Blood Flow in the Bronchial Artery of the Anesthetized Dog

Bruner, H. D.; Schmidt, Carl F.

doi:10.1152/ajplegacy.1947.148.3.648

Cited by 99 publications

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“…Inflation of the lungs decreases bronchial vascular resistance in dogs (Bruner & Schmidt, 1947;Goetz, Rohman, Dee, Haller & State, 1960) and, since this is prevented by lung denervation (Lung, 1979), it may be a pulmonary reflex. Lung (1979) concluded that it was mediated by pulmonary C fibres which are stimulated by large lung inflations and our results are consistent with this view; in our experiments lung inflations were kept to low pressure to stimulate pulmonary stretch receptors rather than C-fibre receptors.…”

Section: Discussionmentioning

confidence: 99%

Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs.

Şahin

Webber

Widdicombe

1987

The Journal of Physiology

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SUMMARY1. With pentobarbitone-anaesthetized dogs, the cranial tracheal arteries have been independently perfused on both sides, to measure vascular resistance. Blood pressure and contractions of tracheal muscle were also measured.2. Capsaicin was injected intravenously to stimulate lung C-fibre receptors. In breathing and in paralysed artificially ventilated dogs it decreased tracheal vascular resistance and blood pressure, and contracted tracheal muscle. The effects were abolished or far smaller after bilateral cervical vagosympathectomy.3. Veratrine was injected intravenously to stimulate slowly adapting pulmonary stretch receptors and cardiac receptors. In breathing and in artificially ventilated dogs it lowered tracheal vascular resistance and blood pressure, and had variable effects on tracheal muscle tone. The vascular effects were prevented by vagotomy.4. Veratrine injected into the left atrium caused similar vascular changes to intravenous administration. The changes were prevented by vagotomy. Veratrine causes a tracheal vasodilatation by action on cardiac receptors. 5. Inflation of the lungs in artificially ventilated dogs, to stimulate slowly adapting pulmonary stretch receptors, had no effect on tracheal vascular resistance but decreased blood pressure and tracheal muscle tone, the latter being prevented by vagotomy.6. Bilateral carotoid arterial occlusion, to decrease the discharge in carotid sinus baroreceptors, had no effect on tracheal vascular resistance but increased blood pressure and contracted tracheal muscle, the last two responses being greatly reduced by cutting the sinus nerves.7. It is concluded that stimulation of lung C-fibre and cardiac receptors causes a reflex tracheal vasodilatation, but that no changes in the tracheal vascular bed occur with stimulation of slowly adapting pulmonary stretch receptors or inhibition of carotid sinus baroreceptors.

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Section: Discussionmentioning

confidence: 99%

Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs.

Şahin

Webber

Widdicombe

1987

The Journal of Physiology

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“…One possible mechanism is that the response is due to dilatation of the pulmonary vascular bed proper and another, that it is the result of a reflex alteration in bronchial vasomotor tone causing a redistribution ofblood between the bronchial and pulmonary vascular systems (Berry & I. de B. Daly, 1931). This latter explanation does not seem unreasonable in view ofthe finding that the vagus nerve functionally innervates the bronchial vascular bed (Bruner & Schmidt, 1947). The decision as to which of these two explanations is the correct one can only be decided by experiments in which chemoreceptor reflexes are tested under conditions which preclude the exchange of blood between the bronchial and pulmonary vascular systems (I. de B.…”

Section: Discussionmentioning

confidence: 99%

The effects of stimulation of the carotid body chemoreceptors on pulmonary vascular resistance in the dog

Daly¹,

Daly²

1957

The Journal of Physiology

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In a previous study we investigated the effects of carotid sinus baroreceptor reflexes on pulmonary vascular resistance (Daly & Daly, 1957b, c). An examination has now been made of the reflex effects of stimulation of the carotid body chemoreceptors on the lesser circulation and the results which have been briefly reported elsewhere (Daly & Daly, 1957a) are presented in this paper. METHODSDogs of 14-7-19-6 kg body weight were anaesthetized with chloralose (0-1 g/kg intravenously) after premedication with morphine hydrochloride (1 mg/kg subcutaneously). The chest was opened in the mid-sternal line and the lungs ventilated by means of a Starling 'Ideal' pump at constant pressure, which varied from 8 to 15 cm water in different experiments. During expiration the lungs collapsed passively against a resistance of 2-2-5 cm water. Changes in tidal air volume were measured by the method of Konzett & Rossler (1940). Both phrenic and recurrent laryngeal nerves were crushed to minimize mechanical effects on the lungs.Perfusion of the carotid bodies. Reflex effects from the carotid body chemoreceptors were elicited by temporarily changing the perfusate from arterial blood to venous. For this purpose both carotid bifurcation regions were isolated from the circulation by ligation of all branches of the common and external carotid arteries. The veins draining the carotid bodies were, however, carefully preserved. Perfusion of the carotid sinus and body on both sides was carried out through the common carotid arteries. The arrangement of the two Dale-Schuster pumps used for the perfusion is shown in Fig. 1

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“…Histamine, methacholine and isoprenaline increase bronchial blood flow in sheep when administered directly into the bronchial artery; adrenaline injected similarly reduces bronchial blood flow, and nicotine has a variable effect (Parsons et al, 1985). Histamine (Bruner & Schmidt, 1947;Yamatake & Yanaura, 1978), methacholine (Lakshminarayanan et al, 1985), isoprenaline (Yamatake & Yanaura, 1978) and prostaglandins E2 (Yamatake & Yanaura, 1978) 'Author for correspondence. 2Present address: Research Institute for Military Medicine,Central Military Hospital Tilkka,Mannerheimintie 164,00280 Helsinki 28,Finland. and F2, (Lakshminarayanan et al, 1985) increase bronchial blood flow in dogs, although one report (Yamatake & Yanaura, 1978) describes a vasoconstriction with prostaglandin F2.. Aerosolised histamine increases both bronchial blood flow and airflow resistance, and it is suggested that the action of histamine on bronchial arterioles is mediated by H2-receptors .…”

Section: Introductionmentioning

confidence: 99%

Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

Laitinen

Widdicombe

1987

British J Pharmacology

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IVarious doses of mediators were tested on tracheal vascular resistance in dogs anaesthetized with pentobarbitone. Tracheal vascular resistance was determined by perfusing the cranial tracheal arteries at constant flows and measuring inflow pressures. 2 All drugs produced dose-related changes in vascular resistance. 3 The peptides bradykinin, substance P and vasoactive intestinal peptide (VIP) each had similar vasodilator potencies and were much more powerful than histamine, methacholine and salbutamol.4 Platelet activating factor (Paf) was a weaker dilator than the peptides. Prostaglandins D2, E, and F2,, had wide dilator potency ranges, PGE, being very effective even at low concentrations.5 Phenylephrine, an a-adrenoceptor agonist, was the only drug tested that always increased vascular resistance. 6 All the drugs studied also had effects on the contralateral tracheal vascular resistance.

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Blood Flow in the Bronchial Artery of the Anesthetized Dog

Cited by 99 publications

References 0 publications

Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs.

Lung and cardiac reflex actions on the tracheal vasculature in anaesthetized dogs.

The effects of stimulation of the carotid body chemoreceptors on pulmonary vascular resistance in the dog

Dose‐related effects of pharmacological mediators on tracheal vascular resistance in dogs

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