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Biomedical subjects

A Schettini

Publications and source records attributed to A Schettini.

At least 19 recordsLinked to original sources
PubMed1991

Contribution of brain distortion and displacement to CSF dynamics in experimental brain compression.

The present study was designed to determine the contribution of brain distortion and displacement to changes in cerebrospinal fluid (CSF) dynamics [pressure-volume index (PVI), compliance (C), and outflow resistance (Ro)] during progressive brain compression and the effect of compression on brain mechanical properties. In 10 dogs measurements were made of CSF dynamics, brain elastic behavior, cerebral perfusion pressure, local cerebral blood flow, and suprainfratentorial intracranial pressure (ICP) during the incremental expansion of a supratentorial extradural balloon. PVI appeared more as a measure of the compressibility of the cerebral vascular compartment than of intracranial bulk compliance. Reciprocal changes in CSF dynamics behaved as expected when the balloon expanded predominantly supratentorially causing a moderate increase in ICP. A significant increase in ICP, however, caused a rise in PVI and a decrease in compliance. Under these conditions PVI alone could not differentiate between a falling cerebral perfusion pressure and an increasing suprainfratentorial ICP gradient. In contrast, the compliance decreased with balloon expansion while the outflow resistance showed an inverse correlation with compliance and a linear correlation with baseline ICP; Go, an elastic response parameter, consistently decreased, implying that C, Ro, and Go can be used as a trend of intracranial compensatory reserve during intracranial mass expansion.

Animals↗
PubMed1990

Brain tissue elasticity and CSF elastance.

In the analysis of the pressure-volume relationship of the intracranial system, the concept of brain elastance, sometimes called tissue elastance or CSF elastance, is often used. It is generally designated as Ecsf and is calculated as the slope of the pressure-volume curve of the system. Variations in Ecsf are related to, for example, changes in the buffering capacity of the system which, however, could be influenced by the cerebral vascular volume, compressibility of the meningeal membranes, and compressibility of the subpial brain tissue. Our interest is in isolating the effect of controlled changes in the intracranial system with changes in the subpial tissue only. Here we discuss the measurement of brain tissue elasticity and describe two experimental conditions in which simultaneous measurements showed distinct differences between the behaviour of the system CSF elastance and brain tissue elastic behaviour.

Animals↗
PubMed1989

Attenuation of decompressive hypoperfusion and cerebral edema by superoxide dismutase.

This study tested the hypothesis that ischemia-reperfusion injury initiated by the superoxide anion radical is a major component of postdecompression hypoperfusion and cerebral edema, and could be attenuated by superoxide dismutase (SOD). A supratentorial extradural balloon was placed in 20 fasting, lightly anesthetized, mechanically ventilated dogs and inflated in 0.5-ml increments (0.07 ml/sec) at 15-minute intervals. The end-point of balloon expansion was the onset of an isoelectric electroencephalogram, near-arrest of hemispheric cerebral blood flow (CBF) (measured by H2 clearance), and the appearance of a suprainfratentorial intracranial pressure gradient, which was held for 15 minutes. The in vivo development of brain edema was detected by measuring brain elastic response (BER) extradurally, and was correlated with postmortem measurement of brain water content (gravimetry); blood-brain barrier integrity was tested by Evans blue dye given after the insult. After decompression, the dogs were randomly assigned to one of four treatment groups: Group I received hyperventilation (PaCO2 28 +/- 1 mm Hg, mean +/- standard deviation); Group II received furosemide (2.4 mg/kg) and pentobarbital (10 mg/kg) every 8 hours; Group III received 20% mannitol in a 1.4-gm/kg bolus plus furosemide, 0.5 mg/kg; and Group IV received SOD, 15,000 U/kg every 15 minutes for 3 hours. At 4 hours of decompression Group IV had significantly greater recovery in local CBF and BER than Groups I, II, and III (p less than 0.05). The 24-hour survival rate was 20% for Group I, 60% for Group II, 80% for Group III, and 100% for Group IV. The survival rate appeared to correlate with a variable degree of postmortem intraparenchymal hemorrhages, blood-brain barrier disruption, and moderate to severe brain edema for Groups I, II, and III. In contrast, Group IV had the least brain edema (p less than 0.05) and Evans blue dye extravasation (p less than 0.05) and the fewest intraparenchymal hemorrhages. These data support the hypothesis that, under the experimental conditions described here, the superoxide anion plays a major role in the pathophysiology of postdecompression ischemic edema.

Animals↗
PubMed1988

Brain tissue elastic behavior and experimental brain compression.

This study was designed to test the hypothesis that the progressive expansion of an extradural mass causes detectable changes in brain mechanical response properties, in particular the nonlinear elastic behavior, before any significant changes in intracranial cerebrospinal fluid pressure can be detected. In 10 chronically prepared and anesthetized dogs, incremental inflation (0.07 ml/s) of an extradural balloon caused 1) a progressive fall in the brain nonlinear elastic parameter (G0, mmHg/mm2), 2) nonsignificant changes in brain tissue elasticity (G0, mmHg/mm), 3) a disproportionate progressive rise in subpial tension, and 4) a progressive fall in local cerebral blood flow (H2 clearance), despite a modest decrease in cerebral perfusion pressure (extracranial). In previous brain compression experiments (Brain Res. 305: 141-143, 1984) we have shown that the compression site becomes compacted and stiffer (increased G0) and its nonlinear elastic parameter (G0) increases markedly. These earlier findings, coupled with the present observation of a loss in tissue nonlinearity distally to the compression site, are most likely the major mechanisms by which, with a rapidly expanding intracranial mass, tissue pressure gradients and brain displacement, including transtentorial herniation, develop.

Animals↗
PubMed1984

Brain elastic behavior in experimental brain compression: influence of steroid therapy.

In chronically prepared dogs we studied the influence of large doses of steroids on experimentally increased brain stiffness. The latter was quantified by measuring brain elastic response, in terms of the (instantaneous) initial tangent, Go (mm Hg/mm). After epidurally induced brain compression (45 min), Go increased and remained elevated in spite of steroid therapy. The data suggest that steroids are ineffective in congestive hyperemia consequent to ischemic compression.

Animals↗
PubMed1984

Calculation of brain elastic parameters in vivo.

In an earlier study [Am. J. Physiol. 232 (Regulatory Integrative Comp. Physiol. 1): R27-R30, 1977], we defined the concept of brain elastic response in vivo as measured by a pressure-depth ratio (G0) derived from a graphic analysis of the elastic response tests. These tests have shown that brain elastic response in vivo is sensitive to changes in the intracranial system and that the response is nonlinear. In this study we identify a second parameter, G0, a second-order pressure-depth ratio that characterizes the nonlinear behavior and, along with G0, can be evaluated from a mathematical relation that models the experimental results obtained from the elastic response test. The equation is a logarithmic function relating the pressure and the subpial insertion depth. From this we obtain G0 and G0 as the slope and curvature of the response function at the subpial position. In animal experiments we correlated the changes in these parameters with those of cerebral hemodynamics during hemorrhagic and drug-induced hypotension. The calculated values of G0 and G0 are reproducible and reflect changes in cerebral blood flow and/or volume.

Animals↗
PubMed1984

Application of the coplanar principle to dynamic epidural pressure measurements.

The application of the coplanar principle to dynamic epidural pressure measurements was investigated in vitro. The authors used a coplanar pressure-displacement transducer, commonly employed to measure the viscoelastic properties of brain tissue in vivo. The present studies were performed using canine dura and a specially constructed fluid-filled chamber. The accuracy of the technique was assessed by comparing the pressure in the chamber recorded by the coplanar transducer to the pressure measured by a transducer directly vented to the chamber. The results show that the coplanar principle remained valid for dynamic measurements with the transducer under a variety of conditions.

Epidural Space↗
PubMed1982

Osmotic and osmotic-loop diuresis in brain surgery. Effects on plasma and CSF electrolytes and ion excretion.

In 22 patients to be operated on for brain tumors or cerebral aneurysms, the effect of osmotic diuresis was compared with that of osmotic-loop diuresis on plasma and cerebrospinal fluid (CSF) electrolytes, and water and ion excretion. Mannitol or mannitol plus furosemide were used to reduce brain bulk. After treatment with thiopental and hyperventilation, patients received randomly a rapid infusion of mannitol (1.4 gm/kg), or mannitol (1.4 gm/kg) plus furosemide (0.3 mg/kg). Brain shrinkage was considerably greater and more consistent with mannitol plus furosemide than with mannitol alone. However, hyponatremia, hypokalemia, hypochloremia, and hyperosmolality were also more marked (p less than 0.05) with mannitol plus furosemide than with mannitol. The rate of water and ion excretion was even more striking. At 30 minutes after absorption of mannitol alone, water excretion peaked at 17 ml/min, and gradually decreased to 3.8 ml/min 70 minutes later. With mannitol plus furosemide, during an identical time course, initial water excretion was 30 ml/min, followed by a further rise to 42 ml/min and then a decline to 17 ml/min. At peak diuresis after mannitol, Na+ and Cl- excretion average 0.57 and 0.62 mEq/min, respectively. This compares with mean values of 3.7 and 4.12 mEq/min for Na+ and Cl-, respectively, after mannitol plus furosemide. Although optimum brain shrinkage is achieved with osmotic-loop diuresis, the rapid electrolyte depletion (Na+ and Cl-) must be corrected to avoid altered sensorium during the patients' postoperative course.

Adult↗
PubMed1979

Brain water and electrolyte distribution during the inhalation of halothane.

The brain concentration of Na+, K+ and Cl-, water content and total brain osmolality were measured in six normocapnic dogs under pentobarbitone narcosis (30 mg kg-1). These studies were repeated in six additional dogs after exposure for 1 h to the inhalation of halothane 1% (end-tidal); there was an increase (P less than 0.05) in Na+, Cl- and water content but no change in K+ content in the grey matter, but in the white matter only Cl- increased (P less than 0.05). These findings were associated with a decrease in total brain osmolality (P less than 0.05) and a negative brain-cisternal c.s.f. osmotic gradient. The changes in the grey cortical matter were interpreted as a pattern of metabolic brain oedema related to interference with water-ion transport mechanisms across cell membranes. The observed brain-c.s.f. osmolality deficit could be related to a time-lag in the intracellular water-solute adjustment or to a deficit in osmotically active brain amino acids induced by the anaesthetic agent, or both.

Animals↗
PubMed1978

Effects of halothane and sodium thiopentone on surface brain pressure and brain electrical impedance in dogs with normal intracranial tension.

The effects of the inhalation of halothane and the i.v. administration of thiopentone on surface brain pressure and brain electrical impedance, at a frequency of 1 kHz, were investigated in 14 chronically implanted dogs. In dogs with normal PaCO2, halothane, at inspired concentrations of 0.8, 1.2, 1.5 and 2.0%, produced increases in brain pressure and impedance. Thiopentone i.v. and hyperventilation preceding the administration of halothane lessened, but did not prevent, the increases in brain pressure and impedance. Thiopentone 35 mg kg-1 decreased both pressure and impedance. The dose-related (P less than 0.01) increase in surface brain pressure was attributed to cerebral vascular expansion; the increase in impedance was not dose related and was interpreted as a loss of conductivity in brain extracellular space (e.c.s.). This loss could be a result of a decrease in both brain e.c.s. volume and its electrolyte concentration resulting from intracellular translocation and electrical inactivation of available ions in brain e.c.s. caused by increased cation binding. These phenomena might be related to the interaction between the anaesthetic molecule and cell proteins. The present study suggests that, in contrast to thiopentone, halothane induced a reversible ionic imbalance in the central nervous system.

Anesthesia, General↗
PubMed1977

On measurement of brain elastic response in vivo.

The elastic response behavior of brain tissue in vivo has been shown to be sensitive to the physiological environment of the brain and thus represents a useful parameter for identifying effects of controlled changes on the system. Here we describe a method for measuring brain elastic response using an epidural pressure-depth transducer and a minimum number of insertions. The method also serves to identify the nonlinear response of brain tissue.

Animals↗
PubMed1976

Elastic behavior of brain tissue in vivo.

A measurement system and a test sequence have been developed to determine the in vivo elastic response of brain tissue in terms of a pressure-depth ratio. This parameter appears sensitive to changes in the tissue environment that may occur due to the influence of, e.g., anesthetic agents, hyperventilation, etc., and thus may be useful in evaluating such influences. The measurements are made with the dura-arachnoid membranes intact, thus maintaining the influence of the cerebrospinal fluid compartment on the response behavior of the brain tissue that comprises the subpial region. As an integral part of the test, the procedure also serves to determine the depth or position of the subpial region and thus assures that the subsequent pressure-depth measurements invole brain tissue response. Finally, some discussion is given to relating the measured pressure-depth ratio to the classical elastic modulus. Values of the pressure-depth ratio and the corresponding elastic modulus for seven dogs are given.

Animals↗