[Evaluation of the stretch of the bladder wall during filling].
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Biomedical subjects
Publications and source records attributed to M G Clement.
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We studied the respiratory response to infusion of prostacyclin (PGI2) in 7 anaesthetized pigs in an attempt to understand whether the changes in pattern of breathing were due to a direct action of the substance or to the concomitant hypotensive effect. The depth and frequency of breathing were analyzed in terms of the threshold-inhibition curve for termination of inspiration (VT/TI relationship) and of bulbo-pontine rhythm, estimated from inspiratory and expiratory time during occlusion of the airways at the end expiratory level (TE/TI relationship). This provide the central respiratory rhythm when the phasic lung volume receives no input from pulmonary stretch receptors. The hypotension induced by PGI2 increased pulmonary ventilation mainly through a change in VT and caused a slight rightward displacement of VT/TI relationship without modifying the slope of the curve. This effect seems to be vagally mediated. PGI2 also changed the bulbo-pontine rhythm. Our results show that PGI2 modifies the vagal discharge and bulbo-pontine rhythm by two opposite mechanisms: hypotension and an apparent direct action on carotid and aortic baroreceptors.
Cardiovascular and pulmonary effects of prostacyclin (PGI2) were investigated in the anaesthetized pig before and after vagosympathectomy at 1',2',3',4',5',10',15' and 20' after the beginning of the infusion. The animals were perfused with PGI2,2ug/kg/min for 4 min. We measured the following parameters : mean arterial pressure, heart rate, cardiac output, stroke volume, mean pulmonary arterial pressure, mean wedge pressure, left stroke work, total systemic resistance, total pulmonary resistance, tidal volume, respiratory frequency, minute volume, lung resistance and compliance, end-tidal CO2, transpulmonary pressure. Our findings suggest that the hypotension observed is due to a reduction in total peripheral resistance by a direct effect of PGI2 on the vascular bed without inhibition of the sympathetic nervous system. Prostacyclin does not directly modify cardiac function and produces a decrease in preload by venous dilation. The changes in pattern of breathing are related to the hypotensive effect of PGI2.
The perfusion of octopamine in pig produces an increase of cardiac output with decrease of pulmonary vascular resistances. The changes in lung circulation depend by a direct action of this drug on nervous control of vascular walls because when the pulmonary shunt increase the effect is not correlated to changes a pattern of breathing.
In anaesthetised pig the intravenous perfusion of 2 micrograms/Kg/min/4 min of PGI2 induces within 30'' respiratory changes that spontaneously disappear after perfusion. The PGI2 induces a decrease of respiratory frequency while total pulmonary resistance increases significantly. This changes of pattern of breathing are correlated to tonus of vagus nerve and after vagosimpathectomy are not present. The relationship of tidal volume/frequency has been evaluated according to the blood pressure variation.
The hemodynamic response of pig perfused by PGI2 (2 micrograms/kg/mm/4 min) has been studied before and after vagosympathectomy. Prostacyclin produces hypotension, which depends to an reduction of total peripheral resistances, without cardiac involvement. A venous dilatation is also present with reduction of preload and of systolic volume. The authors conclude assessing that prostaciclyn act by peripheral mechanism.
In anaesthetised and tracheotomised pig, the reflex of panting has been evaluated. The thermal tachypnea showed two phases: initially respiratory frequency increases likely to body temperature but at 41,4 degrees C is observed apnea. When temperature rose above 42 degrees C the respiratory frequency further increased the changes in blood CO2, O2 and pH were not significant. During apnea is present a slight alkalosis.
The dynamic work of breathing (Wdyn) has been measured during thermal tachypnea in pig anaesthetized and tracheotomized. During euthermia Wdin(cm H2O/R1/min-1) increases with ventilation (L.P.S.) according to Wdyn = 1,09 V2 + 1,33 V3; when body temperature rose above 39 degrees C for a given ventilation Wdyn decreases. In all animals has been observed a change of airways size and probably of respiratory tract of Weibel.
PGF2 alpha was injected into different parts of the circulatory system (intravenously by femoral and jugular veins, into the pulmonary artery, into the ascending or descending aorta and into the internal carotid artery at a level above the sinus and carotid body) of anaesthetized spontaneously breathing pigs. It caused changes in respiratory and cardiovascular variables. In vagosympathectomized animals the changes in pattern of breathing produced by PGF2 alpha were greatly reduced and total lung resistance was increased. This may indicates more than one site of action of PGF2 alpha, lung resistance being influenced by a direct action of PGF2 alpha and by an immediate reflex while the pattern of breathing being modulated by vagal efferents from the lungs.
The effects of vagosympathectomy, asphyxia, hypoxia and hypercapnia on the breathing of anaesthetised pigs are described. Vagosympathectomy caused changes in cardiovascular variables and in the pattern of breathing characteristic of the loss of stretch receptor activity. After vagosympathectomy the linear relationship between tI and tE was abolished. Hypoxia in intact animals produced changes in minute ventilation by peripheral chemoreceptor drive. When this drive was removed by vagosympathectomy the central depressing effects of hypoxia were revealed as a slowing of breathing and reduction in minute volume. The central depressing effect of hypoxia on respiration was very potent in the pig and very clearly seen in asphyxia. Vagosympathectomy caused a reduction in frequency of breathing and respiratory arrest occurred when a dead space of only moderate size was used. Breathing slowed from the moment of connection of the dead space to produce respiratory arrest within 2 min. The pig lung has been considered similar to the human lung on morphometric and physiological grounds but these results show that there are very important species differences in response to asphyxia.
In dogs the authors have recorded from single fibres of the vagus nerve the action potentials originating from rapidly adapting receptors (irritant receptors) of the tracheo-bronchial tree activated both by inflation and deflation and by i.v. injection of histamine. A gross localization between extrapulmonary airways was established for 196 such receptors by probing the structures containing them. For 82 receptors a precise localization was determined within the extrapulmonary airways and for 51 receptors, localized in the lung parenchyma, a further precise localization was established along the intrapulmonary airways be dissecting the lung tissue. 66.9% of these receptors were found to be in the intrapulmonary airways and 33.1% in the extrapulmonary airways. Their distribution along the tracheo-bronchial tree resulted as follows: 4.75% in the higher 2/3 of the trachea, 9.25% in the lower 1/3 of the trachea and the carina, 19.0% in the main bronchus, 25.0% in the lobar bronchi, 36.8% in bronchi having a diameter larger than 1 mm and 5.2% in bronchi having a diameter smaller than 1 mm. Therefore the concentration of irritant receptors increases going from the upper trachea to the lobar bronchi and then sharply decreases reaching the smaller airways.
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