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Biomedical subjects

F Lioy

Publications and source records attributed to F Lioy.

At least 19 recordsLinked to original sources
PubMed1988

Effects of carbon dioxide on hindlimb vascular resistance in the acute spinal cat.

A cervical (C2) spinal section was carried out in anaesthetized, neuromuscularly blocked cats and the vascularly isolated hindlimbs were independently perfused at constant flow with blood taken from the abdominal aorta. One leg was denervated by sectioning the lumbar sympathetic chain. The animals were hyperventilated in 100% O2 and 5% or 10% CO2 in O2 was administered without altering the rate or tidal volume of the respirator. Increasing paCO2 (mm Hg) from 16.36 +/- 0.84 to 37.48 +/- 1.03 and to 62.23 +/- 2.23, induced a significant early vasoconstriction (P1) followed by a later more prolonged vasoconstriction (P2) in the innervated leg, while only a significant P2 response was present in the sympathetically denervated leg. A significant increase in systemic arterial pressure (SAP) was also observed with no change in heart rate (HR). After bilateral adrenalectomy increasing paCO2 from 17.16 +/- 0.66 to 37.96 +/- 1.21 and to 64.20 +/- 1.55, induced smaller but significant P1 and P2 responses in the innervated leg but only a significant P2 response was induced in the denervated leg. These results suggest that the early vasoconstriction was mainly due to activation of lumbar sympathetic neurons, while the late vasoconstriction was caused by the release of adrenal catecholamines and possibly other unidentified vasoconstrictor substances.

Administration, Inhalation↗
PubMed1985

Regional hemodynamic effects of changes in PaCO2 in the vagotomized, sino-aortic de-afferented rat.

Rats were anesthetized with urethane (1.5 g/kg i.p.) paralyzed with gallamine (3 mg/kg, i.v.), artificially ventilated and the vagi, carotid sinus and aortic nerves were cut. PaCO2 levels of 16.4 +/- 0.8, 23.3 +/- 1.6, 32.3 +/- 1.8 and 51.9 +/- 2.2 mm Hg were obtained by hyperventilation in 0%, 3%, 5% and 8% CO2 in O2, respectively. Radioactive microspheres labelled with 57Co or 113Sn were injected into the left ventricle and cardiac output and regional blood flows were determined by the 'arterial reference sample' method. Increasing PaCO2 induced an increase in systemic arterial pressure which was predominantly due to a significant increase in total peripheral resistance, while the increase in cardiac output was much less pronounced and no changes in heart rate were observed. The effect of increasing PaCO2 on regional vascular resistance (VR) was not uniformly distributed. CO2 induced a dilatation in the cerebral, bronchial and hepatic artery vascular beds. Coronary VR was not affected while vasoconstriction was induced by CO2 in the other vascular territories. This vasoconstriction was most significant in skeletal muscle, skin, pancreas, large intestine and kidneys. In most of these territories the vasoconstrictor effect of CO2 was observed at PaCO2 levels above 23.3 mm Hg, while between 16.4 and 23.3 mm Hg there was either no change or a decrease in VR. Propranolol and phentolamine (1 mg/kg and 10 mg/kg, i.v., respectively), which caused a 78% +/- 2% adrenergic blockade, significantly reduced the CO2 pressor and vasoconstrictor effects. Our experiments show that, after peripheral chemoreceptor denervation in the rat: (a) there is a direct relationship between PaCO2 and VR mediated by the sympathetic nervous system over the whole range of PaCO2 values from hypocapnia to hypercapnia, and (b) the various vascular territories contribute to a different extent to the CO2-induced changes in total peripheral resistance.

Animals↗
PubMed1984

Pressor effect of CO2 in the rat: different thresholds of the central cardiovascular and respiratory responses to CO2.

Rats were anesthetized with urethane and the vagi, aortic and carotid sinus nerves were sectioned bilaterally. Hypocapnia was induced by artificial hyperventilation with 100% O2. Administration of 5% CO2 in O2, without alteration of the respiratory rate or tidal volume, induced significant increases in mean systemic arterial pressure ( mSAP ) in rats with intact central nervous system (CNS) and after midcollicular section (36 +/- 4 and 34 +/- 2 mm Hg, respectively; mean +/- S.E.). Smaller but significant increases in mSAP (17 +/- 3 mm Hg) were induced by inhalation of 5% CO2 after section of the spinal cord at the C4 level. Ganglionic blockade with hexamethonium completely abolished the pressor response to CO2. In hypocapnic (paCO2 15.5 +/- 0.7 mm Hg) apneic rats with intact CNS, after denervation of the peripheral chemoreceptors, inhalation of 1.5% CO2 in O2 increased paCO2 to 22.3 +/- 1.2 mm Hg and mSAP by 16 +/- 1 mm Hg, but the animals remained apneic for up to 45 min of continuous CO2 administration. Higher FICO2s induced further immediate increases in mSAP and, after delays of up to 6-7 min, also a resumption of central rhythmic respiratory activity (monitored by the intercostal muscles or phrenic nerve electrogram). The paCO2 threshold for this respiratory response was 25 +/- 1 mm Hg. When rhythmic respiratory activity resumed, a further slight increase in mSAP and the appearance of respiratory modulated oscillations of the SAP were observed in most animals. When, after a period of CO2 inhalation, 100% O2 was again administered to the animals mSAP fell immediately, reaching the control level within 20-30 s, while the respiratory activity, if present, disappeared only after 1.5-2 min. From these experiments we conclude that in the hypocapnic rat, after denervation of the peripheral chemoreceptors: (1) CO2 induces a neurogenic hypertensive response even in the absence of rhythmic respiratory activity; (2) the central chemosensitive sites appear to be located in the ponto-medullary region and in the spinal cord; and (3) the central mechanisms responsible for the pressor response have a lower CO2 threshold and a much shorter latency than those responsible for the initiation of the rhythmic respiratory activity.

Animals↗
PubMed1981

Cardiovascular control by medullary surface chemoreceptors.

The cardiovascular and respiratory effects of superfusion of the ventral surface of the medulla with acid hypercapnic or alkaline hypocapnic solutions have been studied in anaesthetized, paralyzed, artificially ventilated cats. Peripheral chemoreceptor and baroreceptor denervation was achieved by section of carotid sinus, aortic and cervical vagus nerves. Systemic arterial and central venous pressure, hindquarters blood flow, heart rate and phrenic nerve activity were recorded. Acid hypercapnic (pH 6.8, pCO2 85 mm Hg) superfusion caused increases in systemic arterial pressure, phrenic nerve activity and heart rate, and a decrease in hindquarters blood flow. Alkaline hypocapnic (pH u.i, pCO2 less than 10 mmHg) superfusion caused opposite effects. These experiments indicate a significant role of the chemoreceptors of the ventral surface of the medulla in cardiovascular control.

Animals↗
PubMed1981

Role of carotid and central chemoreceptors in the CO2 response of sympathetic preganglionic neurons.

In anesthetized, vagotomized, paralyzed, artificially ventilated cats with aortic nerves cut, we recorded the response of 28 sympathetic preganglionic neurons (SPNs) of the cervical sympathetic trunk of changes in arterial pCO2. We observed the effects on these responses of: (i) surgical denervation of carotid sinus chemoreceptors in normoxia (paO2 110 mm Hg); and (ii) hyperoxia (paO2 greater than 350 mm Hg) which is known to depress peripheral chemoreceptor sensitivity to CO2. Stimulus-response curves, obtained by rebreathing at constant paO2, were used to detect the effects of these manoeuvres. The present experiments have confirmed previous observations demonstrating the CO2-sensitivity of this neuron population. The population average firing rate, as a function of paCO2, describes a sigmoid curve, increasing continuously between 20 and 90 mm Hg and asymptotically approaching plateaus at the highest and lowest paCO2 values. Carotid sinus nerve section caused a decrease of the average response of the population at all paCO2 values, resulting in a displacement to the right of the response curve, in a decrease in slope and maximum values. On the assumption that the CO2 response curve after carotid sinus nerve section is due to central chemoreceptor input, and that there is a simple addition between the effects of central and carotid chemoreceptors, the difference between CO2 response curves ("difference curves") before and after denervation represents the contribution of the carotid chemoreceptors. A comparison of this "difference curve" with the curve obtained after denervation reveals that the contribution of the carotid chemoreceptors is of the same magnitude as that of the central chemoreceptors up to a paCO2 value of 60-70 mm Hg. Beyond this value, the carotid contribution declines and becomes a smaller component of the total response, whereas the contribution of the central chemoreceptors continues to increase. Similar results were obtained with rebreathing in hyperoxia, after correction for the central excitatory effect of hyperoxia. Hyperoxia never caused a depression of the CO2 response of units after section of the carotid sinus nerve. Observation of the effects of the two manoeuvres on individual SPNs leads to the conclusion that in approximately half of the CO2-sensitive units there is an overlap of central and peripheral chemoreceptor input. The remainder of the CO2-sensitive units receive input only from the central chemoreceptors.

Animals↗
PubMed1979

Baroreceptor influence on a spinal cardiovascular reflex.

A stretch of the walls of the thoracic aorta, performed in vagotomized cats without obstructing aortic flow, induces increases in heart rate, myocardial contractility, and arterial pressure. These reflex responses are still present after high spinal section. Cats under chloralose-urethane anesthesia were vagotomized and one carotid sinus was isolated and perfused with arterial blood at constant flow. The contralateral carotid sinus nerve and both aortic nerves were sectioned. A stretch of the walls of the thoracic aorta between the 7th and 10th intercostal arteries induced a reflex increase in mean arterial pressure 29 +/- 2 mmHg (mean +/- SE). Stepwise increases of carotid sinus pressure (CSP) or electrical stimulation of the carotid sinus nerve induced stepwise decreases of this reflex response. At maximal baroreceptor stimulation (CSP 212 +/- 9 mmHg) the reflex response to aortic stretch was reduced by 42%. These experiments show that this spinal cardiovascular reflex is at least partially under the inhibitory control of the baroreceptor input.

Animals↗
PubMed1979

Evaluation of a screen oxygenator suitable for small animal organ perfusion.

A small vertical screen oxygenator was built using a stainless steel screen enclosed in a Plexiglas box as the oxygenating surface. The unit was primed with 35 ml dextran-diluted blood (Hct 25.1 +/- 0.6%. mean +/- SE) and tested in cats with a partial cardiopulmonary bypass circuit. An oxygen saturation of more than 95% was always obtained, even when the incoming venous saturation was as low as 15%. The O2 exchange capacity was minimally affected by changes in blood flow (1.5 to 70 ml/min) through the unit. CO2 extraction was not flow limited over the range tested. Output PCO2 was 33.3 +/- 0.6 mmHg and pH was 7.29 +/- 0.02. These results were obtained when 3% CO2 in O2 was passed through the oxygenator chamber at 1.0 to 5.0 l/min. The performance of the unit was stable for periods up to 4 h. The small priming volume and reliable performance make this oxygenator suitable for organ perfusion in small experimental animals.

Animals↗
PubMed1978

CO2-dependent component of the neurogenic vascular tone in the cat.

Complete vascular isolation of the hindlimbs was performed in vagotomized cats under Sodium Pentobarbital anesthesia. The hindlimbs were perfused at constant flow with blood kept at a constant and physiological PO2, PCO2, and pH values by means of a specially designed pump-oxygenator system. The animals were hyperventilated with different CO2 mixtures (0%, 5%, 7% and 10% in O2) thereby changing blood gases and pH levels in the upper body but not in the hindlimb vascular bed. At body PaCO2 (mm Hg) of 13.7 +/- 1.0 (means +/- SE), 30.6 +/- 1.05, 40,4 +/- 0,9 and 58.4 +/- 2.9 the hindlimb perfusion pressure (mm Hg) was, respectively 124 +/- 7.6, 138 +/- 7.4, 156 +/- 11.9 and 187 +/- 15.1. These changes in perfusion pressure were still present after complete peripheral chemoreceptor denervation but were abolished after section of the spinal cord at the T5 level. Since hindlimb perfusion pressure fell when body PaCO2 was lowered below physiological levels it is concluded that part of the neurogenic vascular tone of the hindlimbs is maintained by a CO2 mediated stimulation of supraspinal structures.

Animals↗
PubMed1978

Reflex effects of thoracic aorta wall stretch on regional vascular resistance.

In anesthetized, vagotomized cats with both carotid arteries occluded, a stretch of the walls of the thoracic aorta, performed without obstructing aortic flow, induced a significant reflex increase in arterial pressure (35 +/- 2-26 +/- 1 mmHg; systolic-diastolic). This pressure increase was accompanied by significant increases in peripheral resistance in the superior mesenteric (+30%), renal (+23%), and external iliac (+23%) vascular beds. The increase in iliac resistance observed in the skinned leg was comparable with that observed in the contralateral intact limb. All these vascular responses were drastically reduced by the administration of phenoxybenzamine. After alpha-adrenergic blockade no signs of reflex vasodilatation could be detected during aortic stretch in any of the vascular beds examined.

Animals↗
PubMed1977

Inhibition by atropine, phenoxybenzamine and propranolol of the autonomic nervous system of the domestic fowl.

Because of the paucity and inconsistency of information on blockage of the chicken autonomic nervous system for extended periods, the effects of atropine, phenoxybenzamine and propranolol in the anesthetized hen were examined. It was found that cholinergic blockade by atropine was very short lived. For effective (80%) parasympathetic blockage a priming dose of 0.25 mg./kg;, followed by an infusion at the rate of 17.5 microgram/kg./min., was required. Similarly, inhibition of the beta-sympathetic system required propranolol in a priming dose of 0.25 mg./kg. and an infusion of 5 microgram/kg./min. The alpha-sympathetic inhibitor, phenoxybenzamine, was effective when given as a single dose of 5 mg./kg. Using these levels of inhibitor it was possible to ensure blockade in all cases for periods of two hours or more.

Acetylcholine↗
PubMed1971

Passive vasodilatation of the hind limb after sympathetic preganglionic stimulation.

1. The post-vasoconstriction dilatation (PVCD) observed after release of carotid clamping has been attributed to baroreceptor stimulation. However, PVCD has been observed in baroreceptor deafferented animals following cessation of stimulation of the diencephalon or of chemoreceptor fibres.2. The effects of preganglionic (ventral roots) and post-ganglionic (sciatic nerve) stimulation upon the vascular resistance of the hind limb of anaesthetized cats and dogs was investigated. The limb was vascularly isolated and perfused at constant flow with the animal's own arterial blood. The animals were atropinized and neuromuscular block was obtained with gallamine triethiodide.3. PVCD was observed upon cessation of stimulation of intact preganglionic fibres or of their peripheral stump.4. PVCD was dependent upon the existence of neurogenic vasomotor tone in the vessels, but independent from baroreceptor influences.5. PVCD was never observed after cessation of stimulation of the post-ganglionic fibres.6. Similar results were obtained after removal of the skin of the perfused limb.7. The possibility that the post-vasoconstriction dilatation observed in these experiments is due to the existence of a preganglionic inhibitory system is discussed.

Animals↗
PubMed1971

Coronary blood flow, oxygen delivery rate and cardiac performance.

1. Studies have been made on the isolated blood-perfused heart of dogs in which isometric tension development at various settings of resting tension (RT) was measured at various levels of O(2) delivery rates controlled by altering (a) coronary blood flow (CBF), (b) O(2) capacity or (c) O(2) saturation of the perfusate. Measurements were also made of O(2) consumption and vascular perfusion resistance.2. The capacity of the left ventricle to develop tension at any given setting of resting tension was found to be directly correlated with changes in O(2) delivery rate using any of the above three methods of altering the latter.3. The slopes of the curves relating resting tension to developed tension are positively correlated with total O(2) delivery to the heart.4. The O(2)-dependent metabolic effect upon tension production was found to be slow in development, in contrast to the Frank-Starling effect, which reached full development in the first heart beat after a change in resting length and tension.5. The O(2) consumption of the isometrically contracting heart is strongly correlated with the O(2) delivery rate at all particular values of resting tension and related developed tension.6. The metabolic state of the myocardium as determined by the rate of O(2) delivery within physiological ranges is (a) a direct major determinant of the tension-producing capacity of the heart muscle and (b) determines the magnitude of adaptation via the Frank-Starling mechanism.

Animals↗