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Biomedical subjects

A Crockard

Publications and source records attributed to A Crockard.

At least 37 records · Page 2Linked to original sources

Staphylococcal infection of the odontoid peg.

An epidural abscess secondary to osteomyelitis of the odontoid peg produced a sudden left-sided weakness. Appropriate antibiotics, transoral evacuation of the pus and subsequent posterior atlanto-axial fusion were associated with a full recovery.

Abscess↗

The time course of intracranial pathophysiological changes following experimental subarachnoid haemorrhage in the rat.

The rat subarachnoid haemorrhage (SAH) model was further studied to establish the precise time course of the globally reduced CBF that follows and to ascertain whether temporally related changes in cerebral perfusion pressure (CPP) and intracranial pressure (ICP) take place. Parallel ultrastructural studies were performed upon cerebral arteries and their adjacent perivascular subarachnoid spaces. SAH was induced by a single intracisternal injection of autologous arterial blood. Serial measurements of regional cortical CBF by hydrogen clearance revealed that experimental SAH resulted in an immediate 50% global reduction in cortical flows that persisted for up to 3 h post SAH. At 24 h, flows were still significantly reduced at 85% of control values (p less than 0.05), but by 48 h had regained normal values and were maintained up to 5 days post SAH. ICP rose acutely after haemorrhage to nearly 50 mm Hg with C-type pressure waves being present. ICP then fell slowly, only fully returning to control levels at 72 h. Acute hydrocephalus was observed on autopsy examination of SAH animals but not in controls. Reductions in CPP occurred post SAH, but only in the order of 15%, which could not alone account for the fall in CBF that took place. At 48 and, to a lesser extent, 24 h post SAH, myonecrosis confined largely to smooth muscle cells of the immediately subintimal media was observed. No significant changes in the intima or perivascular nerve plexus were seen. Within 24 h of haemorrhage, a limited degree of phagocytosis of erythrocytes by pial lining cells took place. However, early on the second day post SAH, a dramatic increase in the numbers of subarachnoid macrophages arose from a transformation of cells of the pia-arachnoid. This period was characterised by intense phagocytic activity, erythrocytes, fibrin, and other debris being largely cleared over the next 24 h. At 5 days post SAH the subarachnoid macrophage population declined, cells losing their mobile active features to assume a more typical pia-arachnoid cell appearance once more. Our studies indicate that this increasingly utilised small animal model of SAH develops global cortical flow changes only acutely, and it is likely that early vasospasm, secondary to released blood products rather than pressure changes per se, is responsible for the initial cerebral ischaemia that develops. Interestingly, both cerebral arterial vasculopathy and perivascular macrophage phagocytic activity are most marked at approximately 48 h following SAH in the rat, a time at which a phase of delayed cerebral arterial narrowing has previously been documented.

Animals↗

Serial determinations of regional cerebral blood flow in the rat using simple chronically implanted platinum wire microelectrodes.

The ability to reliably obtain serial determinations of regional cerebral blood flow (rCBF) over time in small animals using simple and inexpensively constructed platinum-wire microelectrodes has been investigated. Repeated measurements of local cortical flow were obtained on a daily basis using the hydrogen clearance technique in a group of 18 animals, in each of which, 6 electrodes were chronically implanted. Our studies have shown the simple microelectrodes utilised to give a low variability of results, as well as being well tolerated and provoking minimal tissue reaction even over prolonged periods of time. Under identical steady-state conditions, serial determinations of rCBF were obtained for up to one week, with a maximum variation in mean values of only 12%, a result that compares favourably with the known serial determination error for the technique in the shorter term.

Animals↗

5-Hydroxytryptamine demonstrated immunohistochemically in rat cerebrovascular nerves largely represents 5-hydroxytryptamine uptake into sympathetic nerve fibres.

This study has re-examined, by immunohistochemistry, a proposed serotonergic innervation of major cerebral vessels in the rat. Previous studies had demonstrated a dense perivascular plexus of 5-hydroxytryptamine immunoreactive nerve fibres upon major cerebral vessels in this and many other species. The present work has shown, however, that 5-hydroxytryptamine immunoreactive nerve fibres are rarely observed in cerebral vessels prepared by perfusion-fixation in situ, and only form a well-developed plexus in vessels prepared, as in previous studies, by immersion-fixation. Prior treatment with a predominantly noradrenergic uptake inhibitor desmethylimipramine but not the serotonergic uptake inhibitor fluoxetine produced a major diminution in the 5-hydroxytryptamine immunoreactive plexus visualized in these immersion-fixed vessels. In addition, 5-hydroxytryptamine immunoreactive nerves were only occasionally observed in immersion-fixed vessels from animals that had been pretreated with 6-hydroxydopamine to produce adrenergic denervation. The removal, firstly, of vessel-contained blood, by left ventricular perfusion with Krebs' solution, prior to vessel dissection and immersion-fixation, resulted in an absence of 5-hydroxytryptamine immunoreactivity in perivascular nerves. Immunoreactivity could then be restored by briefly incubating vessels in Krebs' solution containing either blood or 5-hydroxytryptamine before fixation. It would appear therefore that 5-hydroxytryptamine is rarely present under normal circumstances in the perivascular nerves of major cerebral vessels, and that previous descriptions of a dense serotonergic nerve plexus represent 5-hydroxytryptamine in blood released during vessel dissection being taken up via the noradrenaline-uptake system into perivascular sympathetic nerves. The possibility is thus raised that 5-hydroxytryptamine uptake and interaction within perivascular adrenergic nerves could occur in those cerebrovascular disorders where blood is released.

Adrenergic Fibers↗

Alterations in serotonin and neuropeptide Y content of cerebrovascular sympathetic nerves following experimental subarachnoid hemorrhage.

The effect of an experimental subarachnoid hemorrhage (SAH) upon neurotransmitter content in sympathetic nerves supplying the major cerebral arteries of the rat has been examined by immunohistochemical analysis and high performance liquid chromatography with electrochemical detection (HPLC-ECD). In particular, changes that occur in sympathetic nerve content of the vasoconstrictor agents serotonin (5-HT) and neuropeptide Y (NPY), which are colocalized with noradrenaline, were assessed. Subarachnoid hemorrhage was induced by a single injection of autologous arterial blood into the cerebrospinal fluid (CSF) space of the cisterna magna. The density of 5-HT-containing and NPY-containing perivascular nerve fibers per unit area of vessels was measured at defined intervals from 15 min to 5 days post-SAH. In addition, an HPLC study was performed to quantify the actual amounts of 5-HT and noradrenaline present in circle of Willis vessels at 3 h post-SAH. Comparison was made with sham-operated animals and animals that received a cisternal injection of buffered saline in place of blood. Our results reveal a major increase in cerebrovascular sympathetic nerve content of serotonin, arising by uptake, presumably from subarachnoid blood clot, within the first 3 h post-SAH. Neuropeptide Y content, however, decreased from 3 up to 48 h posthemorrhage. By 3 days post-SAH, when the majority of subarachnoid clot had resorbed, the sympathetic nerve content of both NPY and 5-HT was restored to normal. This pattern of change was not observed in either sham-operated or saline-injected controls.

Animals↗

Ultrastructure of serotonin-containing nerve fibres in the middle cerebral artery of the rat and evidence for its localization within catecholamine-containing nerve fibres by immunoelectron microscopy.

This study has examined the ultrastructural characteristics of serotonin (5-HT)-like immunoreactive (5-HT-I) nerves in the perivascular plexus of a major cerebral blood vessel and their relationship with catecholaminergic (CA) nerves. This was achieved by immunohistochemistry for 5-HT used alone and in combination with simultaneous 5-hydroxydopamine (5-OHDA) false transmitter preloading to demonstrate catecholaminergic nerves examined by electron microscopy. About 15% of perivascular nerves showed some 5-HT-like immunoreactivity. These nerves were characterised by a predominance of small pleomorphic vesicles with a diameter of 40-50 nm and a few large granular vesicles about 100-150 nm diameter. 5-HT-I nerves were found at all levels of the perivascular plexus, from the outer adventitia where they were formed together with non-reactive nerves into bundles by Schwann cells and their processes, to more singly at the adventitia-media border, sometimes in close apposition to smooth muscle cells, separated by some 125 nm. Examination of animals treated by 5-OHDA preloading revealed that 5-HT-I nerves were almost invariably identified as catecholaminergic. However, CA nerves did not always show 5-HT-like immunoreactivity, some 25% only being doubly labelled in this study. Treatment of animals with the catecholaminergic nerve uptake blocker desmethylimipramine resulted in abolition of 5-HT-like immunoreactivity. These results provide direct ultrastructural evidence for the localisation of 5-HT within the perivascular catecholaminergic nerves of a major cerebral vessel and suggest that the contained 5-HT is mainly derived by uptake rather than synthesis within them.

Animals↗

Discovertebral destruction in ankylosing spondylitis complicated by spinal cord compression.

A 56 year old man with ankylosing spondylitis and discovertebral destruction presented with signs of spinal cord compression that was the result of the soft tissue reaction occurring at the level of the discovertebral destruction. This case emphasises the importance of early recognition, use of appropriate imaging techniques (computed tomographic myelography or magnetic resonance), and operative intervention in the management of this rare complication of ankylosing spondylitis.

Humans↗

Experimental penetrating head injury: some aspects of light microscopical and ultrastructural abnormalities.

A high velocity model of penetrating head injury has been developed in the rhesus monkey and a lower velocity model in the baboon. It is apparent that pathological changes are widespread and develop early although the pathogenesis of the diffuse vascular changes is unknown. The present study involved the sampling of grey and white matter from 20 monkeys with high velocity injury, and 10 baboons with low velocity injury together with similar material from a number of normal control animals. 30 minutes after a high velocity injury swelling of perivascular astrocytes was present, sometimes associated with an increase in extracellular fluid. Animals with lower velocity injuries survived for some hours. Astrocytic swelling and perivascular oedema associated with cellular necrosis was frequently found in this group. The pathogenesis of these lesions is discussed.

Animals↗

An ultrastructural study of experimental high velocity penetrating head injury.

Experimental high velocity missile brain injury in the rhesus monkey produces widespread swelling of perivascular astrocytes within 30 min of injury. Possible mechanisms for this lesion include a direct effect of force, chemical mediation secondary to the extravasation of blood, alterations in the permeability of the blood brain barrier and ischaemia. The implications of this findings for the function of the blood brain barrier, for neurotransmission and for neuronal survival are discussed.

Animals↗

Cytochemistry of normal lymphocyte subsets defined by monoclonal antibodies and immunocolloidal gold.

The cytochemical reactivities of 3 acid hydrolases, alpha-naphthyl acetate esterase (ANAE), acid phosphatase and beta-glucuronidase were investigated in normal peripheral blood lymphocyte subsets defined by monoclonal antibodies OKT3, 4, 8 and FMC4 (anti-Ia). A combined monoclonal antibody-immunocolloidal gold/cytochemical staining procedure was used to determine enzyme activities and distributions of reaction product in each subset. Cytochemical profiles for each lymphocyte subset were defined. The majority (greater than 85%) of T cells (OKT3+) were positive for all 3 enzymes whereas a minority (less than 40%) of B cells (FMC4+) displayed reactivity. The cytochemical profiles of T helper/inducer (OKT4+) and T suppressor/cytotoxic (OKT8+) cells were not significantly different and corresponded to that observed for OKT3+ cells; thus none of these enzymes can be used to distinguish normal lymphocyte subsets cytochemically. ANAE reactions were further analysed, in the respective subsets, on the basis of dot-like or scattered/diffuse reactivity. The ratios of cells displaying dot-like: scattered/diffuse reactivity, in the respective subsets, were OKT3+, 5.4:1; OKT4+, 8.1:1; OKT8+, 2.4:1; FMC4+, 0.4:1. The cytochemical profiles and ANAE reactivities of T cell subsets identified by monoclonal antibodies differ from those displayed by T cell subsets defined by Fc receptors and confirms that there is little correlation between subsets defined by these two methods.

Acid Phosphatase↗

Cerebrovascular effects of prostaglandin inhibitors in the gerbil.

Autoregulation of cerebral blood flow (CBF) to mean arterial blood pressure (MABP) of 40-50 mm Hg has been demonstrated in the spontaneously breathing gerbil anaesthetised with barbiturate (60 mg/kg). CO2 reactivity has also been assessed at 2.8% change CBF/mm Hg change in arterial PCO2. In six animals pretreated with indomethacin (3 mg/kg), autoregulation was preserved although the resting CBF was significantly reduced, but CO2 reactivity was completely abolished. 1-n-Butyl imidazole, a specific thromboxane synthetase inhibitor, was used in six other animals (3 mg/kg), and this abolished CO2 reactivity while preserving autoregulation; the effect of this agent has not been described previously. Both drugs inhibit different pathways of prostaglandin metabolism and may interfere with normal CO2 reactivity in several ways. Two explanations are that prostaglandins constitute the final common pathway in effecting cerebrovascular response to CO2 or, alternatively, that the free radicals and ionic fluxes generated during prostaglandin metabolism are a coincidental source of the hydrogen ion changes required.

Animals↗

Cytochemistry of acid hydrolases in chronic B- and T-cell leukemias.

Four acid hydrolases, acid phosphatase (AP), alpha-naphthyl acetate esterase (ANAE), beta-glucuronidase, and N-acetyl-beta-glucosaminidase, were determined cytochemically in peripheral blood lymphocytes from 50 patients with B and T chronic lymphocytic and prolymphocytic leukemias (CLL, PLL) and related disorders. Strong positive reactions were characteristic of the T-cell leukemias while the reactions were weak or negative in B-CLL and B-PLL. Differences in the cytochemical profile of T-CLL and T-PLL were noted. In both, beta-glucuronidase and N-acetyl-beta-glucosaminidase were positive; these enzymes are therefore good cytochemical markers of the chronic T-cell leukemias. AP and ANAE gave different results according to the disease process; AP was strong in T-CLL and variable in T-PLL, while ANAE was strongly positive in T-PLL, but weak or negative in T-CLL. The findings in T-CLL, a proliferation of T gamma lymphocytes, were similar to those of normal T gamma cells. In T-PLL, the findings did not relate to the membrane phenotype as defined by monoclonal antibodies.

Acetylglucosaminidase↗

A model of focal cortical contusion in gerbils.

An experimental model of focal laceration and contusion in gerbils is described. Associated with this injury are systemic changes which are neurogenically mediated and result in an immediate reduction in blood pressure, bradycardia, and generalized reduction in cerebral blood flow. There is generalized edema, as judged by a decreased specific gravity in the brain, probably related to reduced blood flow; superimposed on this, there is an edema gradient which is maximal close to the injury. This, in turn, affects the local capillary bed and prevents any local increase in flow. A separate group studied over a longer time period (6 hours) did not reveal egress of Evans blue into the surrounding tissue and this is in contrast to reports from cold-injury studies.

Animals↗