Biomedical subjects

A Chodobski

Publications and source records attributed to A Chodobski.

25 records · Page 2Linked to original sources

PubMed1992

Atrial natriuretic peptide does not alter cerebrospinal fluid formation in sheep.

Because the choroid plexus has been shown to have a high density of atrial natriuretic peptide (ANP) binding sites, we investigated the effect of intracerebroventricular and intravenous administrations of ANP on cerebrospinal fluid (CSF) formation. CSF formation rate was measured in conscious sheep with a dye-dilution method using blue dextran 2000 as an indicator substance. During the experiment animals were partially restrained in a sling, and their ventricular systems were perfused with artificial CSF containing the indicator substance. ANP (alpha-human ANP) administered centrally at rates of 0.015-15 ng/min, resulting in CSF ANP concentrations ranging from physiological to pharmacological CSF hormone levels, was found not to influence CSF formation. Similarly, intravenous administration of ANP at a rate of 10 ng.kg-1.min-1 did not affect CSF formation, i.e., decreases in CSF formation rate in all experiments involving ANP administration were not significantly different from those observed in time control experiments. Our results suggest that ANP does not significantly affect CSF production in sheep. It is possible that the lack of effect of ANP on CSF formation is associated with the predominance in the choroid plexus of clearance receptors over biologically active receptors.

Animals↗

PubMed1990

Effect of arginine vasopressin on CSF composition and bulk flow in hyperosmolar state.

To find out whether central arginine vasopressin (AVP) plays a role in regulation of cerebrospinal fluid (CSF) composition and of CSF bulk flow (CSFbf) in acute hyperosmolar state, the experiments were performed on 16 anesthetized cats in which the ventriculocisternal system was perfused either with artificial CSF (aCSF; 8 control experiments) or with aCSF containing AVP (10 microU/min, 8 experiments) before, during, and after intravenous infusion of 5% NaCl. In both series, hyperosmotic infusion significantly increased CSF osmolality (CSFosmol) and sodium (CSFNa) and potassium (CSFK) concentration and reduced CSFbf. Administration of AVP significantly influenced the dynamics of changes in CSFNa and slightly affected changes in CSFK concentration induced by infusion of hyperosmotic saline, while it did not modify changes in CSFosmol) and CSFbf. In control experiments, CSFbf was significantly related to plasma and CSF osmolalities and sodium concentrations, whereas in AVP experiments these relationships were markedly suppressed. The results suggest that during acute hyperosmolar state AVP significantly influences sodium handling in CSF and may play a role in adaptation of the brain to hyperosmolality.

Animals↗

PubMed1989

Cerebral regulation of renal sodium excretion in sheep infused intravenously with hypertonic NaCl.

1. The natriuretic response to intravenous infusion of 2 M-NaCl was investigated in six conscious sheep. This hypertonic NaCl load resulted in relatively small, physiological (2-3 mmol l-1) increases in plasma Na+ concentration and was followed by a natriuresis with a maximum mean urinary sodium excretion 5 times higher than pre-infusion values. 2. Intravenous infusion of isotonic NaCl, delivering the same Na+ load as hypertonic NaCl infusion, did not induce natriuresis. This suggested, therefore, that with the hypertonic sodium load administered in the present study, the rise in plasma Na+ and/or tonicity rather than increase in blood volume is important in evoking the natriuretic response. 3. Intracerebroventricular infusion of low-Na+ artificial cerebrospinal fluid (CSF) reduced CSF Na+ concentration, decreased plasma vasopressin (AVP) levels and caused a copious water diuresis. This was associated with excessive loss of water and large increases in plasma Na+ concentration and osmolality. 4. The natriuresis induced by intravenous hypertonic NaCl load could be blocked by lowering CSF Na+ concentration in situations where water diuresis was either prevented or reduced by intravenous infusion of AVP or by delayed intracerebroventricular infusion of low-Na+ CSF, respectively. 5. The results of the present study provide further evidence that renal sodium excretion can be controlled by the central nervous system.

Animals↗

PubMed1986

Effect of ammonia intoxication on cerebral blood flow, its autoregulation and responsiveness to carbon dioxide and papaverine.

Cerebral blood flow (CBF) was measured in anaesthetised cats with 133Xe clearance method under normal conditions and with hyperammonaemia. Elevation of blood ammonia concentration by an intravenous infusion of ammonium acetate caused an increase in CBF and a parallel decrease in cerebrovascular resistance (CVR). These parameters reached, however, plateau at an arterial blood ammonia level exceeding 500 mumol/l. Cerebrovascular reactivity to CO2 diminished following elevation of blood ammonia concentration and at arterial blood ammonia level exceeding 500 mumol/l it was virtually abolished. In contrast, hyperammonaemia influenced neither cerebrovascular responsiveness to papaverine nor autoregulatory properties of the cerebral circulation. It is concluded, therefore, that hyperammonaemia exerts some dilatatory effect on cerebral vessels and severely impairs chemical regulation of CBF but does not elicit cerebral vasomotor paralysis.

Ammonia↗

PubMed1986

Intracranial pressure, cerebral blood flow, and cerebrospinal fluid formation during hyperammonemia in cat.

Intracranial pressure (ICP), cerebral blood flow (CBF), and the cerebrospinal fluid (CSF) formation rate were examined in anesthetized cats during ammonia intoxication. Hyperammonemia, evoked by intravenous infusion of ammonium acetate, caused a significant increase in ICP when the arterial blood ammonia level exceeded 400 mumol X liter-1. A progressive elevation of blood ammonia concentration was followed by a gradual rise in CBF, measured by the xenon-133 clearance technique. At an arterial blood ammonia level exceeding 500 mumol X liter-1, the CBF reached a plateau at 30% above the mean control value. Increase in ICP correlated weakly, but significantly, with the increase in CBF (R = 0.489, p less than 0.005). Elevation of the arterial blood ammonia level to 780.4 +/- 25.5 mumol X liter-1 for 2 hours elicited a significant gradual increase in CSF formation rate, measured by the ventriculocisternal perfusion method with iodine-125-albumin as an indicator substance. A maximum increase in CSF flow of 81% was noted at the end of the ammonium acetate infusion. It is suggested that hyperammonemia increases ICP both by cerebral vasodilatation and by enhancement of the CSF formation rate.

Ammonia↗

PubMed1986

Chemical regulation of the cerebral blood flow in cats with rostro- or prepontine transection of the brainstem.

Cerebral blood flow (CBF) and its response to hypercapnia were evaluated in cats with brainstem transected either at rostropontine (pretrigeminal preparation) or prepontine (cerveau isole preparation) level. Additionally, the effect of pentobarbital on CBF response to hypercapnia and to papaverine were examined. CBF was measured with 133 Xe intracarotid injection method. Cortical EEG activity was recorded. In rostropontine cats cerebral vessels responded with a dilatation to hypercapnia. In prepontine cats CBF response to CO2, was absent, where-as that to papaverine maintained. In rostropontine cats administration of pentobarbital, even in very low doses, caused disappearance of CBF response to hypercapnia, leaving that to papaverine. Our results support the idea that a neurogenic mechanism is involved in chemical regulation of CBF. The rostra1 part of the pontine reticular formation may be responsible for this neurogenic control.

Animals↗

PubMed1985

The effect of stimulation of the reticulo-hypothalamic-hippocampal systems on the cerebral blood flow and neocortical and hippocampal electrical activity in cats.

The effect of stimulation of the medial and lateral reticulo-hypothalamic-hippocampal (RHH) systems on cerebral blood flow (CBF) and electrical activity of the hippocampus and neocortex was examined in 19 encéphale isolé cats. ECoG was recorded from posterior sigmoid gyri and marginal gyri and hippocampal activity from dorsal hippocampus. Changes in hippocampal activity were evoked by electrical stimulation of RHH systems. CBF was measured by external monitoring of the clearance of 133Xe given as a single bolus in the carotid artery. Stimulation of the lateral system resulted in desynchronisation of ECoG and hippocampal activity without changes in CBF. Stimulation of the medial system elicited desynchronisation in ECoG modulated by theta-like synchrony, theta activity in the hippocampus and a 45% CBF increase. After atropine administration, low frequency, high voltage waves appeared in both ECoG and hippocampal activity, but no change in CBF was observed. During stimulation of the medial system there were no changes in the type of electrical activity but the CBF response was still preserved (increase by 50%). Stimulation of the lateral system did not change either the type of electrical activity or the CBF. The results indicate that the two systems of neuronal pathways, which mediate two different patterns of electrical response in the dorsal hippocampus but similar ECoG activity in the neocortex, elicit different CBF responses. It is argued that the alterations of electrical activity of the neocortex and hippocampus mediated by these two pathways depend on the cholinergic system, whereas the CBF changes depend on a different mechanism.

Action Potentials↗