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Biomedical subjects

H G Sullivan

Publications and source records attributed to H G Sullivan.

15 recordsLinked to original sources
PubMed1979

The CSF pressure-volume relationship before and after cardiac arrest in the cat.

The CSF pressure-volume (P-V) function was evaluated before and after cardiac arrest in 15 cats. The CSF volume change was produced by bolus loading (loading rate, greater than 0.1 mL/s) of the CSF space. Comparison of the CSF P-V function before and after cardiac arrest was made over a CSF pressure range of 5 to 46 mm Hg and for a CSF volume change of up to 9% of total CSF volume. After cardiac arrest, all CSF P-V curves were well described by the mathematical model konwn to be valid under normal physiological conditions. In eight animals, there was no significant difference between the prearrest and postarrest P-V functions. For the seven animals demonstrating a significant difference between prearrest and postarrest P-V data, all but one of the postarrest P-V curves were within the normal range. These results suggest that the shape of the CSF P-V curve is not substantially altered by cardiac arrest. We conclude that under normal circumstances material properties of brain tissue are the most important factors in determining the configuration of the CSF P-V curve and that under normal circumstances cerebral hemodynamic factors do not affect the shape of this curve.

Animals↗
PubMed1979

Bolous versus steady-state infusion for determination of CSF outflow resistance.

For rapid changes in cerebrospinal fluid volume an exponential relationship was demonstrated between CSF pressure and CSF volume in 15 cats. This relationship was valid over a CSF pressure range from 7 to 50 mm Hg and for acute increases of up to 9% to total CSF volume (approximately 13 ml for humans). Our data agree well with previous reports for the cat. A similar relationship has been shown in the dog and in humans. It has been claimed that, given the equations for CSF bulk flow and the exponential relationship between CSF pressure and CSF volume, one can calculate CSF outflow resistance by observing the decay of CSF pressure after a bolus injection into the CSF space. This claim was evaluated in an additional 18 cats. In these animals CSF outflow resistance calculated by the bolus method was compared with resistance calculated by a steady-state infusion method over the CSF outflow resistance range of 74 to 293 mm Hg/ml min-1. Resistance calculated by the bolus method underestimated resistance calculated by the steady-state method, and this underestimate grew larger with increasing resistance. The bolus technique is therefore not a valid method for determining CSF outflow resistance. The explanation offered for these results is that the decay of CSF pressure after a bolus injection into the CSF space occurs not only because of runoff of the injected volume of CSF but also because of "pressure relaxation" of the brain parenchyma around the CSF space. The phenomenon of pressure relaxation was not considered in developing the equation for calculation of CSF outflow resistance by the bolus technique. The time dependency of pressure relaxation allows for a fundamental element of hysteresis within the CSF space. A method of quantifying this element of hysteresis is suggested.

Animals↗
PubMed1979

Surgical removal of bilateral papillomas of the choroid plexus of the lateral ventricles with resolution of hydrocephalus. Case report.

The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.

Cerebral Ventricle Neoplasms↗
PubMed1978

Vascular permeability alterations to horseradish peroxidase in experimental brain injury.

Protein uptake and transport within the brain stem vasculature of mechanically brain injured cats was studied by means of both light and electron microscopy utilizing intravenously injected horseradish peroxidase as the protein tracer. In animals sustaining low grade head injuries not of sufficient intensity to elicit either microscopic, intraparenchymal hemorrhages or subtle, neuropathological responses, peroxidase extravasation was noted both in the vascular walls and in the surrounding parenchyma of the ventromedial aspect of the brain stem. At the ultrastructural level as early as 3 min after brain injury, occasional arterioles, venules and capillaries displayed peroxidase leakage. In serial sections large endothelial segments of these vessels revealed the peroxidase reaction product within numerous vesicles which often shared continuity with tubular and vacuolar profiles. Such vesicular activity apparently moved the peroxidase from the luminal surface to extrude it into the basal lamina. From the perivascular basal lamina, the reaction product flooded the interstices of the surrounding brain stem parenchyma where occasional neural, glial and pericytic elements incorporated the peroxidase within coated invaginations, vesicles, tubules and vacuoles. In that protein leakage was consistently observed despite the apparent integrity of both the endothelial tight junctions and their cell membranes, it is concluded that the vesicular transport of horseradish peroxidase across the endothelia of the brain stem vasculature represents a possible mechanism of blood-brain barrier dysfunction in mechanical brain injury.

Animals↗
PubMed1977

Significance of intracranial hypertension in severe head injury.

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.

Brain Injuries↗
PubMed1977

The physiological basis of intracranial pressure change with progressive epidural brain compression. An experimental evaluation in cats.

Sequential cerebrospinal fluid (CSF) pressure-volume studies were carried out in seven cats during the expansion at a constant rate of an epidural balloon. The same studies were performed in three control cats. Beginning after 20 minutes of inflation and continuing to the point of pupillary dilatation there was a progressive increase in the pressure-volume index (volume required to change intracranial pressure (ICP) by tenfold). During the course of balloon inflation, there was also a progressive increase in CSF elastance (instantaneous ICP change per unit change in CSE volume). At the point of pupillary dilatation there was a marked, abrupt increase in the pressure-volume index and an equally dramatic decrease in CSF elastance. The CSF outflow resistance increased to a variable extent during balloon inflation. The plot of the CSF pressure versus balloon volume (the mass lesion pressure-volume curve) was of the classical configuration with an initial relatively flat segment and a final steep segment. A hypothesis is presented that interprets the shape of the mass lesion pressure-volume curve in terms of changes occurring in the elastic properties of the tissues surrounding the CSF space and the volume of the CSF space. It is proposed that this hypothesis will explain most of the commonly observed variations in CSF pressure. Confusion regarding the ICP-volume relationships has arisen because of lack of specificity regarding which anatomical spaces are being perturbed.

Animals↗
PubMed1976

Fluid-percussion model of mechanical brain injury in the cat.

Mechanical brain injury was produced in 36 cats with a fluid-percussion model in which brain damage or dysfunction is produced by a single, brief, hydraulically-induced pressure transient that is conducted through the brain. Fluid-percussion injury induce elastic deformation of the brain resembling the brain deformation known to occur following head impact. Physiological responses and pahtological changes following injury were expressed as a function of peak pressure. Macroscopic central nervous system lesions concentrated at the pontomesencephalic junction, cervicomedullary junction, and in the cerebellar tonsils were consistently observed at and above 2.6 atmospheres (atm). At higher levels of injury (greater than or equal to 3.2 atm) there was extensive basal subarachnoid hemorrhage. At very high levels of injury (greater than 4.0 atm) hemorrhagic contusions were noted at the cerebral hemisphere impact site. A spectrum of neuronal alterations was identified in the damaged areas. Computer analysis showed correlation of electroencephalographic (EEG) changes with the neuropathological changes, since EEG recovery became severely impaired above 2.6 atm. No EEG changes were noted below 1.5 atm. From 1.5 to 2.2 atm there was a physiological response to injury but no significant changes were seen on neuropathological examination. This range of injury should permit further studies of the more subtle changes following mechanical brain injury without intraparenchymal hemorrhage or subarachnoid hemorrhage. The fluid-percussion model relates brain deformation following mechanical loading to a single pressure transient that is easily measured and controlled. Further quantitative investigation into the pathobiology of mechanical brain injury following graded brain deformation is thus made possible.

Animals↗