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Biomedical subjects

A M Allen

Publications and source records attributed to A M Allen.

At least 127 records · Page 7Linked to original sources
PubMed1971

Tyzzer's Disease of Rabbits: Isolation and Propagation of Bacillus piliformis (Tyzzer) in Embryonated Eggs.

Bacillus piliformis (Tyzzer) was isolated from the liver of rabbits with Tyzzer's disease and serially passaged in embryonated hens' eggs. Weanling rabbits given the 32nd egg passage developed lesions typical of Tyzzer's disease and died. B. piliformis was reisolated from the liver of these rabbits in embryonated eggs. Outside the host cell, the motile vegetative phase appeared to be unstable, and no means was found to preserve its viability; the results of titrations were believed to be dependent upon the resistant stage or spore. The spore withstood repeated freeze and thaw and was resistant to heat treatment of 56 C for 1 hr but not 80 C for 0.5 hr. None of several antibacterial substances tested in embryonated eggs was completely inhibitory; B. piliformis was resistant to sulfamethazine and chloramphenicol. The taxonomic position of this pleomorphic, gram-negative, sporeforming, pathogenic bacterium which appears to grow only in certain cells of several species remains unresolved.

Journal Article↗
PubMedDate not supplied

A new model of concussive brain injury in the cat produced by extradural fluid volume loading: I. Biomechanical properties.

This study presents a new device for producing experimental, concussive head injury together with a detailed description of biomechanical features of fluid percussion brain injury in the cat. Anaesthetized cats were subjected to multiple (N = 3) or single injuries (N = 87). The variables studied in repeated injury experiments included the volume of fluid injected intracranially, rate of fluid flow, and the associated pressure transients recorded extracranially in the injury device and intracranially at supratentorial and infratentorial sites. Peak fluid flow increased with increasing volumes of fluid loaded intracranially. Extracranial pressure peaks and durations increased when volume loading was increased. Extracranial and intracranial pressure transients were similar at all recording sites. The form of pressure transients recorded in single injury experiments was similar to that recorded in multiple injury experiments. In single injury experiments, the extracranial pressure peaks and durations also increased with increased intracranial fluid volume loading. The slopes describing the relationships between intracranial volume loading and extracranial pressure transients were significantly different in single and multiple injury experiments. Details of the design and use of the head injury device are also discussed.

Animals↗
PubMedDate not supplied

A new model of concussive brain injury in the cat produced by extradural fluid volume loading: II. Physiological and neuropathological observations.

This study examined physiological and histopathological changes in the cat produced by a new experimental fluid injury device. Spontaneously breathing (N = 14) and artificially ventilated (N = 45) cats were subjected to systemically varied magnitudes of fluid percussion brain injury. Within certain injury ranges, increasing magnitudes of fluid percussion injury produced increasing durations of apnea, as well as greater transient increases in mean arterial blood pressure, intracranial pressure and cerebral perfusion pressure. Acute increases in intracranial pressure may have been related to cerebral vasodilatation produced by the systemic hypertension following brain injury. Injuries associated with pressure transients greater than 10 atm ms produced concussive responses, including irreversible apnea in spontaneously breathing cats and temporary pupillary dilatation, increases in heart rate and mean arterial blood pressure in artificially ventilated cats. Injuries greater than 39 atm ms frequently produced histopathological and physiological indices of significant irreversible brain damage, including fixed and dilated pupils, systemic cardiovascular hypotension and deteriorating blood gases. Injury magnitudes less than 20 atm ms did not produce macroscopic evidence of histopathology, intermediate injury ranges produced increasing evidence of subarachnoid and petechial hemorrhage while injury levels greater than 40 atm ms frequently produced significant histopathology including massive hematomas. Injury greater than 10 atm ms resulted in opening of the blood-brain barrier, as assessed by extravasation of horseradish peroxidase. Injury greater than 19 atm ms produced suppression of EEG amplitudes which did not recover for up to 40 minutes after injury. These data provide detailed information on the physiological and histopathological consequences of fluid percussion injury in the cat and indicate that this modified fluid percussion apparatus can produce graded levels of brain injury similar to those previously reported for fluid percussion injury.

Animals↗
PubMedDate not supplied

Interactions of angiotensin II with central catecholamines.

There is a large body of anatomical and functional evidence supporting an interaction between brain angiotensin and central catecholamine systems. Angiotensin II AT1 receptors have been identified on dopamine containing cells in the substantia nigra and striatum of human brain using receptor autoradiography. Using in vivo microdialysis we have demonstrated that locally administered angiotensin II stimulates dopamine release from the striatum of conscious rats. Since some angiotensin receptor antagonists and angiotensin converting enzyme inhibitors can cross the blood brain barrier it is possible that they interact with the brain catecholaminergic systems.

Angiotensin II↗