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Biomedical subjects

L Fedina

Publications and source records attributed to L Fedina.

At least 19 recordsLinked to original sources
PubMed1998

[Influence of auxiliary materials on the proportion of effective particle size of metered-dose suspension type aerosols].

The aim of the present study was to formulate suspension type inhalation aerosols by various types of auxiliary materials, and to select the formulation with the highest proportion of the effective particle size. The examined suspension type aerosol contained sodium cromoglycate as an active compound. For the stabilization of the suspension, the applied surface active ingredients were oleic acid and oleyl oleate, and dimethyl siloxane polymer was selected as hydrophobizing agent. Factorial design was used for the optimization of the experimental results. On the basis of our results, the correct types and amounts of auxiliary materials can be selected to obtain the therapeutically effective formulation.

Administration, Inhalation↗
PubMed1996

[Usage modeling test in aerosols formulations].

Authors emphasize the importance of "usage-modelling" test concerning the uniformity of doses in the case of aerosol formulations, containing propellants or supplied with atomising devices. Weight measurement was carried out to identify the uniformity of doses per actuation keeping non-use periods in the case of water-based solutions with different density and suspension containing HFC propellants. It can be concluded that uniformity of doses--applying non-use periods during the testing time--significantly depends on the composition, the density of the formulation and the spraying mechanism of the atomising device.

Aerosols↗
PubMed1993

Differential sympathetic reactions during cerebral ischaemia in cats: the role of desynchronized nerve discharge.

1. Sympathetic nerve discharge (SND) of three postganglionic nerves with different functions and anatomical locations was simultaneously recorded at rest and during severe cerebral ischaemia (Cushing reaction). The three nerves, controlling the heart (inferior cardiac nerve), visceral (renal nerve) and skeletal muscle circulation (vertebral nerve), were selected with the assumption that their activity pattern will represent the differential central autonomic command to the major players of the circulatory response to cerebral ischaemia. 2. Changes in the power density spectra of the nerve signals, and in the pairwise coherence functions, elicited by the cerebral ischaemia, were evaluated separately for the rhythmic (R-SND, i.e. between 0 and 6 Hz) and high-frequency (HF-SND, i.e. between 12 and 100 Hz) components of the nerve signals. 3. The sympathetic nerve response to cerebral ischaemia developed in two phases. Phase 1 was a massive R-SND reaction and phase 2 was characterized by SND desynchronization and by the emergence of HF-SND. The power of HF-SND occupied a wide band between 12 and 80 Hz with maximum between 20 and 30 Hz. All three nerves were involved in the Cushing response but the magnitude and character of the reactions were specific for each nerve. In the cardiac nerve, the power of the rhythmic component of the discharge increased almost twice the control and remained dominant during the whole reaction, strongly modulating HF-SND during the second phase. In the vasomotor nerves, R-SND was suppressed during phase 2 and HF-SND occupied 65% of the total power of the signal. Near equal R- to HF-SND proportions, however, were reached on different activity levels in renal and vertebral nerves. Whereas total renal SND did not change, the power of the vertebral SND increased more than twice. In addition, desynchronization in the vertebral SND was preceded by a massive R-SND reaction during phase 1, which was missing in the renal nerve. 4. For all possible nerve pairs, R-SND was highly coherent before the reaction and remained so during intracranial pressure elevation, regardless of the direction and magnitude of the changes in absolute and/or relative power of this component in different nerves. On the other hand, HF-SND never correlated between any of the nerve pairs indicating that this component in each nerve originated from specific sources of regional sympathetic activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Effect of preexisting brain ischemia on sympathetic nerve response to intracranial hypertension.

The performance of the sympathetic nervous system during sustained moderate cerebral ischemia (CI) was examined in the present study. For this purpose, a Cushing response was elicited repeatedly during incomplete global CI in anesthetized artificially ventilated cats after vagotomy and baroreceptor denervation. In control animals without CI, sympathetic activity in response to brief elevation of intracranial pressure (ICP) showed a well-repeatable two-phase reaction. During CI there was a progressive deterioration of background sympathetic nerve discharge (SND) over a period of 30 min. SND response to repeated elevation of ICP was initially similar to control response but later with progression of CI was seriously changed. 1) Instead of the usual hyperactivation, sympathetic nerve activity was depressed during intracranial hypertension. 2) The characteristic desynchronized activity either appeared later during the reperfusion period or remained absent. The progressive loss of SND response to raised ICP in developed CI was compared with the changes seen in experiments in which repeated ICP elevations were superimposed on asphyxia. These findings suggest that the sympathetic component of the Cushing reaction strongly depends on the actual state of brain stem autonomic circuits and may be seriously altered in pathological situations involving ischemic brain injury.

Animals↗
PubMed1990

Comparison of methods eliciting cerebral ischaemic pressor response in the cat.

Three methods of intercepting the blood supply to the brain were tested by means of X-ray angiography and by monitoring the pressor response following cerebral ischaemia. The methods were: (1) occlusion of carotid and basilar artery; (2) occlusion of carotids and vertebral arteries in the cervical canal of the third vertebra; (3) occlusion of carotid and subclavian arteries. The X-ray angiographs showed that in most cases we could close the accessory sources of the cerebral circulation and drastically reduce the blood supply to the brain of the cat. With all three methods the cerebral ischaemia evoked strong blood pressor elevation, which was weaker however when the carotid and basilar artery were clamped, in comparison with the other two methods. This may be explained by the existence of small arteries supplying the lower brain stem and originating intracranially from the vertebral artery near to the junction of the vertebral and anterior spinal artery.

Animals↗
PubMed1989

Transplantation of cultured embryonic spinal cord grafts into the hemisected spinal cord of adult rabbits.

Spinal cord fragments from 20-day-old rabbit embryos cultivated for 1 week were transplanted into the hemisected and intact spinal cord of adult rabbits. The morphological changes at the site of intervention were investigated by light and electron microscopy 3, 12, and 29 weeks following implantation. In 80% of the animals the procedure was successful. The implants grew in volume, the cells matured, and many new neural processes with myelinization and synapse formation appeared. The histological findings indicate the survival, maturation, and integration of transplanted cultured embryonic spinal cord tissue in the lesioned adult spinal cord.

Animals↗
PubMed1989

Two-phase change of sympathetic rhythms in brain ischemia, Cushing reaction, and asphyxia.

The present study was designed to determine the extent to which the brain stem neural networks, normally capable of synchronizing the sympathetic nerve discharge (SND) into 2- to 6- and 10-Hz rhythmic fluctuations, contribute to the control of autonomic reactions during brain hypoxia and/or hypercapnia. Vertebral, cardiac, and renal nerve discharges were recorded electrophysiologically in 34 anesthetized, curarized, and artificially ventilated cats. The sympathetic nerve responses to cerebral ischemia (elicited by reducing the blood supply to the brain), intracranial pressure elevation (Cushing reaction), and systemic asphyxia were tested with special focus on the rhythmic structure of the SND. It has been found that there are two phases of SND changes during cerebral ischemia differing mainly in the frequency content of the signals and less in the compound action potential amplitude. During the first phase the rhythmic generators controlling the tonic sympathetic outflow are more strongly activated, which is reflected in a stronger, more regular, and more widespread manifestation of these rhythms on the efferent neurograms. After some time the normal SND structure abruptly changes to a desynchronized activity with loss of the three main sympathetic rhythms and responsiveness to baroreceptor reflex activation. The same stereotyped changes can be observed regardless of the way in which the brain hypoxia and/or hypercapnia has been produced. Nor does the denervation of peripheral baro- and chemoreceptors substantially alter the general pattern of the responses.

Animals↗
PubMed1986

Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part I: Observations at the time of intracranial hypertension.

The origin and pathomechanism of vegetative disturbances in patients suffering from subarachnoid haemorrhage are not completely clarified. Since some of these alterations in vegetative functions may well be attributed to acute changes in sympathetic activity, we initiated a study to investigate this modality in experimentally induced subarachnoid haemorrhage. Experiments were performed on 51 cats, anaesthetized with alpha-chloralose and urethane, immobilized and artificially ventilated. Compound electrical discharges of the left vertebral, cardiac and renal sympathetic nerves, ECG, EEG, end-tidal CO2, systemic arterial blood pressure and intracranial pressure were recorded on a polygraph. Subarachnoid haemorrhage was simulated by the injection of 1-5 ml of fresh, autologous blood into the cisterna magna. Mock cerebrospinal fluid was also injected as a control. Our results showed that in induced subarachnoid haemorrhage, not the blood itself but the intracranial pressure elevation might be responsible for the strong increase in sympathetic efferent activity. With the direct recording of the electrical activity of the three sympathetic nerves, we were able to verify the sympathetic overactivity underlying the cardiovascular disturbances during intracranial pressure elevation. Regarding the mechanism of the overactivity, most probably not the ischaemia or hypoxia, but the mechanical distortion of the medulla could be the adequate stimulus of the sympathetic overactivity and the Cushing response during intracranial pressure elevation.

Animals↗
PubMed1986

Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part II: Observations during the "early vasospasm" period.

The efferent activity of the vertebral, cardiac and renal sympathetic nerves was recorded during the so-called "early vasospasm" period, 25-30 minutes after experimentally induced subarachnoid haemorrhage. Experiments were performed on 51 cats with methods described in Part I of our publication. The animals were held either in a sphynx-like position (Pos. I), or in head-down position (Pos. II), when the level of the cisterna magna was 2-3 cm below the level of the spinal cord, facilitating the injected blood to flow in to, and remain at the base of the brain. According to our results during the "early vasospasm" period, we could not observe such changes in the sympathetic efferent activity, which could be specific for this period. With the gradual decrease in the intracranial pressure, the sympathetic overactivity ceased, and in most cases the level of activity was similar to that of the preinjection period. Our results also indicate that because of the remarkable variability of the activity of the renal sympathetic nerve during the intracranial pressure elevation, recording the activity of one sympathetic nerve only may give misleading results concerning the activity of the whole sympathetic system.

Animals↗
PubMed1975

Facilitation from contralateral primary afferents of interneuronal transmission in the Ia inhibitory pathway to motoneurones.

The action of volleys in contralateral primary afferents on transmission in the Ia inhibitory pathways to motoneurones was investigated with intracellular recording from motoneurones. Ia IPSPs in flexor as well as most extensor motoneurones were regularly facilitated by volleys in contralateral high threshold muscle, cutaneous and joint afferents in spinal cats under chloralose anaesthesia. In decerebrate cats with a low pontine lesion transmission in Ia inhibitory pathways was not facilitated but rather depressed by volleys in these afferents. The recurrent effects from motor axon collaterals were investigated on inhibitory transmission from different contralateral afferents to motoneurones. Previous investigations have shown that the interneurones mediating the reciprocal Ia inhibition receive recurrent inhibition via motor axon collaterals and Renshaw cells. Now a strong positive correlation was revealed between recurrent depression of IPSPs evoked from different contralateral afferents and facilitation of Ia IPSPs by the same afferent volleys. These results suggest that the recurrent depression of IPSPs from different contralateral primary afferents depends on their excitatory convergence onto the Ia inhibitory interneurones, which then partly mediate the IPSP evoked in the motoneurone from these afferents.

Animals↗
PubMed1975

Specific baroreceptor control of vertebral and cardiac sympathetic activity.

The effect of bilateral carotid occlusion (BCO) on the activity of the vertebral and cardiac sympathetic efferent nerves was studied in gallamine-immobilized and artificially ventilated cats under chloralose-urethane anaesthesia. Electrical activity of the vertebral and cardiac nerves (VNA and CNA), their integram, arterial blood pressure and respiration were recorded. BCO led to an increase in VNA persisting throughout the occlusion period, while merely a transient increase took place in CNA. When blood pressure was kept at a constant level or the depressor nerves was transected, CNA responded to BCO with a lasting increase. Electrical stimulation of the central stump of the left depressor nerve inhibited CNA much more than VNA. It is assumed that the selective inhibition of CNA, after a transient increase, arises as a consequence of a rise in blood pressure, i.e. of consecutive aortic baroreceptor excitation.

Action Potentials↗