Biomedical subjects

J T Hoff

Publications and source records attributed to J T Hoff.

At least 91 records · Page 5Linked to original sources

PubMed1990

Brain edema and cerebrovascular permeability during cerebral ischemia in rats.

Focal cerebral ischemia was produced by occluding the left middle cerebral artery in 769 rats. Permeability of the blood-brain barrier to small or large molecules was evaluated qualitatively using Evans blue or sodium fluorescein and quantitatively using the transfer indexes of iodine-125-labeled bovine serum albumin or [14C]sucrose. Water content was determined using wet and dry weights and sodium and potassium contents using flame photometry. Cortical tissue in the middle cerebral artery territory was sampled less than or equal to 14 days after occlusion. A significant increase in the albumin transfer index was first found 12 hours after occlusion, and the index remained approximately the same until water content peaked 3 days after occlusion. In contrast, the sucrose transfer index increased gradually, significantly correlated with increases in the water and sodium contents. Tissue staining by sodium fluorescein was more extensive than that by Evans blue. As edema fluid decreased gradually 4-10 days after occlusion, the albumin and sucrose transfer indexes increased markedly. These findings indicate that disruption of the blood-brain barrier to small molecules is accompanied by accumulation of edema fluid during the later stages of ischemia. Opening of the barrier to serum protein is probably related to the resolution of edema.

Animals↗

PubMed1990

Products of cells from gliomas: VIII. Multiple-well immunoperoxidase assay of immunoreactivity of primary hybridoma supernatants with human glioma and brain tissue and cultured glioma cells.

To test the feasibility of primary screening of hybridoma supernatants against human glioma tissue, over 5000 combinations of hybridoma supernatants with glioma tissue, cultured glioma cells, and normal central neural tissue were screened with a new multiple-well (M-well) screening system. This is an immunoperoxidase assay system with visual endpoints for screening 20-30 hybridoma supernatants per single microscope slide. There were extensive differences between specificities to tissue and to cultured glioma cells when both were screened with M-wells and when cultured cells were screened with standard semi-automated fluorescence. Primary M-well screening with glioma tissue detected seven hybridoma supernatants that specifically identified parenchymal cells of glioma tissue and that were not detected with cultured cells. Immunoreactivities of individual supernatants for vascular components (nine supernatants), necrosis (five supernatants), and nuclei (three supernatants) were detected. Other supernatants bound multiple sites on glioma tissue and/or subpopulations of neurons and glia of normal tissue. The results show that primary screening with glioma tissue detects a number of different specificities of hybridoma supernatants to gliomas not detected by conventional screening with cultured cells. These are potentially applicable to diagnosis and therapy.

Antibody Specificity↗

PubMed1990

Hearing preservation following suboccipital removal of acoustic neuromas.

Advances in the diagnosis and intraoperative management of acoustic neuromas have greatly reduced the incidence of neurologic deficits following their removal. Ninety-three patients underwent acoustic tumor removal during a 41/2-year period, and hearing preservation was attempted in 20 cases. Hearing was preserved in 65% of the entire series, and excellent results were obtained in tumors less than 1.5 cm. No patient with a tumor greater than 1.5 cm had serviceable hearing preserved when total tumor removal was performed. Two patients, one with neurofibromatosis and one with an acoustic neuroma in an only-hearing ear, had planned partial tumor removal with preservation of hearing. Preoperative auditory brainstem response results were not predictive of postoperative hearing preservation. Intraoperative auditory brainstem response monitoring demonstrated that loss of wave V consistently correlated with loss of hearing postoperatively, whereas persistence of wave V (with a latency prolongation not exceeding 3.00 ms) was predictive of successful hearing preservation regardless of latency increases.

Audiometry, Evoked Response↗

PubMed1990

Blood-to-brain sodium transport in ischemic brain edema.

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Role of blood-brain barrier permeability in focal ischemic brain edema.

We studied how changes in BBB function are related to the development of ischemic brain edema. Focal cerebral ischemia was produced by left MCA occlusion in rats. The permeability of the BB to small or large molecules was evaluated qualitatively by the extravasation of EB or NaFl dyes and quantitatively by the uptake index of 125I-BSA or 14C-sucrose. Brain water content was determined by specific gravity. Measurements were made from the cortical core of the MCA territory within 14 days of occlusion. Water content progressively increased within 2 days of occlusion and then gradually decreased up to 14 days. Lightly stained EB areas were located only in the proximal portion of the ischemic core. The incidence of NaFl extravasation was similar to that of EB within 2 days of occlusion but was greater than that of EB 3 days after occlusion. NaFl staining diffusely extended into the ischemic core. Although the index of 125I-BSA increased only slightly within 2 days of occlusion, a marked increase in 125I-BSA was found after 3 days. The index of 14C-sucrose increased gradually after occlusion, reaching a peak at 8 days. These findings indicate that the change in BBB permeability is minimal in ischemic brain tissue when the accumulation of edema fluid is maximal and suggest that BBB alteration in ischemic brain tissue may be associated with the stabilization or resolution of the ischemic lesion.

Animals↗

PubMed1990

An osmotic gradient in ischemic brain edema.

We studied how the osmotic pressure gradient between blood and the brain is related to the development of ischemic brain edema. Focal cerebral ischemia was produced by left MCA occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, water content of the brain tissue was measured by wet and dry weight, and the tissue sodium and potassium contents were assayed by flame photometry. Permeability of BBB was tested by EB. These measurements were made from the cortical core of MCA territory at various intervals from 1 hr to 14 days after occlusion. Brain osmolality increased from 311 +/- 2 mOsm/kg (M +/- SE) to 329 +/- 2 mOsm/kg (n = 7, p less than 0.01) by 6 hrs after occlusion. Serum osmolality did not significantly change. The osmotic gradient between blood and the brain was about 26 mOsm/kg. Brain osmolality then decreased to 310 +/- 2 mOsm/kg by 12 hr after occlusion and remained about the same level for up to 14 days. Water content progressively increased within 1 day, then gradually decreased by 14 days. Sodium plus potassium content of the brain tissue did not increase and EB extravasation was not seen within 6 hr of occlusion. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Brain osmolality is not related to tissue electrolyte change and BBB disruption to protein.

Animals↗

PubMed1989

Mechanical prophylaxis of venous thrombosis in patients undergoing craniotomy: a randomized trial.

A randomized, prospective clinical trial of 70 patients undergoing craniotomy was performed to compare and evaluate two forms of mechanical prophylaxis of deep vein thrombosis. Thirty-eight patients received antiembolism stockings, whereas 32 patients received external pneumatic compression. Prophylaxis was begun preoperatively and continued intraoperatively and post-operatively until the patients were ambulatory. Impedance plethysmography was used to detect deep vein thrombosis both preoperatively and postoperatively. Two patients, one from each group, developed thromboembolic complications postoperatively. Impedance plethysmography showed false-positive findings in two additional patients. There were no deaths. The data suggest that either form of mechanical prophylaxis is effective against the development of deep vein thrombosis in this high-risk patient population.

Clinical Trials as Topic↗

PubMed1989

Discitis caused by the Centers for Disease Control microorganism Group Ve-1.

An unusual case of discitis in a 60-year-old, insulin-dependent, diabetic man is presented. Radiographs of the lumbar spine demonstrated changes associated with infection of the intervertebral disc space. Cultures from the L5-S1 disc space grew the microorganism designated by the Centers for Disease Control as Group Ve-1, an organism that has had questionable clinical significance in the past, and has not been reported as a pathogen in an intervertebral disc space.

Anti-Bacterial Agents↗

PubMed1989

Cerebral edema induced by arachidonic acid: role of leukocytes and 5-lipoxygenase products.

Arachidonic acid is released from cellular phospholipid membranes after brain injury associated with vasogenic edema. Intracerebral injection of arachidonic acid results in rapid breakdown of the blood-brain barrier, followed by an increase in brain water and sodium content. This effect is diminished by a 5-lipoxygenase inhibitor, but is unaffected by indomethacin, an inhibitor of cyclooxygenase. Leukocytes are rich in 5-lipoxygenase and mediate posttraumatic extracellular edema in other tissues. We sought to determine whether leukocytes are necessary for arachidonic acid-induced vasogenic edema and whether they are the primary source of 5-lipoxygenase activity. Intracerebral injection of arachidonic acid (10 micrograms) was performed in 21 rats divided into three groups. One hour after injection, the area of Evans blue stain extravasation on the corona slice through the needle tract was quantitated by polar planimetry and taken as a measure of blood-brain barrier permeability. Control animals (n = 7) had a 3.44 +/- 0.19 mm2 area of Evans blue cortical stain. Rats (n = 7) pretreated with a lipoxygenase inhibitor (BW755C) had a significant decrease (P less than 0.05) in the area of Evans blue extravasation was not significantly different from that seen in the control animals. Intracerebral injection of saline or eicosapentaenoic acid showed only minimal staining along the needle tract (0.14 +/- 0.08 mm2). We have confirmed the role of the 5-lipoxygenase products in arachidonic acid-induced vasogenic edema. The primary source of cerebral 5-lipoxygenase activity does not appear to be in leukocytes and is most likely within the brain parenchyma.

Animals↗

PubMed1989

Brain edema: a classification based on blood-brain barrier integrity.

Brain edema is a frequent complication of a variety of brain injuries and disorders. Two primary types of brain edema can be distinguished depending upon the integrity of the blood-brain barrier. With intact-barrier edema, the permeability of the blood-brain barrier is normal and brain edema results from a disturbance in ionic homeostasis. This type of edema is typically associated with swelling of the brain cells and a contraction of the extracellular space. In open-barrier edema, the permeability of the blood-brain barrier is increased and brain edema results from the oncotic forces generated by an influx of serum proteins into brain. In this case, the edema fluid accumulates primarily in the extracellular space. To a greater or lesser extent, both types of edema occur simultaneously in the majority of clinical conditions; however, one form usually predominates and demands the attention of both the scientist and clinician. Furthermore, classification of brain edema based upon blood-brain barrier integrity is useful to focus research on common mechanisms for brain edema formation and to direct therapy. This review considers intact-barrier and open-barrier edema with regard to their (a) histological features, (b) biophysical forces, (c) possible biochemical mediators, (d) mechanisms of resolution, and (e) implications for therapy.

Blood-Brain Barrier↗

PubMed1988

Ischemic brain edema and the osmotic gradient between blood and brain.

The relationship of the osmotic pressure gradient between blood and brain, and the development of ischemic brain edema was studied. Focal cerebral ischemia was produced by left middle cerebral artery occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, brain water content by wet-dry weight, and tissue sodium and potassium contents by flame photometry. Permeability of the BBB was tested by Evans blue. Measurements were made from the ischemic cortex within 14 days of occlusion. Brain osmolality increased from 311 +/- 2 to 329 +/- 2 mOsm/kg by 6 h after occlusion. Serum osmolality did not change significantly. The osmotic gradient between blood and brain peaked at approximately 26 mOsm/kg. Brain osmolality then decreased to 310 +/- 2 mOsm/kg by 12 h after occlusion and remained at about that same level. Water content increased progressively within 1 day of occlusion, then gradually decreased by 14 days. Brain tissue sodium plus potassium content did not increase within 6 h of occlusion, and Evans blue extravasation was not seen within that time. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Furthermore, the increase in brain osmolality is not related to tissue electrolyte change or BBB disruption to protein.

Animals↗

PubMed1988

Biomechanics of brain edema in acute cerebral ischemia in cats.

We studied whether the biomechanical properties of brain play an important role in the development of early ischemic brain edema in cats with middle cerebral artery occlusion. Brain tissue pressure, tissue compliance, and tissue resistance were measured from the gray matter in the core and the periphery of the middle cerebral artery territory for 6 hours after occlusion. Regional cerebral blood flow and water content were also measured from the same areas. Ventricular fluid pressure was recorded. Tissue pressure rose gradually in the core, where flow was 6 ml/100 g/min, over 4 hours and then stabilized. The pressure gradient measured between edematous tissue and ventricular fluid was 5.3 mm Hg. Tissue resistance increased 1 hour after occlusion when water content increased to 10 mg/g. Later, when water content increased by 40 mg/g, tissue resistance decreased and tissue compliance increased significantly. In the periphery, where flow was 17.6 ml/100 g/min, tissue pressure rose slightly while tissue compliance and tissue resistance did not change within 6 hours. Our data indicate that as ischemic injury progresses, edema fluid accumulates in highly compliant brain parenchyma, then migrates through highly conductive tissue into the cerebrospinal fluid spaces, driven by the hydrostatic pressure gradient between the edematous tissue and the cerebrospinal fluid.

Acute Disease↗

PubMed1988

The pathogenesis of spinal epidural abscess: microangiographic studies in an experimental model.

An experimental model of spinal epidural abscess was developed in rabbits by injecting Staphylococcus aureus into the posterior thoracolumbar epidural space. This model has been shown to reproduce the neurological, bacteriological, and radiological aspects of the human disease. In this study, the effect of the infectious epidural mass on the vasculature of the spinal cord in paraplegic rabbits was studied using microangiographic techniques. The normal vascular anatomy of the rabbit spinal cord was defined in control experiments. Vascular proliferation was demonstrated in the epidural space surrounding the abscesses. Anterior and paired posterior spinal arteries remained patent in paraplegic rabbits with mild or moderate spinal cord compression and in some cases of severe compression. In animals with severe compression, the anterior epidural venous plexus remained patent, but the dorsal spinal vein was occluded. Occlusion of perforating arteries occurred only with extreme spinal cord compression. These data indicate that the initial neurological deficit associated with experimental spinal epidural abscess is not due to vascular thrombosis.

Abscess↗

PubMed1988

Management of post-traumatic cervical spine instability: operative fusion versus halo vest immobilization. Analysis of 49 cases.

A 5-year retrospective analysis was conducted for all cervical spine fractures associated with neurologic deficit initially treated at the University of Michigan Hospitals. Forty-nine cases of lower cervical spine fracture (C3-C7) were reviewed. Twenty-eight patients underwent early operative fusion followed by immobilization with either halo vests, or hard cervical collars, and 20 patients were initially immobilized in halo vests only. One patient refused treatment and was kept in a hard cervical collar. The average period of immobilization was 3 months. Eight patients in the halo vest group demonstrated radiographic evidence of spinal instability following immobilization (40%). Five of these eight patients subsequently required operative stabilization. Two of these five suffered progression of neurologic deficit secondary to loss of reduction while immobilized. Spinal instability occurred in two of the 28 patients initially fused (7%) (p less than 0.01), and in the patient treated in a collar. The findings indicate: 1) the halo vest does not protect patients with cervical instability from neurological injury, nor does it absolutely immobilize the cervical spine; 2) surgery may be required to provide spinal stability, even after a 3-month orthotic treatment period; and 3) there appears to be an increased rate of spinal stability with fusion and immobilization versus immobilization alone.

Adolescent↗

PubMed1987

Skull x-ray examinations after head trauma. Recommendations by a multidisciplinary panel and validation study.

The value of skull radiography in identifying intracranial injury has not yet been satisfactorily defined. A multidisciplinary panel of medical experts was assembled to review the issue of skull radiography for head trauma. The panel identified two main groups of patients--those at high risk of intracranial injury and those at low risk of such injury--and developed a management strategy for imaging in the two groups. The high-risk group consists primarily of patients with severe open or closed-head injuries who have a constellation of findings that are usually clinically obvious. These patients are candidates for emergency CT scanning, neurosurgical consultation, or both. The low-risk group includes patients who are asymptomatic or who have one or more of the following: headache, dizziness, scalp hematoma, laceration, contusion, or abrasion. Radiographic imaging is not recommended for the low-risk group and should be omitted. An intermediate moderate-risk group is less well defined, and skull radiography in this group may sometimes be appropriate. A prospective study of 7035 patients with head trauma at 31 hospital emergency rooms was conducted to validate the management strategy. No intracranial injuries were discovered in any of the low-risk patients. Therefore, no intracranial injury would have been missed by excluding skull radiography for low-risk patients, according to the protocol. We conclude that use of the management strategy is safe and that it would result in a large decrease in the use of skull radiography, with concomitant reductions in unnecessary exposure to radiation and savings of millions of dollars annually.

Brain Injuries↗

PubMed1987

Perioperative morbidity associated with operative resection of craniopharyngioma: a review of ten years experience.

A ten-year review of perioperative morbidity after operative resection of craniopharyngioma is presented. From 1974 to 1983, 23 patients underwent a total of 34 operations. Patients were subdivided into 95% or greater resection and partial resection groups. Features compared between the two groups included sodium, glucose, temperature, diabetes insipidus, major complications, neurological deficits and death. Patients undergoing 95% or greater resection had significant fluctuations in sodium, temperature and glucose (p less than .01). Diabetes insipidus and major postoperative complications were also significantly elevated in the 95% or greater resection group (p less than .05). Therefore, the extent of surgical resection correlated well with the degree of metabolic dysfunction and major postoperative complications. Careful assessment of surgical morbidity is warranted in the management of patients with craniopharyngioma.

Body Temperature Regulation↗

PubMed1987

Experimental spinal epidural abscess: a pathophysiological model in the rabbit.

To define the pathophysiology of spinal cord dysfunction associated with spinal epidural abscess formation, we developed an experimental model. Spinal epidural abscesses were produced in rabbits by injecting Staphylococcus aureus into the posterior thoracolumbar epidural space under direct vision. Progressive neurological deficits were detected in 18 of 20 animals; severe paraparesis or paraplegia occurred in 75%, and sphincter dysfunction occurred in 55%. Clinical data, including the results of plain spine roentgenography, myelography, and biochemical and bacteriological examination of the cerebrospinal fluid, were recorded. Epidural abscesses with varying degrees of spinal cord compression were confirmed pathologically in 95% of the experimental group. Spinal cord white matter changes included vacuolization, loss of myelin, and axonal swelling. The gray matter of the spinal cords was relatively preserved. There was no microscopic evidence of thrombosis or vasculitis in the major blood vessels supplying the spinal cords. Histopathological changes detected in the spinal cords were more consistent with direct compression of neural tissue than with infarction. The progressive clinical course and the histopathological changes in the spinal cord after compression by abscess closely resembled those of experimental compression of the spinal cord by epidural neoplasm.

Abscess↗

PubMed1987

Effect of dexamethasone on experimental brain abscess.

Dexamethasone has been used to manage brain edema in patients with intracranial abscess. However, its administration has often been delayed or avoided for fear of adverse effects upon normal host responses to infection. An experimental model of brain abscess in the rat was developed to determine if dexamethasone produced adverse effects on immune competence and collagen deposition in the region of the abscess. Sprague-Dawley rats were inoculated with Staphylococcus aureus and treated intraperitoneally each day with either dexamethasone (0.25 mg/kg) or saline solution. Surviving animals were sacrificed at 4, 8, 12, or 18 days after treatment. The brains were examined grossly for abscess formation and microscopically for intensity of the inflammatory response, abscess diameter, and wall thickness. There were no differences in mortality rates, abscess production rates, or abscess diameters when groups were compared. The intensity of inflammatory response was similar in both groups. In the group sacrificed 8 days after inoculation, a delay in collagen deposition was apparent, manifested as a thinner abscess wall in the experimental group (mean: 17.8 mu in dexamethasone-treated animals and 85 mu in saline-treated control animals: p = 1.0041). At 12 and 18 days after inoculation, there was no difference in abscess wall thickness between the control and experimental groups. Therapeutic doses of dexamethasone had little effect on mortality rates, incidence of abscess production, or intensity of inflammatory response in the experimental animals. Thus, dexamethasone did cause a delay in collagen deposition in the walls of experimental brain abscesses, but wall thickness 18 days after inoculation was not affected.

Animals↗