Vergleichende biochemische Untersuchungen an einem autorhythmischen und einem nicht spontan aktiven Gefässmuskel &lt;i&gt;in vitr&lt;/i&gt;&lt;i&gt;o&lt;/i&gt;

Voth, David R.; Lell, D.

doi:10.1159/000157962

Cited by 1 publication

(1 citation statement)

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“…This is not surprising because hypoxia has been found not to be important in the regulation ofthe resistance and capacitance vessels of many other vascular beds (Cuthbert, 1967;Daugherty, Scott, Dabney & Haddy, 1967;Voth & Lell, 1973;Vanhoutte, 1976). Hypercapnia, on the other hand, acts locally on the nasal capacitance vessels, most probably via dilatation of the thick-walled veins and opening up of the arteriovenous anastomoses as excess carbon dioxide or a decrease in pH has been known to be vasodilatatory in many other vascular beds (Daugherty et al 1967;Vanhoutte & Clement, 1968).…”

Section: Discussionmentioning

confidence: 99%

Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog.

Lung¹,

Wang²

1986

The Journal of Physiology

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SUMMARY1. The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed.2. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously.3. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa.4. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery.5. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously.6. Hypercapnic gas challenge (8 % C02, 30 % 02 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance.7. Hypoxic gas challenge (6 % 02 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance.8. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance.9. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy.10. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy.11. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.

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