Biomedical subjects

K Głowicki

Publications and source records attributed to K Głowicki.

10 recordsLinked to original sources

PubMed1992

The possible role of endothelium in prevention of rebleeding in experimental subarachnoid hemorrhage (SAH).

Experiments were performed on six male cats under nitrous oxide in oxygen anesthesia. Animals were paralysed and artificially ventilated. Subarachnoid hemorrhage (SAH) was produced by basilar artery puncture following clivectomy. After 10 minutes (3 cats) and 60 minutes (3 cats) the basilar artery was dissected and fixed for electronmicroscopic examination. Ultrastructural examinations revealed in the cytoplasm of the endothelial cells on the side of the vessel lumen, the presence of spherical or flattened cylindrical structures identified as Weibel-Palade bodies. In the endothelium of the proximal segment, 10 and 60 minutes after puncture, the number of these electron-dense bodies increased, and was higher than in the corresponding distal segment. The possible role of the Weibel-Palade bodies in SAH after-effects is discussed.

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PubMed1991

The respiratory response to magnetic stimulation of the cortex in the unanaesthetized baboon.

Transcranial magnetic stimulation has been used to study cortical input to the respiratory system in unanaesthetized baboons. Single magnetic pulse caused usually a short-latency excitation with subsequent inhibition in stimulated inspiratory phase and change in the amplitude and timing of the respiratory cycle. The results suggest that cortical information is processed by the medullary pattern generator.

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PubMed1985

Influence of vagal input on cerebral blood flow in monkeys and dogs after experimental cerebral vasospasm.

Cerebral blood flow (CBF) was a response to experimental subarachnoid haemorrhage (SAH) in four monkeys ,and three dogs. Decrease in CBF was observed in the white and gray matter and in the flow measured within the internal carotid artery as the result of SAH. Bilateral vagotomy enhanced CBF in the gray matter and blood flow in the internal carotid artery to values exceeding the control ones. Results suggest the existence of a receptor susceptible to subarachnoid haemorrhage and connected with vagal nuclei.

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PubMed1984

Response of respiratory motoneurons to release from vagal inhibition in the rabbit.

Long-lasting effects of vagal input on phrenic (Phr) and external intercostal (EI) motoneuronal output were studied on 16 anesthetized rabbits breathing spontaneously or paralysed and ventilated by a phrenic nerve-driven pump. Withholding of ventilation by tracheal occlusion or by switching off the servorespirator maintained for seven breaths evoked a progressive increase of Phr and EI from breath to breath. This effect was more evident in animals ventilated by servo- respirator. The higher was the gain of the pump (volume-to-phrenic signal ratio) before the maneuvre, the bigger was the rate of increase of the tidal phrenic amplitude from breath to breath at all CO2, levels tested. Vagotomy strongly depressed or eliminated this effect. We conclude that with intact vagus nerve the increase of respiratory motoneuronal output was only partialy due to the gradual increase in chemical drive when ventilation was stopped. The character of the response indicates the existence of a long-lasting component of the Breuer-Hering reflex. Splitting the medulla abolished this prolonged response while preserving the inspiratory vagal inhibition indicates that the neuronal pathways crossing the midline of .the medulla are important for the effect.

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PubMedDate not supplied

Cerebral blood flow in split-brainstem rabbits.

Cerebral blood flow (CBF), mean arterial pressure (MAP) and heart rate (HR) were recorded in anaesthetised, vagotomised, paralysed and artificially ventilated rabbits before and after a mid-sagittal section of the lower brainstem ("split-respiratory centre"). Splitting the medulla elicited first a small decrease and then an increase in CBF, a decrease in HR but no change in MAP. Hypoxia reduced CBF but did not modify MAP or HR. Hypercapnia did not significantly affect any of these parameters. It is concluded that a midline section of the rabbit's medulla and lower pons does not impair CBF and therefore the decrease in output from the respiratory controller, observed in split-brainstem animals, is not likely to be elicited by alterations in CBF.

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PubMedDate not supplied

Minute ventilation changes in rabbits during experimental hypothermia.

The effect of experimental hypothermia on changes of the electrophysiological equivalent of minute ventilation (Veq) was studied in rabbits under urethane-chloralose general anaesthesia with muscle relaxation and artificial ventilation. The animals were subjected to bilateral vagotomy prior to the experiment. During normothermia (37.5 +/- 0.7 degree C) and hypothermia (29.9 +/- 1.7 degrees C) the animals were given for breathing a hypercapnic mixture of gases (CO2 5% with O2 95%) and asphyxia was produced by switching off the respirator. The arterial blood pressure, blood flow in the common carotid artery, end-expiratory CO2 concentration, "integrated" phernic nerve activity and brain-stem temperature were recorded. The partial pressure of carbon dioxide and oxygen, hydrogen ion concentration and arterial acid-base balance were determined with correction for temperature changes. The equivalent of minute ventilation (being the product of the frequency and amplitude of "integrated" phrenic nerve activity) decreased in hypothermia by 91%, with a simultaneous fall of PaCO2 from 33,48 +/- 3.84 mmHg to 23.40 +/- 3.59 mmHg (by 30%). The hypercapnic stimulus applied during hypothermia produced a fivefold lower Veq value than in normothermia and under control conditions (despite a similar value of PaCO2 of 28.89 +/- 3.12 mmHg). The Veq value approaching that found under normal conditions in normothermia was observed during hypothermia only when asphyxia was induced when the value of PaCO2 was 37.07 +/- 8.74 mm Hg and that of PaO2 was 37.41 +/- 29.11 mmHg. During hypothermia the blood flow in the common carotid artery decreased by 16% when the animals were breathing the hypercapnic mixture. The analysis of the obtained results showed a direct effect of temperature on respiratory activity generation and regulation of arterial blood flow to the brain. It may be supposed also that hypothermia raises the response threshold to CO2 level in the breathed air.

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PubMedDate not supplied

Effect of lowered temperature on respiratory rhythm generation in rabbit.

It was tried in this study to determine the effects of temperature and carbon dioxide on the respiratory drive under experimental hypothermia in rabbits under urethane-chloralose anaesthesia after muscle-relaxant administration, after bilateral vagotomy and during artificial ventilation with a biologically-controlled respirator. Hypercapnia was produced in the animals during normothermia (37.3 +/- 0.7 degrees C) and hypothermia (30.0 +/- 1.5 degrees C). The basic physiological parameters and efferent activity of the phrenic nerve were recorded, and arterial blood gasometric parameters were determined. The electrophysiological equivalent of minute ventilation (Veq) decreased during hypothermia by 33% on the average while the PaCO2 value was unchanged. The hypercapnic stimulus applied during hypothermia failed also to raise the Veq value to its initial level. A 9% fall of blood flow was observed in the common carotid artery when the animals received a hypercapnic gas mixture for breathing during hypothermia. The results obtained in this study and earlier observations confirm unequivocally the hypothesis of a direct influence of temperature lowering on respiratory rhythm generation and regulation of arterial blood flow to the brain.

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PubMedDate not supplied

Changes of minute ventilation in rabbits in experimental hyperthermia.

The relative effect of the temperature on respiratory rhythm generation was studied in muscle-relaxed, artificially ventilated and bilaterally vagotomized rabbits under general anaesthesia (urethane and chloralose). Hypercapnia was produced during normothermia (38.8 +/- 0.6 degrees C) and hyperthermia (40.5 +/- 0.3 degrees C). The basic physiological parameters, efferent phrenic nerve activity and gasometric determinations in arterial blood were recorded. In the animals ventilated with a classic respirator hyperthermia produced a 118% increase of Veq value with a simultaneous 28% rise of the partial pressure of CO2. An increase of the stroke volume of the respirator during hyperthermia (in a degree sufficient for achieving PaCO2 value equal to the control value during normothermia) produced a 2% fall of Veq value due to an 8% fall in amplitude of the respiratory movements without changes of respiratory rate. Breathing in of a hypercapnic mixture caused a 131% rise of Veq above the control value in normothermia. This rise was due both to the increased respiratory rate and respiratory amplitude. During ventilation by means of a respirator controlled by phrenic nerve activity hyperthermia increased the electrophysiological equivalent of minute ventilation by 34%, with a 109% rise in the respiratory rate and with no change in PaCO2. Breathing of a hypercapnic mixture increased Veq without inducing any statistically significant changes in the respiratory rate and amplitude. The analysis of the results suggests that the effect of raised temperature on respiratory rhythm generation is manifested mainly as an impairment of the respiratory amplitude. Maintaining of minute ventilation proportional to the magnitude of respiratory drive is decisive in this phenomenon.

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PubMedDate not supplied

"Paradoxical" effect of carbon dioxide on common carotid artery blood flow in rabbits during hypothermia and hyperthermia.

The relative effects of temperature and CO2 on the blood flow in the common carotid artery (CCBF) were investigated in vagotomized, paralyzed rabbits under urethane-chloralose general anaesthesia with artificial ventilation. During hypothermia a 52% fall of CCBF was observed in rabbits ventilated by the classic method. Administration of a hyperkapnic mixture for breathing caused a further 16% CCBF fall, with a simultaneous rise in PaCO2 by 23%. During ventilation with a respirator triggered by phrenic nerve activity hypothermia caused a 30% CCBF fall without changes in PaCO2 value. Administration of the hyperkapnic mixture for breathing caused, in these circumstances, a 9% CCBF fall with a 7% PaCO2 increase. Hyperthermia caused during ventilation by the classic method a 42% rise in CCBF and a 22% PaCO2 rise. The hyperkapnic mixture given for breathing decreased the CCBF by 9% and increased the PaCO2 by 15%. On the other hand, during ventilation with the respirator triggered by phrenic nerve activity no changes were observed in these parameters. This suggests that the thermic stimulus exerts a direct effect on the regulation of the blood flow to the brain, and during hypothermia it prevails over the stimulus produced by CO2.

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PubMedDate not supplied

Differentiation of respiratory reflexes by electrical stimulation and cold blockade of the vagus nerve in rabbits.

Using cold blockade of conduction in the myelinated nerve fibres respiratory effects were studied evoked by centripetal stimulation of the vagus nerve. The experiments were carried out on rabbits under general anaesthesia with halothane and with artificial ventilation. The vagus nerves were cut in the neck and one of them was adapted for stimulation of its proximal part. Electrical stimulation was applied in expiration using impulse frequency 50/sec. The direction of the response (i.e. prolongation or shortening of the expiration phase during stimulus application) served for determination of the excitation threshold of the afferent fibres from slowly-adapting and rapidly-adapting pulmonary mechanoreceptors. It was found that the conduction in the afferent fibres from the slowly-adapting pulmonary receptors could be blocked selectively with cooling temperatures 8-10 degrees C.

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