Papers already published report that in the normal mammals so far examined (man, dog and rat, both sexes) oxytocin dilates a number of vascular beds (Lloyd, 1959a, b;Lloyd & Pickford, 1961; see Haigh, Kitchin & Pickford, 1963). This dilator effect is converted to a constrictor one following chemical blockage of ganglia or peripheral sympathetic nerves, after surgical sympathectomy of the part, and after administration of reserpine. The same change is also induced by subcutaneous or intravenous administration of oestrogens, or when the animal (rat) is in natural oestrus. As a first step towards elucidating the mechanism of the identical change in the response to oxytocin induced by procedures as diverse as oestrogen administration and interference with the sympathetic nervous system, it was decided to attempt restoration of the dilator effect of oxytocin after having caused the appearance of the constrictor one. This paper is chiefly concerned with experiments made to this end on a number of dogs and on two monkeys. Brief reference to some of these results has already been made (Haigh, Lloyd & Pickford, 1964;Pickford, 1964). METHODSThe observations were made on a number of dogs of both sexes and on two female monkeys. All but two of the experiments were acute ones in which the animals were anaesthetized with pentobarbitone, 26 5 mg/kg body weight, given intravenously; the animals also received heparin, 5 mg/kg body weight intravenously. Mean blood pressure was recorded by mercury manometer from the carotid artery. Blood flow through the hind limb was measured by means of a Pavlov (1887) stromuhr inserted between the cut ends of the femoral vein. When preparations were complete a period of 25-40 min was allowed before observations were begun.Chronic observations were made in one female and one male dog and, in these, leg flow was measured by means of venous occlusion plethysmography. The diaphragm of the plethysmograph was specially designed with an irregular ovoid opening shaped like the cross-section of a dog's leg. The leg was inserted through this into a thin rubber bag made of two breadths of 2 in. diameter colostomy tubing sealed together; in the usual way the rubber bag was attached to the rim of the diaphragm across the opening of the plethysmograph. 36-2
SUMMARYThe mammalian tachykinin neuropeptides substance P (SP) and neurokinin A (NKA) are present in the airways of several species and are involved in control of bronchomotor tone. We investigated the effect of SP and NKA on various respiratory and cardiovascular parameters in anaesthetized sheep. Dose-dependent decrease in dynamic compliance (CdYf) and increase in respiratory resistance (RL) occurred with intravenous administration of SP. The predominant effect of NKA was on Cdyn with little or no effect on RL. Consequently SP is a more potent bronchoconstrictor than NKA in the sheep and affects both central and peripheral airway tone. The sensitivity to SP and NKA and the order of potency found suggests the NK-1 receptor predominates in sheep airways. Atropine and the ganglion blocker hexamethonium markedly reduced the bronchoconstriction caused by SP. SP and NKA were equipotent in causing a significant reduction in respiratory rate. SP caused a fall in mean blood pressure while NKA caused mild vasoconstriction. Neither peptide affected heart rate. We concluded that SP is a more potent bronchoconstrictor than NKA in the sheep and that the mechanism of action is mainly indirect involving modulation of postganglionic cholinergic nerve endings.
The influence of vagotomy on resting arterial blood gases (PaCO2 and PaO2) and on the ventilatory responses to hypercapnia and hypoxia was studied in three different species of anaesthetized animals. After bilateral cervical vagotomy resting PaCO2 generally declined. In the dog, where this was studied more fully, resting PaCO2 declined significantly (8.13+O067 mm Hg) over several hours, but PaO2 changes were not significant.After vagotomy tidal volume (VT), but not frequency (f), increased with increasing chemical drive. It is concluded that the increase in frequency in response to increased CO2 or decreased 02 is dependent on the vagal mechanisms. [1880] suggested that stimulation of the vagus was ineffective in animals made apnoeic by hyperventilation. Rice [1938] reported that hypercapnia produced by increased respiratory dead space caused a decrease in the effectiveness of the vagal reflexes while Woldring [1965] showed that the sensitivity of the inspiratory muscles to a given change in lung volume in anaesthetized cats varied with the level of arterial PaCO2.Although it is well known that the vagus nerves are the afferent pathway for a number of respiratory reflexes affecting rate and depth of breathing and there is some information on the minute volume/end tidal PaCO2 relationship after vagotomy, it is not clear what influence the vagi exert on maintenance of a normal arterial CO2 tension. The present study endeavours to establish a more quantitative relationship between the effects of vagotomy on arterial blood gas tension in the resting state as well as during hypercapnia and hypoxia in three different species. METHODSExperiments were carried out in thirteen rabbits (body weight 1-9-3-7 kg), twenty dogs (7419-2 kg) and twelve sheep (22-0-43-0 kg). Food was withheld for 12 hr before the experiment but the animals were allowed free access to water.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.