Effect of aminophylline on regional perfusion distribution in the lungs.

Isawa, Toyoharu; Teshima, Takeo; Hirano, Tomio; Shiraishi, Kimio; Matsuda, Takashi; Konno, Kiyoshi

doi:10.1620/tjem.128.345

Cited by 4 publications

(5 citation statements)

References 11 publications

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“…Judging from the fact that isoproterenol can reverse the hypoxia-induced regional pulmonary vasoconstriction, stimulation of the fl-adrenergic system can modify the pulmonary vascular response to alveolar hypoxia. Once the fl-adrenergic system is blocked, stimulation of the f3-adrenergic system by isoproterenol is no longer feasible, and pulmonary vascular responses to the regional 02 tensions occur as expected from the previous reports (Isawa et al 1978b(Isawa et al , 1979(Isawa et al , 1980. Porcelli and Bergofsky (1973) reported that enhanced pulmonary pressor responses to hypoxia occurred during fl-blockade, and they attributed this enhancement to the unmasking of additional but previously antagonized a-receptors.…”

Section: Effect Of Propranolol Per Sesupporting

confidence: 54%

“…We also have indicated that the pulmonary vascular response is primarily regulated by regional alveolar oxygen tensions (Isawa et al 1978a(Isawa et al , 1979(Isawa et al , 1980, but stimulation of j3-adrenergic receptor by isoproterenol was found to modify the regional pulmonary vascular response to hypoxia in this study. Judging from the fact that no significant changes occurred in the rest of the lungs which breathed air spontaneously, /3-stimulation could reverse only the hypoxia induced regional pulmonary vasoconstriction.…”

Section: Effect Of Propranolol Per Sementioning

confidence: 41%

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Effect of isoproterenol on regional pulmonary perfusion and its blockade by propranolol.

Isawa

Teshima

Hirano

et al. 1981

Tohoku J. Exp. Med.

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Section: Effect Of Propranolol Per Sesupporting

confidence: 54%

Section: Effect Of Propranolol Per Sementioning

confidence: 41%

Effect of isoproterenol on regional pulmonary perfusion and its blockade by propranolol.

Isawa

Teshima

Hirano

et al. 1981

Tohoku J. Exp. Med.

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“…GRANT et al (1976) demonstrated in coatimundi that the Q increased in hyperoxia, but no change occurred in VA, resulting in a reduction of the VA/ ratio. IsAWA et al (1978) also reported that the Q measured in dog increased in hyperoxia, suggesting an occurrence of the hyperoxic recruitment and/or the regional vasodilatation. In our laboratory, Shibuya et al (in submission) showed that the Q increased in 7O° hyperoxia, but not in 40°c hyperoxia in man.…”

Section: Discussionmentioning

confidence: 87%

Evaluation of uneven distribution of VA/Q ratio from data on exchange of respiratory gases.

et al. 1986

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A new approach has been developed for evaluating uneven distribution of ventilation/perfusion ratio, VA/Q, based on a twocompartment model with a reciprocal VA/Q relation. The VA/Q ratios were expressed by j • (1-p)/ p and µ • p/(1-p), where p and p were referred to as the "ideal" VA/Q ratio and unevenness factor, respectively. During steady state breathing, arterial blood was analyzed for Pot and P02, and end-tidal Pco2 as well as the gas exchange ratio, R, was measured. After steady state breathing a rebreathing experiment was performed, and the arterial-venous 02 content difference, (a-v)Co2, was measured, and then, multiplying it by R, the venous-arterial C02 content difference, (v-a) Cco2, was obtained. Referring to these values the mixed venous Pot and Pco2 were estimated from arterial Pot and Pco2, using the 02 and C02 dissociation curves. The VA/Q line and iso-R line were drawn to find p, and further, total arterial, and alveolar Pot and Pco2 of the twocompartment model were computed by changing both p and the mixing weight factor, cIi. The 1i value was determined so as to make the above Pot" P02-locus pass through the measured arterial Pot and Pco2. The p value was selected so that the computed alveolar Pco2 fitted to the end-tidal one. The experiments were performed on 8 normal subjects in normoxia and hyperoxia with PIo2 245 Torr. The mean .P values in normoxia and hyperoxia were 0.50 and 0.56, respectively. The mean p values in normoxia and hyperoxia were 0.438 and 0.428, respectively. The VA/Q ratio was decreased in hyperoxia because of a decrease in VA value.Key words : VA/Q unevenness, two-compartment model, 02-C02 gram, normoxia and hyperoxia. dia- WAGNER et al. (1974) elaborated a method for computing the distribution of VA/Q ratio in the lung by using a number of inert gases. However, for clarifying the Pot and Pco 2 distributions in physiological and pathological conditions, it is

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“…One concern with all drugs given to pa tients with hypoxic chronic obstructive pul monary' disease, which have a potential ino tropic or vasodilator action, is that they may produce further ventilation/perfusion mis matching and worsen arterial blood gas values [ 14], Such an effect has been variably demon strated with calcium channel blockers, hydral azine and P-adrenergic agonists [26][27][28], Ibo pamine even in these patients with severe air flow limitation and type II respiratory failure did not worsen hypoxaemia, as measured continuously by ear-oximetry, or intermit tently throughout the study in arterial blood.…”

Section: Discussionmentioning

confidence: 99%

“…Digoxin is not recommended [13] and even drugs which have both vasodilator and ino tropic properties may potentially worsen gas exchange in patients with severe chronic ob structive pulmonary disease, by worsening ventilation/perfusion mismatching [14], Ibopamine. an ester of dopamine, when given by mouth, has been shown to improve cardiac performance in patients with congestive heart failure secondary to ischaemic heart disease or idiopathic congestive cardiomvopathv [ 15,16].…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic Effects of Ibopamine on the Pulmonary Circulation and Right Ventricular Performance in Patients with Chronic Obstructive Pulmonary Disease

1992

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We have studied the effects of ibopamine, an oral dopamine derivative, on pulmonary hemodynamics and blood gas values when given as a single oral dose (100 mg) to patients with severe hypoxic chronic obstructive pulmonary disease. A small but significant increase in mean pulmonary arterial pressure from 29 ± 8 to 32 ± 7 mm Hg (p < 0.01) was noted 30min after ibopamine was given associated with a small increase in cardiac index. No other consistent hemodynamic changes were observed, and no alteration in blood gas values or oxygen saturation occurred. These results do not indicate a role for ibopamine in the treatment of patients with hypoxic chronic obstructive pulmonary disease and pulmonary hypertension, but, in addition, do not indicate any major deleterious effects of ibopamine on pulmonary hemodynamics or blood gas values in such patients.

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Effect of aminophylline on regional perfusion distribution in the lungs.

Cited by 4 publications

References 11 publications

Effect of isoproterenol on regional pulmonary perfusion and its blockade by propranolol.

Effect of isoproterenol on regional pulmonary perfusion and its blockade by propranolol.

Evaluation of uneven distribution of VA/Q ratio from data on exchange of respiratory gases.

Hemodynamic Effects of Ibopamine on the Pulmonary Circulation and Right Ventricular Performance in Patients with Chronic Obstructive Pulmonary Disease

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