Responses of the Bronchial Veins in a Heart-Lung-Bronchial Preparation

Aramendı́a, Pedro F.; Letona, J Martínez López de; Aviado, Domingo M.

doi:10.1161/01.res.10.1.3

Cited by 31 publications

(16 citation statements)

References 7 publications

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“…However, the present data do not agree with the results obtained by Martinez et al (1961) and Aramendia et al (1962), who reported that histamine caused dilatation and 5-HT caused a biphasic effect in the bronchial artery of the dog in vivo.…”

Section: Discussioncontrasting

confidence: 99%

“…Some actions of many of these mediators on various bovine blood vessels, including the pulmonary vasculature, have been described previously (Eyre, 1971;Burka & Eyre, 1974a;1977;Holroyde & Eyre, 1975 Aviado, 1962). It appears from the literature, that a bronchial vessel has never previously been studied in vitro, probably because the vessel, being very small, is difficult or impossible to obtain from the usual laboratory animal species.…”

Section: Introductionmentioning

confidence: 77%

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Preliminary Pharmacological Characterization of the Bovine Isolated Bronchial Artery Strip: A New Preparation

Arowolo

Eyre

1980

British J Pharmacology

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1This paper describes a preliminary pharmacological study of the isolated helical strip of bovine bronchial artery under isotonic conditions in Krebs-Henseleit solution. 2 The tissue contracted to histamine and 5-hydroxytryptamine (5-HT), actions which were selectively antagonized by mepyramine and methysergide respectively. Histamine was not inhibited by metiamide and 5-HT was not affected by morphine.3 Slow reacting substance of anaphylaxis (SRS-A), prostaglandin F2. (PGF2X) and PGE2 were spasmogenic, whereas PGE1 caused relaxation. No potential antagonists of these agents were tested. 4 Carbachol, at all concentrations, caused contractions of the bronchial artery which were completely, irreversibly blocked by atropine. 5 The spasmogenic action of phenylephrine was selectively blocked by dibenamine. Vessel strips which were partially contracted to histamine, relaxed to isoprenaline and salbutamol. The action of isoprenaline was inhibited similarly by either propranolol or practolol. The evidence therefore suggests the presence of functional a, I, and #2-adrenoceptors.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 77%

Preliminary Pharmacological Characterization of the Bovine Isolated Bronchial Artery Strip: A New Preparation

Arowolo

Eyre

1980

British J Pharmacology

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“…The major hemodynamic and neural determinants of bronchopulmonary flow have been studied by several groups over the past four decades. The majority of investigators (3)(4)(5)(6)(7)(8)(9) have found that systemic arterial pressure, independent of cardiac output, is one of the principal factors determining bronchopulmonary shunt flow. Although the exact anatomic location of the connections between the bronchial and pulmonary circulations is a subject of some controversy (10, 1 1), all agree that the pulmonary arterial and venous pressures, reflecting the "outflow pressure" ofthe bronchopulmonary anastomoses, are also principal determinants.…”

Section: Introductionmentioning

confidence: 99%

Acute alveolar hypoxia increases bronchopulmonary shunt flow in the dog.

Warren¹,

Powell²

1986

J. Clin. Invest.

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To study the effects of alveolar hypoxia on canine bronchopulmonary shunt flow, a biventricular bypass preparation was employed. The preparation allowed a constant and sensitive measure of changes in pulmonary venous blood flow. In 16 of 18 dogs with intact bronchial arteries, alveolar hypoxia caused an increase in pulmonary venous return both under conditions of constant pulmonary arterial inflow and under conditions of no pulmonary arterial inflow, suggesting bronchopulmonary shunting. This effect was accompanied by systemic vasodilation despite vagotomy and ganglionic blockade, and was abolished by division of all bronchial vessels. Ibuprofen, 3 mg/kg, and indomethacin, 15 mg/kg, in dogs with intact bronchial vessels, abolished both the increase in pulmonary venous return and the systemic vasodilatation caused by hypoxia. Thus, alveolar hypoxia directly augments bronchopulmonary flow, most likely through release of one or more vasodilating prostaglandins.

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“…Changes of flow in the diminutive precapillary anastomoses between the bronchial and the pulmonary vascular network are most unlikely to cause the initial rise of pressure in the pulmonary artery. Furthermore the results of the elegant animal experiments by Martinez et al (1961) and Aramendia, de Letona, and Aviado (1962) suggested that the flow from the pulmonary artery into the bronchial veins via anastomotic channels was not reduced by norepinephrine. Finally, whether an increase of blood flow could have been the cause of the early rise of pulmonary arterial pressure should be examined.…”

Section: Discussionmentioning

confidence: 99%

Effects of Norepinephrine on Human Pulmonary Circulation

Bousvaros¹

1962

Heart

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The vasoconstrictive action of norepinephrine on the pulmonary vessels has been consistently demonstrated in animals by histological techniques (Patel and Burton, 1957) or by preparations in which pulmonary blood flow could be regulated at will and continuously measured (Rose et al., 1955;Borst, Berglund, and McGregor, 1957;Eliakim and Aviado, 1961); but such techniques are not applicable in man. Pulmonary vasoconstriction following the administration of norepinephrine has not been demonstrated unequivocally in man; although Patel, Lange, and Hecht (1958) reported significant increases of pulmonary vascular resistance during steady-state administration of norepinephrine and interpreted this as indicating pulmonary arteriolar constriction, Fowler et al. (1951) under similar conditions obtained no such increase. Investigating the effect of norepinephrine on the pulmonary circulation in a group of patients with aortic regurgitation, Regan et al. (1959) found no change in pulmonary vascular resistance, whereas an increase was noted in their normal controls. In view of these contradictory reports further investigation of the subject was undertaken. MATERIAL AND METHODSThe study was carried out in two parts. In 13 subjects (group A) "steady-state" observations of pressures and blood flow in the pulmonary circulation were made before and during infusion of norepinephrine: pulmonary vascular resistance was thus computed. In 9 additional subjects (group B) the moment-to-moment changes of pressure across the pulmonary vascular bed were observed, following a single injection of norepinephrine. While flow, and thus resistance, changes could not be measured by this method, rapid transients that would not be discernible by the "steady-state" method could be observed.Group A. In this group there were 6 patients with isolated pulmonary stenosis, 1 with atrial septal defect, 3 with small ventricular septal defect, and 2 others, one of whom had been in heart failure three years before after an infundibular resection for the tetralogy of Fallot. There was also one person investigated for a praecordial systolic murmur, in whom no hlmodynamic abnormality was found. All subjects were familiar with the laboratory surroundings and had practised breathing through the mouthpiece of the close-circuit spirometer which measured the oxygen consumption. Right heart catheterization was performed with the subjects mildly sedated and in the post-absorptive state: single lumen, end-hole catheters were introduced from a medial antecubital vein and in each case the diagnostic data were first collected. For the observations control blood samples, oxygen consumption, and pressures were obtained, and this was followed by intravenous administration of norepinephrine at a concentration of 8 ,ug./ml. in isotonic saline. The rate of administration was adjusted to produce stable systemic hypertension of moderate degree; and the amount thus given

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Responses of the Bronchial Veins in a Heart-Lung-Bronchial Preparation

Cited by 31 publications

References 7 publications

Preliminary Pharmacological Characterization of the Bovine Isolated Bronchial Artery Strip: A New Preparation

Preliminary Pharmacological Characterization of the Bovine Isolated Bronchial Artery Strip: A New Preparation

Acute alveolar hypoxia increases bronchopulmonary shunt flow in the dog.

Effects of Norepinephrine on Human Pulmonary Circulation

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