This paper describes the methods of prevention of delayed neurological deficit (DND) in patients with subarachnoid haemorrhage (SAH) due to ruptured intracranial aneurysm. To prevent the decrease in the cerebral flow, vasodilators, inhibitors of platelet aggregation and synthesis of endogenous prostaglandins, stimulators of prostacyclin synthesis of its analogue should be applied. It is also recommended to use the inhibitors of phosphodiesterase, blockers of serotonin and of calcium channel (particularly nimodipine). Therapy with the immunosuppressive drugs helps to prevent DND. With all those therapeutical methods DND is still a serious complication following SAH.

Cerebral Arteries↗

PubMedDate not supplied

[Spasm of intracranial arteries or spastic syndrome in ruptured cerebral aneurysm?].

Cerebral vasospasm is the most serious complication of intracranial hemorrhage rupture. For example, the resulting neurological deficits affect more than 30 thousand patients in North America. Subarachnoid hemorrhage is accompanied by the release of more than 50 endogenous substances, most possessing vasoconstrictory activities. There are many theories explaining the pathogenesis of vasospasm following SAH. The most popular is the theory of direct vasoconstrictory activity of releasing substances on a vessel wall. The other one describes the narrowing of vessel lumen as a result of angiopathic process. The other theories include the vasoactive, neurotoxic and ++immuno-aggressive concepts of neurological deficit in following aneurysm rupture. The relationship between the vasospasm and the neurological deficit is also discussed.

Cerebral Arterial Diseases↗

PubMedDate not supplied

Split-respiratory centre in the dog.

Explore the source record for details and available documents.

Animals↗

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.

Animals↗

PubMedDate not supplied

Decrease of oxygen difference between arterial blood and cerebrospinal fluid after intravenous injection of sodium bicarbonate in hyperoxic patients, anaesthetized, paralyzed and artificially ventilated.

In the subjects being prepared to neurosurgical treatment an i.v. injection of NaHCO3 (2 mEq/kg) elicited a significant increase in PCSFO2 from 69 +/- 6.4 (SEM) Torr to 75.5 +/- 3.9 (SEM) Torr. This change ws accompanied by a significant drop of PaO2 from 150.5 +/- 6.0 Torr to 138.0 +/- 5.8 Torr. Metabolic alkalosis (pH 7.54 +/- 0.02 SEM) elicited by bicarbonate administration was accompanied by arterial blood hyperoxia. Both these factors reduce the cerebral flow (CBF). We suppose that changes in the blood--CSF oxygen relationship reflect the presence of a mechanism which might protect the CNS against a decrease in CBF.

Adult↗

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.

Animals↗

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.

Animals↗

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.

Animals↗

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.

Animals↗

PubMedDate not supplied

Reversal of oxygen difference between arterial blood and cerebrospinal fluid in the rabbit.

The experiments were carried out in rabbits under general anaesthesia with muscle relaxation and artificial ventilation with atmospheric air. Samples of arterial blood and cerebrospinal fluid were obtained. Of particular interest was reversal of the oxygen gradient, that is PaO2 less than PCSFO2 at arterial blood hypoxia below 65 Torr. The animals were given then acetazolamide intravenously which was followed by acidification and increased partial oxygen pressure in the arterial blood. At the same time the oxygen gradient between the arterial blood and cerebrospinal fluid (CSF) practically disappeared. Administration of a hypoxic breathing mixture reversed again the oxygen gradient. It is worth stressing that the pH of the arterial blood showed no statistically significant fall. In view of this it is postulated that Bohr's effect is not responsible for the reversal of the oxygen gradient although it has been suggested by Jankowska and Grieb [13]. We put forward the hypothesis that the rate of oxygen passage on the arterial side of the blood-brain barrier is not identical in both directions, and its passage from the blood into the CSF decreases with increasing arterial hypoxia. This mechanism of "oxygen trap" may be the cause of reversal of the oxygen gradient between the arterial blood and CSF in hypoxia.

Animals↗

PubMedDate not supplied

Effect of acute haemorrhage and autotransfusion on respiration in the pig.

The effect of haemorrhage and transfusion of blood on minute ventilation, VE, in eight anaesthetized pigs was studied by bleeding the animals from the jugular vein and retransfusion of the same quantity of blood. Bleeding the pig from the jugular vein at approximately 50 ml/min, during 2 min, decreased V/ by 8.4 +/- 5.6 per cent of the pre-bleeding control valve (p = 0.0004) and when the same quantity of blood was retransfused the VE increased by 11.8 +/- 12.4 per cent (p=0.03). The possible mechanisms are discussed. We conclude that: a) mechanoreceptors localized in pulmonary circulation play an important role in the VE response during the first seconds of venous haemorrhage and venous transfusion, b) autotransfusion from moving legs and its effect on pulmonary mechanoreceptors may explain in part hyperpnoea at the onset of muscular exercise.

Animals↗