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T Dóczi

Publications and source records attributed to T Dóczi.

At least 55 records · Page 3Linked to original sources
PubMed1993

Volume regulation of the brain tissue--a survey.

Though the brain bulk has been considered to be constant in several pressure homeostasis studies, the central nervous tissue may be responsible for the accommodation of extracerebral masses exceeding the volume regulation capacity of the cerebral blood and cerebrospinal fluid. Volume buffering of the nervous tissue may even be functioning in parallel, in conjunction with the "fluid" compartments. Of the existing volume regulatory models, the following are discussed: osmotic feedback (buffering) preventing major fluid shifts in osmotic or pressure disequilibrium at the blood brain barrier (BBB), and the 4-compartment model, which under steady-state conditions can be regarded as an analogue of systemic tissue volume regulation, i.e. secretion of fluid at the BBB, bulk flow of interstitial space fluid (ISF) in the brain and absorption via the cerebrospinal fluid (CSF). The most recent data are presented, confirming that accommodation of space occupation by the nervous tissue is achieved via shrinkage of the extracerebral fluid (ECF), while the cell volume remains relatively constant. These findings confirm Hakim's classical hypothesis, based on biomechanical considerations, that the brain behaves like a sponge. The data presented in this survey point to a more general hypothesis: the brain interstitial space can vary in volume according to physiological and pathological stress, within certain bounds this being a reversible process which does not affect brain function. The potential role of the central neuro-endocrine system in brain volume regulation is discussed. Vasopressin (AVP) and atriopeptin (ANP) probably, function within the brain via a paracrine mechanism, as physiological regulators of brain cell and ISF volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Significance of the rate of systemic change in blood pressure on the short-term autoregulatory response in normotensive and spontaneously hypertensive rats.

Cerebral autoregulation, the physiological regulatory mechanism that maintains a constant cerebral blood flow (CBF) over wide ranges of arterial blood pressure, was investigated in normotensive and spontaneously hypertensive rats by means of laser-Doppler flowmetry. Systemic arterial hypertension was produced at rates ranging from 0.02 mm Hg/second to 11 mm Hg/second by constant infusion of epinephrine and norepinephrine. Systemic arterial hypotension was produced at rates ranging from -0.03 mm Hg/second to -12 mm Hg/second, either by bleeding the animals into a reservoir or by compressing the abdomen. In those cases with a low rate of change in systemic arterial blood pressure (SABP), the measurements lasted for 5 +/- 2 minutes, and in those with a high rate of change in SABP, measurements lasted for 40 +/- 30 seconds. The purpose was to record the time of onset and course of autoregulation in the basal ganglia in response to slow or rapid changes in SABP. CBF in the basal gray matter remained at baseline values (i.e., autoregulation was functioning) if the rate of increase of SABP did not exceed a critical value (0.10 mm Hg/second in the normotensive rats; 0.35 mm Hg/second in the spontaneously hypertensive rats). When hypertension was produced at faster rates, CBF followed arterial blood pressure passively, and no autoregulatory response was observed for 2 +/- 1 minutes. Hypotension did not change the baseline CBF when it was not produced at a rate faster than -0.4 mm Hg/second in normotensive rats and -0.15 mm Hg/second in spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Determination of the cerebrovascular reserve capacity by using acetazolamide as well as transcranial Doppler and SPECT tests].

The aim of this study was the development of a simple bedside test to assess cerebrovascular reserve capacity using transcranial Doppler sonography. We tried to validate the increase in blood flow velocity as cerebrovascular reserve capacity in 20 (3 normal, 7 TIA, 10 completed stroke) patients. They were studied using transcranial Doppler sonography and rCBF SPECT before and after injection of 1 g acetazolamide. Their increases in blood flow velocity and changes in cerebral blood flow correlated significantly in the symptomatic hemispheres (p less than 0.001). Blood flow velocity between the two hemispheres (symptomatic and asymptomatic) was not significantly different at rest. We offer these simple and reliable methods in clinical studies to clarify the frequency of ischemic stroke of hemodynamic origin.

Acetazolamide↗
PubMed1992

[The role of combined SPECT studies of regional cerebral blood flow and volume in the detection of intracranial vascular malformations].

Brain perfusion (rCBF) (99mTc--HMPAO) and blood volume (rCBV) (99mTc--RBC) investigations were performed by SPECT on 13 patients with intracranial AVM. In each cases the rCBF revealed a decreased tracer uptake at the site of the AVM. In the rCBV SPECT, abnormal AVM structures with increased radioactivity were detected in 92% of cases. In all of the patients surgical resection of the AVM was also carried out. In the cases where the rCBF disturbance was equal or larger than the rCBV abnormality the surgical complications were more frequent it was concluded that combined rCBF--rCBV method is suitable to detect the AVM-s, and to clarify their haemodynamic effects. It is helpful in planning the surgical intervention, and in the follow-up.

Arteriovenous Malformations↗
PubMed1991

Measurements of regional cerebral blood flow and blood flow velocity in experimental intracranial hypertension: infusion via the cisterna magna in rabbits.

Cerebral blood flow velocity, as measured in the intracranial segment of the internal carotid artery by transcranial Doppler sonography via the transorbital route, and regional cerebral blood flow and volume in corresponding cortical areas, as measured by the hydrogen clearance technique, were recorded for eight New Zealand White rabbits subjected to infusion via the cisterna magna to elevate intracranial pressure. In the lower range of autoregulation, that is, at perfusion pressures between 80 and 40 mm Hg and even lower, the changes in cerebral blood flow velocity and cerebral blood flow showed a strong correlation (0.86) under conditions of standard pCO2 (PaCO2 = 35 +/- 2 mm Hg). Autoregulation was exhausted at 40 mm Hg, and the cerebrovascular resistance was minimal. Below this perfusion pressure, the cerebral blood flow and volume dropped sharply, whereas the cerebrovascular resistance gradually increased, indicating that, despite the maximally dilated resistance vessels, intracranial hypertension causes vascular resistance to increase, possibly via blocking of the venous outflow. Our results confirmed that noninvasive and easily (even at bedside) applicable measurements of changes in cerebral blood flow velocity could be a substitute for the cumbersome and expensive isotope measurements of cerebral blood flow in patients with intracranial hypertension.

Animals↗
PubMed1990

[Effect of extra- and intra-cranial vascular anastomosis on regional blood flow, studied by SPECT using 99m-Tc HMPAO].

Thirty-two patients suffering from occlusive cerebrovascular disease were investigated by means of 99mTc-HMPAO brain SPECT before and one month after EC-IC bypass operation. The regional cerebral blood flow was unchanged postoperatively in 19 patients, increased in 7 cases, and deteriorated in 6 patients. One patient died in the postoperative period and in another no follow-up SPECT could be performed. It is concluded that the regional cerebral blood flow, even in the absence of a morphological deficit on CT, was not improved by the operation in the majority of cases.

Adult↗
PubMed1990

[Regional cerebral blood flow studied by single photon emission computed tomography (SPECT)].

Clinical experience based on regional cerebral blood flow investigations with 99mTc HMPAO SPECT in 164 patients is reported. The pharmacokinetics of the 99mTc HMPAO are summarised, and the important indications of the investigations are interpreted in case reports (stroke, surgical solution of intracavernous aneurysm, Alzheimer and multiinfarct types of dementias). The literature data suggest that the diagnostic possibilities with this method are good in other diseases too, this area is surveyed briefly.

Alzheimer Disease↗
PubMed1990

Do the skull and dura exert influence on brain volume regulation following hypo- and hyperosmolar fluid treatment?

The present studies were performed to determine the response of the brain water and electrolytes to acute hypoosmolality and hyperosmolality in animals with intact skull and dura, in comparison with those subjected to extensive bilateral or unilateral craniectomy and dural opening. Four to 5 weeks following extensive unilateral or bilateral craniectomy and dural opening in rats, a 50 mosm/kg decrease in plasma osmolality was produced by systemic administration of distilled water ("water intoxication"), or a 28 mosm/kg increase in plasma osmolality was produced by systemic administration of either 1 M NaCl or 1 M mannitol in 0.34 M NaCl. Tissue water, Na, and K contents were determined after 120 minutes. Tissue water accumulation or water loss was proportional to the decrease or increase in plasma osmolality. However, the tissue water accumulation following "water intoxication" was less (40% of the predicted value) than that predicted for ideal osmotic behaviour. The brain tissue was also found to shrink less than predicted on the basis of ideal osmotic behaviour (40% of the predicted value after mannitol treatment, and 60% after NaCl administration). This non-ideal osmotic response of the brain tissue is consistent with the finding in other studies and indicated a significant degree of volume regulation. Water and electrolyte changes were not different in operated and non-operated animals, demonstrating no effects of extensive skull and dura defects on tissue volume regulation under hypo- and hyperosmolar conditions of a degree that may be encountered under clinical circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The effect of skull and dura on brain volume regulation after hypo- and hyperosmolar fluid treatment.

This study was performed to determine the response of brain water and electrolytes to acute hypo-osmolality and hyperosmolality in animals with intact skulls and dura, in comparison with those subjected to extensive bilateral or unilateral craniectomy and opening of the dura. In rats, 4 to 5 weeks after extensive unilateral or bilateral craniectomy and opening of the dura, a 50-mOsm/kg decrease in plasma osmolality was produced by systemic administration of distilled water ("water intoxication"), or a 28-mOsm/kg increase in plasma osmolality was produced by systemic administration of either 1 M NaCl or 1 M mannitol in 0.34 M NaCl. Tissue water, Na. and K contents were determined after 120 minutes. Tissue water accumulation or water loss was proportional to the decrease or increase in plasma osmolality. The tissue water accumulation after "water intoxication," however, was less (40% of the predicted value) than that predicted for ideal osmotic behavior. The brain tissue was also found to shrink less than predicted on the basis of ideal osmotic behavior (40% of the predicted value after mannitol treatment, and 60% after NaCl administration). This nonideal osmotic response of the brain tissue is consistent with the finding in other studies and indicated a significant degree of volume regulation. Water and electrolyte changes did not differ between animals operated on and those not operated on, a fact which demonstrates that there are no effects of extensive skull and dura defects on tissue volume regulation under hypo- and hyperosmolar conditions encountered under clinical circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Regulation of brain water and electrolyte contents: the opposite actions of central vasopressin and atrial natriuretic factor (ANF).

Considerable evidence indicates that regulation of the ionic environment of the brain is coordinated by a central neuroendocrine system capable of affecting the capillary endothelium, the choroid plexus, and the astroglia. All three cell groups are responsible for precise control of brain volume through adjustment of cell water and electrolyte content. With these considerations in mind, we have attempted to elucidate the possible involvement of the central vasopressin (AVP) and atrial natriuretic factor (ANF) systems in the regulation of the water and ion homeostasis of the brain tissue of rats: Vasopressin-positive vascular connections, investigated by immuno-electronhistochemistry, were found in close or direct contact with brain microvessels. Central administration of AVP (125 ng) or DDAVP (0.5 micrograms), with or without an accompanying water load, brought about a 1-1.3% water accumulation. Brain oedema caused by experimental subarachnoid haemorrhage had a different course in Wistar and Brattleboro DI rats, the latter being unable to synthetize AVP. These findings suggest that the centrally released AVP leads to brain water accumulation by increasing the water permeability of capillaries, and may facilitate the production of brain oedema in various pathological conditions. On the other hand, central administration of synthetic rat ANF (2 micrograms) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. The better understanding of these hormone receptors and their manipulations have exciting clinical implications.

Animals↗
PubMed1988

Reverse pinocytosis induced in cerebral endothelial cells by injection of histamine into the cerebral ventricle.

Histamine dihydrochloride (10 micrograms of 500 micrograms/ml) was infused during 1 min into the lateral cerebral ventricle of rats, which resulted in a significant stimulation of pinocytosis in the endothelial cells. Systemic injections of mepyramine or metiamide could not prevent this activation. In contrast, ranitidine, injected with histamine was able to inhibit the stimulation of pinocytosis. Albumin exudation from the blood was not found. There was also no change in water and electrolyte contents of the brain tissue. The results suggest that histamine reaching the abluminal membrane can activate the pinocytosis in the cerebral endothelial cells in the reverse direction, i.e., from brain to blood, without opening the blood-brain barrier.

Animals↗
PubMed1988

Increased concentration of atrial natriuretic factor in the cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage and raised intracranial pressure.

Plasma and cerebrospinal fluid (CSF) atrial natriuretic factors/peptides (ANFs/ANPs) were measured in 26 patients with normal or raised intracranial pressure (ICP) by means of an instant radioreceptor assay. All 26 patients were suffering from aneurysmal subarachnoid hemorrhage (SAH), and 11 had also developed raised ICP (ICP greater than 20 mm Hg). In SAH patients with normal ICP, the plasma levels of ANF were 20 to 200 pg/ml (mean +/- SE, 89 +/- 68 pg/ml); in the 11 SAH patients with raised ICP, however, ANF levels were 14 to 262 pg/ml (mean 114 +/- 79 pg/ml). The difference was not statistically significant. The ANF/ANP plasma levels in 6 healthy volunteers were 15 to 167 pg/ml (mean 77 +/- 32 pg/ml). Although the ANF/ANP concentration in the CSF of patients with normal ICP did not reach the lower limit of detectability (i.e., 4 pg/ml) in any case, in those with elevated ICP it was 14 to 120 pg/ml (mean 49 +/- 37 pg/ml). This difference was statistically highly significant. The results of this preliminary study suggest that the ANF/ANP concentration in human CSF is 1 to 2 orders lower than that in the plasma and that there is no significant correlation between ANF/ANP levels in the CSF and the plasma. After SAH in patients with raised ICP, there was an accompanying increase in the ANF/ANP concentration in the CSF, but the ANF/ANP concentration in the plasma was not changed significantly. Accordingly, a central ANF/ANP release might be hypothesized to play a causative or adaptive role in the neuroendocrine regulation of ICP dynamics, although this may simply be an epiphenomenon.

Adult↗
PubMed1987

Effects of intraventricularly injected isoosmolar glycerol on brain water and electrolytes in the rat.

The infusion of isoosmolar glycerol (0.35 mol/dm-3) into the ventricles of laboratory rats for 120 minutes led to an increase in the serum osmolality by 11 mosm/kg and to hypernatremia. The brain water content of the cerebral hemispheres decreased by 0.9% (P less than 0.05). A corresponding intraventricular infusion of saline or d-glucose did not cause significant changes in these parameters. These findings support the view that glycerol, even in a dose incapable of creating a major osmotic gradient between plasma and brain, could have a beneficial effect in the control of intracranial volume-pressure perturbations. It is hypothesized that, besides acting as an osmotic dehydrating agent in certain concentrations, glycerol influences the central neuroendocrine system responsible for brain ion and volume homeostasis. By its presumed reduction of central and peripheral vasopressin release through lowering the cerebrospinal fluid sodium concentration, it may help in decreasing the brain water content.

Animals↗
PubMed1987

Regulation of brain water and electrolyte contents: the possible involvement of central atrial natriuretic factor.

The intraventricular administration of 0.2 or 2 micrograms of synthetic rat atrial natriuretic factor (syn rANF), sequence 101-126 of the precursor, prevented the water accumulation elicited in rat brain by a systemic hypoosmolar fluid load and led to a statistically significant sodium loss from the nervous tissue, while the potassium content remained unaltered. Similar syn rANF administration to rats not treated with a hypoosmolar fluid load caused no significant change in the water, potassium, and sodium content of the hemispheres. In this experiment, a primary systemic action of centrally administered syn rANF with ensuing secondary changes in brain ion and water homeostasis seems unlikely, as the serum osmolality and sodium and potassium concentrations remained unaltered. Thus, a central influence of the intraventricularly administered hormone upon the water and ion balances of the nervous tissue can be hypothesized. The significant loss of sodium may reflect the primary role of volume regulation of the nervous tissue, i.e., the loss of extracellular osmols such as Na+ in response to a hypoosmolar environment. These data lend further support to the concept that a central neuroendocrine system regulates brain ion and volume homeostasis. The possible role of ANF in the management of brain edema should be considered.

Animals↗