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Biomedical subjects

G Miserocchi

Publications and source records attributed to G Miserocchi.

At least 73 records · Page 4Linked to original sources
PubMed1981

Pleural liquid pressure over the interlobar mediastinal and diaphragmatic surfaces of the lung.

Pleural liquid pressure (Pliq) was measured in the interlobar fissures and over the mediastinal apical, cardiac and diaphragmatic surface. When compared to costal values, Pliq was more subatmospheric over the cardiac region at all lung heights by about 5 cm H2O so that a costo-hilar gradient down the interlobar fissures of about 0.7 cm H2O/cm was found. No differences were found for other surfaces. Cardiac values, unlike costal ones, became more subatmospheric on increasing ventilation and heart-rate. On the basis of a Starling equilibrium a costo-hilar gradient of Pliq as well as more negative values in the cardiac surface can be explained if hydrostatic pressure in visceral pleura and/or hydraulic conductivity of parietal pleura are lower on mediastinal as compared to costal side. However the ventilation and heart-beat dependence of Pliq on cardiac region suggest a possible role of lymphatic in setting pleural liquid pressure.

Animals↗
PubMed1981

Change pattern of pleural deformation pressure on varying lung height and volume.

Simultaneous measurements of pleural surface (Ppl) and liquid (Pliq) pressures were made at various lung heights in lateral and supine dogs on increasing lung volume from FRC to 80% TLC by decreasing abdominal pressure. The difference between Pliq and Ppl, /Pdef liq/, i.e. the pressure elicited by the deformation forces of the contacting pleurae over the areas of intervening liquid, was greater in the superior parts at all lung volumes. Previous data on pleural liquid thickness (9) and the present measurements show that an increase of /Pdef liq/ may occur either with a decrease or an increase of 9. delta Pdef liq/delta Ppl over a given range of Ppl, increases progressively from bottom up. For a given height the greater the initial /Pdef liq/, the greater delta Pdef liq/delta Ppl. When /Pdef liq/ was decreased by injecting liquid into the pleural space at FRC, delta Pdef liq/delta Ppl decreased. Hence, delta Pdef liq/delta Ppl depends on the initial Pdef liq, i.e. upon the initial tightness of fitting of the pleural membranes. A model interpretation of this relationship is provided.

Animals↗
PubMed1981

The role of the pneumotaxic mechanism in the tachypnea of pulmonary vagal origin.

The tachypnea due to stimulation of pulmonary vagal irritant and J.receptors with histamine (5%, aerosol) and phenyldiguanide (150 mu g, i.v.) was studied in 11 pentobarbitone anesthetized cats before and after uni (UL) and bilateral (BL) lesion of sites of the pneumotaxic mechanism. BL prolonged the timing parameters of spontaneous and occluded breaths (no phasic input from pulmonary stretch receptors) more under drug stimulation than in control: thus the shortening effect of drug stimulation increased going from intact to BL. Drug stimulation caused a decrease in volume threshold for inspiratory cut-off and this effect was reduced by about 50% by BL. Under hyperoxic iso-PCO2 conditions drug stimulation reduced the respiratory output (indexed by the rate of change of the pressure developed in the airways during occluded breaths) and this effect was left unaltered by BL. The results suggest that the pneumotaxic mechanism plays a role in the reflex respiratory excitatory frequency effect resulting from activation of irritant and J receptors while it seems to be excluded from a control on respiratory output.

Animals↗
PubMed1981

Respiratory modulation by vagal afferents in pigs.

We have studied the role of pulmonary vagal afferents and baroreceptors of the aortic arch on control of breathing in anaesthetized pigs. As in other species (dog, cats and rabbits) the depth and rate of breathing was found to be controlled by a volume-related vagal feed-back loop from pulmonary stretch receptors. Rapid shallow breathing following histamine aerosol and phenyldiguanide i.v. (which are likely to stimulate pulmonary vagal irratant and J receptors) occurred through a decrease in the activation threshold of the inspiratory cut-off mechanism without altering the matching of inspiratory to expiratory time. These results are also similar to those found in cats and rabbits. Histamine caused an increase in pulmonary resistance and a decrease in compliance: these effects were partially vagally mediated and partially due to a direct stimulation of smooth muscles by the drug. It seems, from relating the respiratory to the vascular systemic effect of histamine administration, that pigs have a greater respiratory response than cats or rabbits. A stepwise decrease in blood pressure through haemorrhage under iso-PCO2 and iso-PO2 conditions was found to affect the matching of the expiratory to the inspiratory time without affecting the activation threshold of the inspiratory cut-off mechanism.

Animals↗
PubMed1980

Stereo-EEG and surgery in partial epilepsy with temporo-parieto-occipital foci.

Six cases of partial epilepsy operated on for lesions at the temporo-parieto-occipital junction are presented. Three cases had signs of enlargement of one lateral ventricle at the temporo-parieto-occipital carrefour, three had a lateral homonymous hemianopsia and all showed lateralizing interictal EEG abnormalities. The manifold features of the seizures could not be related to the involvement of one or more definite cortical areas. Since clinical, radiological, scalp EEG investigations provided no sufficient data to map the epileptogenic lesion to be excised, stereo-EEG studies with chronic depth electrodes were performed. Besides permitting the exact delimitation of the epileptogenic lesion, depth EEG gave the clue for interpreting physiopathological mechanisms underlying the electroclinical seizures in each case.

Adolescent↗
PubMed1980

Late results of stereotactic radiofrequency lesions in epilepsy.

Thirty-five patients with partial complex seizures and two patients with generalized epilepsy were treated by stereotactic radiofrequency lesions. Follow-up from 2 to 13 years was available in 30 patients. The stereotactic targets in patients with partial complex seizures were: a) Amygdala; b) Ammon's horns; c) parahippocampal gyrus; d) Fornix. Depending on scalp EEG and depth electrode studies, each patient had one or more target coagulated, unilaterally or bilaterally. In the 2 cases of generalized epilepsy, bilateral Forel field lesions were performed. Late surgical results are discussed in relation to the depth EEG studies and the number and site of stereotactic lesions.

Adolescent↗
PubMed1980

Pattern of breathing and mouth occlusion pressure during acclimatization to high altitude.

Pattern of breathing and mouth occlusion pressure have been investigated during a 6-day sojourn at an altitude of 3457 m in six resting subjects breathing ambient air or an hyperoxic mixture. It has been shown that ventilation increases and alveolar PCO2 decreases, both variables reaching a steady-state after about 4 days at altitude. Changes in ventilation are caused by modifications, at first, in the timing component of the respiratory cycle and later on, in the mean inspiratory airflow. This suggests that the output of the respiratory center is qualitatively modified during the acclimatization period. Mouth occlusion pressure, an index of neuromuscular inspiratory drive, increased on the first day at altitude, remaining constant thereafter. The mean inspiratory flow did not change on the first day, but progressively increased in the subsequent 3 days. The observation that flow increased in the face of a constant neuromuscular inspiratory drive suggests that during acclimatization to altitudes, the progressive increase in ventilation is due to changes in mechanics of the ventilatory pump rather than changes in central neural drive.

Acclimatization↗
PubMed1980

Pleural liquid and surface pressures at various lung volumes.

Simultaneous measurements of pleural surface (Ppl) and liquid (Pliq) pressures at similar lung height were performed in supine dogs from FRC to about 80% TLC. Lung volume was increased by lowering abdominal pressure so that pressure in the lung remained equal to atmospheric. The difference between Pliq and Ppl (i.e. the pressure elicited by the deformation forces of the contacting pleurae over the areas of intervening liquid) increased progressively with the increase of lung volume, being about -7 cm H2O at Ppl=-2.5 cm H2O and -30 at Ppl=-14. The relationship between Pliq and Ppl was similar in the 2nd and 5th intercostal spaces. From this relationship and previous data on pleural surface area, pleural liquid thickness and cells, and pleural microvilli an attempt was made to get indirect information on pleural contact area through cells and microvilli and pleural contact pressure at various lung volumes.

Animals↗
PubMed1980

Control of breathing during acute hemorrhage in anesthetized cats.

We studied in anesthetized cats the ventilatory response to acute blood loss under hyperoxic iso-capnic conditions. From a blood pressure, of approximately 150 down to approximately 70 mm Hg ventilation increased on the average by 2.5 times. The ventilatory response was characterized by two phases: there was an initial phase (down to a PB approximately 100 mm Hg) of increase in frequency due to an excitatory effect on bulbo-pontine respiratory timing which was estimated from the duration of breaths following occlusion of the airways at the end expiratory volume. This effect was mainly due to the withdrawal of inhibitory afferents from the baroreceptors of the aortic arch. To this phase corresponded the phase of vasomotor compensation. Subsequently there was a phase of excitatory effect on the respiratory output which was estimated from the rate of change of the pressure developed in the airways during occluded breaths. This effect was mainly due to afferents from carotid sinuses; a minor role was due to the decrease in inhibitory afferents from carotid baroreceptors while the greater part was likely to be due to the hypoxic stimulation of glomus cells due to reduced blood flow. Following vagotomy above the superior laryngeal and sinus denervation the excitatory effect on respiratory timing and output were reduced to about 30% of that observed in intact cats.

Acute Disease↗
PubMed1979

Histamine and phenyldiguanide induced tachypnea in hypercapnia and hypoxia.

The rapid shallow breathing of pulmonary vagal origin following administration of histamine (H) and phenyldiguanide (PDG) was studied at different levels of hypercapnic and hypoxic stimulation. At all levels of chemical drive H and PDG caused an excitatory effect on timing of breathing and an inhibitory effect on the respiratory output. The latter was evaluated from the mean inspiratory flow rate and the mean rate of change of pressure developed in the lungs during an inspiratory effort against closed airways. The timing effect was greater at low than at high PaCO2 while the opposite was true for the output effect. At all PaCO2, H and PDG decreased the volume-threshold for termination of inspiration (leftward displacement of the VT vs TI relationship) of the VT Vs TI relationship). Hypoxia increased the respiratory output in control as much as with drug stimulation. Moreover, hypoxia did not affect the volume-threshold curve both in control and with H and PDG. We concluded that vagal afferents stimulated by H and PDG (irritant and/or J receptors) interfere with the timing and output response to central chemoreceptors stimulation (CO2 sensitivity) without affecting the response to peripheral chemoreceptors stimulation (mainly hypoxic chemosensitivity).

Animals↗
PubMed1978

The mechanism of rapid shallow breathing due to histamine and phenyldiguanide in cats and rabbits.

In anaesthetized cats and rabbits we analyzed the rapid shallow breathing following exposure to histamine aerosol (mainly an irritant receptor stimulant) and i.v. injection of phenyldiguanide (mainly a J receptor stimulant). Both drugs caused a marked leftward displacement of the tidal volume (VT) vs inspiratory time (TI) relationship (Hering-Breuer threshold curve) without a corresponding increase in inspiratory flow rate so that inspiration was cut off at a lower VT and TI. The leftward displacement of the VT vs TI relationship occurred with a great shortening of the duration of inspiration during occluded breaths (T0I) accompanied by a shortening of the expiratory phase (T0E). These parameters monitored the central respiratory rhythm in absence of the phasic lung volume related vagal loop. It is suggested that the increased central respiratory frequency was due to the augmented firing of fibers from stimulated irritant and J receptors. Stimulation of these endings also caused the TE vs TI relationship to become steeper in cats and to be displaced downwards in rabbits.

Aerosols↗
PubMed1976

Effect of rib cage or abdomen compression at iso-lung volume on breathing pattern.

In anesthetized rabbits a small compression of the rib cage (RC) caused a marked increase of breathing frequency (f), a marked reduction of expiratory duration (Te), a reduction of inspiratory duration (Ti) and tidal volume (VT), while an equal decrease of lung volume produced by abdominal compression(AC) caused a smaller increase of f and no change of Ti, and a slight increase of VT. Similar results occurred when normal end-expiratory volume was maintained during compression. The phenomena disappeared after bilateral vagotomy, whereas persisted after cordotomy in T1. Similar results occurred in dogs (with the exception that VT decreased during AC), whereas in cats only RC increased f by shortening Te. RC caused a marked increase of discharge in 11 out of 19 irritant receptor fibers, whereas AC caused an increase only in 2. In most of the pulmonary stretch receptor fibers the change of activity produced by compression paralleled the lung volume change. The effects of vagal cooling on Ti, Te and the VT-Ti relationship with and without compression suggest irritant receptors as responsible for the different ventilatory pattern during RC and AC.

Abdomen↗
PubMed1976

Role of peripheral and central chemosensitive afferents in the control of depth and frequency of breathing.

In anaesthetized cats the response to hypercapnia was studied during normoxia, hypoxia (increased peripheral chemosensitive afferents, IPA) and after carotid sinus denervation (decreased peripheral chemosensitive afferents, DPA) in terms of: (a) central output to the inspiratory muscles, (b) bulbopontine respiratory activity and (c) threshold-inhibition curve for termination of inspiration (Vr/Ti relationship). IPA increased, whereas DPA decreased the central output, as estimated from the rate of change of the subatmospheric pressure developed in the trachea during occlusion of the airways. IPA and DPA did not modify the bulbo-pontine rhythm, as estimated from the timing of occluded breaths (phasic vagal afferents nil), nor the Vt/Ti relationship, both of which have been shown to vary as a function of PACO2. It is concluded that peripheral chemosensitive afferents influence only the output of the respiratory centres, whereas central chemosensitive afferents influence also the bulbo-pontine respiratory rhythm and the threshold inhibition curve for termination of inspiration.

Animals↗
PubMed1976

Effect of mechanical factors on the relation between rate and depth of breathing in cats.

In anesthetized tracheotomized cats we compared the time sequence of ventilatory events with neurological events (electrical activity of the diaphragm) during the breathing cycle. We found that under control conditions a phase shift existed between the neurological and the spirometric duration of inspiration, amounting to about 150 ms. This phase shift was increased by increasing the time constant of the respiratory system (resistive loading) and decreased by decreasing it (elastic loading). These phase shifts resulted in a difference in the appreciation of the volume responsible for the termination of inspiration (Hering-Breuer inhibition) because the volume corresponding to the end of the neurological event was somewhat smaller than the final tidal volume reached.

Animals↗
PubMed1975

Contribution of hypercapnic stimuli and of vagal afferents to the timing of breathing in anesthetized cats.

In tracheotomized, anesthetized cats, the authors studied the role of phasic and tonic vagal discharge and of hypercapnic stimuli on the timing of breathing. The effect of tonic vagal discharge was separated from that of the other two parameters by comparing the duration of inspiration and of expiration of control breaths with those obtained during occlusions of the airways at FRC (bulbo-pontine activity). The effect of tonic vagal discharge was then separated from that of hypercapnic stimuli by comparing the bulbo-pontine activity before and after vagotomy. Hypercapnia caused shortening of inspiratory and expiratory duration set by the bulbo-pontine pacemaker and increased sensitivity of the respiratory centers for a given phasic vagal input (displacement to the left of the tidal volume vs inspiratory duration relationship). Vagotomy did not modify the bulbo-pontine duration of inspiration nor its possibility to shorten in hypercapnia; by contrast it caused a lengthening of the expiratory time which did not shorten any more in hypercapnia, suggesting that tonic vagal discharge mainly influences the expiratory duration.

Animals↗