 4 µg/kg over 20 min, followed by 3 µg/kg/h) and placebo (P; saline solution) on the strength of the respiratory muscles, the ventilatory endurance and the exercise tolerance in 7 healthy humans. Neither A nor S caused bronchodilatation, as shown by the lack of change in FEV₁. The strength of respiratory muscles, as measured by maximal inspiratory pressure (MIP), and the ventilatory endurance, as measured by sustainable inspiratory pressure (SIP), were not statistically different after A (MIP: 136.5 ± SE 11.6 cm H₂O; SIP: 104.2 ± 8.4 cm H₂O or after S (MIP: 135.7 ± 11.5; SIP: 107.1 ± 10.4) compared to after P (MIP: 127.1 ± 10.1; SIP: 105.0 ± 5.9). Significant changes in 12-min walking distance, perceived exertion rate, anaerobic threshold, maximal work output, maximal O₂ uptake were observed neither after A nor after S. The exchange ratio and heart rate were higher after A and S than after P at some steps of a progressive, symptom-limited, treadmill-based exercise test. This might be the result of metabolic or cardiovascular adaptations elicited by these drugs. We conclude that A or S at therapeutic concentrations have no clinically relevant beneficial effects on ventilatory muscle function and exercise tolerance in healthy subjects.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 98%

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Failure of Aminophylline and Salbutamol to Improve Respiratory Muscle Function and Exercise Tolerance in Healthy Humans

Violante¹,

Pellegrino²,

Vinay³

et al. 1989

Respiration

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“…Conrad and Prosnitz [110] studied the cardiovascular actions of aminophylline-infusion in healthy male volunteers and found that aminophylline exerted a mild positive inotropic effect, but this action could be prevented by pretreatment with the -adrenergic receptor antagonist metoprolol or propranolol. The hemodynamic action of intravenously applied aminophylline was also studied in healthy human subjects and no significant improvement was found on cardiac performance during tread-mill exercise after using of the compound [111]. These findings are in good agreement with the further study of Conradson using theophylline and enprophylline [112].…”

Section: Solvent-treated Caffeine-treatedsupporting

confidence: 74%

Xanthine Derivatives in the Heart: Blessed or Cursed?

Szentmiklósi¹,

Cseppentö²,

Gesztelyi³

et al. 2011

CMC

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Methylxanthines, such as theophylline, have been used to treat cardiorespiratory disorders, whereas caffeine is the most widely consumed psychoactive agent in various soft drinks. Because of the worldwide use of these drugs and the recently synthesized xanthine derivatives, an intensive research on the cardiac actions of these substances is under progress. This review focuses on the molecular mechanisms involved in the actions of xanthine derivatives with special reference to their adenosine receptor antagonistic properties. The main basic and human studies on the action of xanthines on impulse initiation and conduction, as well as the electrophysiological and mechanical activity of the working myocardium will be overviewed. The potential beneficial and harmful actions of the methylxanthines will be discussed in light of the recent experimental and clinical findings. The pharmacological features and clinical observations with adenosine receptor subtype-specific xanthine antagonists are also the subject of this paper. Based on the adenosine receptor-antagonistic activity of these compounds, it can be raised that xanthine derivatives might inhibit the cardioprotective action of endogenous adenosine on various subtypes (A(1), A(2A), A(2B) and A(3)) of adenosine receptors. Adenosine is an important endogenous substance with crucial role in the regulation of cardiac function under physiological and pathological conditions (preconditioning, postconditioning, ischemia/reperfusion injury). Recent clinical studies show that acute administration of caffeine or theophylline can inhibit various types of preconditioning in human subjects. There are no human studies, however, for the cardiovascular actions of long-term administration of these drugs. Upregulation of adenosine receptors and increased effectiveness of adenosine receptor-related cardiovascular functions have been observed after long-lasting treatment with methylxanthines. In addition, there are data indicating that blood adenosine level increases after long-term caffeine administration. Since the salutary actions (and also the adverse reactions) of a number of xanthine derivatives are repeatedly shown, the main goal is the development of novel structures that mimic the actions of the conventional methylxanthines as lead compounds, but their adenosine receptor subtype-specificity is higher, their water solubility is optimal, and the unwanted reactions are minimized.

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“…The mitochondria is the main site of action for members of the apoptosis-regulating protein family exemplified by Bcl-2 family, such as Bcl-2, BNIP3, and Bad (7). Commitment to apoptosis is typically governed by opposing factions of the Bcl-2 family, including pro-apoptotic vs. antiapoptotic family members (13). Pro-apoptotic and anti-apoptotic Bcl2 family members can homodimerize or heterodimerize to each other and appear to interact with and neutralize each other, so that the relative balance of these effectors strongly influences cytochrome c release and cell fate (19).…”

mentioning

confidence: 99%

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis

Lee

Kuo

Bau

et al. 2008

Journal of Applied Physiology

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. The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis. J Appl Physiol 104: 1144-1153, 2008. First published January 17, 2008 doi:10.1152 doi:10. /japplphysiol.00152.2007 nocturnal sustained hypoxia during sleeping time has been reported in severe obesity, but no information regarding the cardiac molecular mechanism in the coexistence of nocturnal sustained hypoxia and obesity is available. This study evaluates whether the coexistence of nocturnal sustained hypoxia and obesity will increase cardiac Fas death receptor and mitochondrial-dependent apoptotic pathway. Methods: 32 lean and 32 obese 5-to 6-mo-old rats with or without nocturnal sustained hypoxia were studied and assigned to one of four subgroups: normoxia lean (NL), normoxia obese (NO), hypoxia lean (HL, 12% O2 for 8 h and 21% O2 16 h/day, 1 wk), and hypoxia obese (HO). The heart weight index, tail cuff plethysmography, echocardiography, hematoxylin-eosin staining, TUNEL assays, Western blotting, and RT-PCR were performed. Results: systolic and diastolic blood pressures in HO were higher than those in NL, and fractional shortening in HO was reduced compared with others. The whole heart weight, the left ventricular weight, the abnormal myocardial architecture, and TUNEL-positive apoptotic cells, as well as the activity of cardiac Fas-dependent and mitochondrial-dependent apoptotic pathway, were significantly increased in obese group or nocturnal sustained hypoxia group and were further increased when obesity and nocturnal sustained hypoxia coexisted, the evidence for which is based on decreases in an anti-apoptotic protein Bcl2 level and Bid and increases in Fas, FADD, pro-apoptotic Bad, BNIP3, cytosolic cytochrome c, activated caspase-8, activated caspase-9, and activated caspase-3. Conclusions: The cardiac Fas receptor-and mitochondrial-dependent apoptotic pathways were more activated in obesity with coexistent nocturnal sustained hypoxia, which may represent one possible apoptotic mechanism for the development of heart failure in obesity with nocturnal sustained hypoxia.

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Effect of Intravenous Aminophylline upon the Incremental Exercise Performance of Healthy Men

Cited by 9 publications

References 0 publications

Failure of Aminophylline and Salbutamol to Improve Respiratory Muscle Function and Exercise Tolerance in Healthy Humans

Failure of Aminophylline and Salbutamol to Improve Respiratory Muscle Function and Exercise Tolerance in Healthy Humans

Xanthine Derivatives in the Heart: Blessed or Cursed?

The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis

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