Biomedical subjects

A C Bain

Publications and source records attributed to A C Bain.

5 recordsLinked to original sources

PubMed2001

Multicenter study of principles-based waveforms for external defibrillation.

STUDY OBJECTIVE: The efficacy of a shock waveform for external defibrillation depends on the waveform characteristics. Recently, design principles based on cardiac electrophysiology have been developed to determine optimal waveform characteristics. The objective of this clinical trial was to evaluate the efficacy of principles-based monophasic and biphasic waveforms for external defibrillation. METHODS: A prospective, randomized, blinded, multicenter study of 118 patients undergoing electrophysiologic testing or receiving an implantable defibrillator was conducted. Ventricular fibrillation was induced, and defibrillation was attempted in each patient with a biphasic and a monophasic waveform. Patients were randomly placed into 2 groups: group 1 received shocks of escalating energy, and group 2 received only high-energy shocks. RESULTS: The biphasic waveform achieved a first-shock success rate of 100% in group 1 (95% confidence interval [CI] 95.1% to 100%) and group 2 (95% CI 94.6% to 100%), with average delivered energies of 201+/-17 J and 295+/-28 J, respectively. The monophasic waveform demonstrated a 96.7% (95% CI 89.1% to 100%) first-shock success rate and average delivered energy of 215+/-12 J for group 1 and a 98.2% (95% CI 91.7% to 100%) first-shock success rate and average delivered energy of 352+/-13 J for group 2. CONCLUSION: Using principles of electrophysiology, it is possible to design both biphasic and monophasic waveforms for external defibrillation that achieve a high first-shock efficacy.

Aged↗

PubMed2001

Dynamic stretch correlates to both morphological abnormalities and electrophysiological impairment in a model of traumatic axonal injury.

In this investigation, the relationships between stretch and both morphological and electrophysiological signs of axonal injury were examined in the guinea pig optic nerve stretch model. Additionally, the relationship between axonal morphology and electrophysiological impairment was assessed. Axonal injury was produced in vivo by elongating the guinea pig optic nerve between 0 and 8 mm (Ntotal = 70). Morphological damage was detected using neurofilament immunohistochemistry (SMI 32). Electrophysiological impairment was determined using changes in visual evoked potentials (VEPs) measured prior to injury, every 5 min for 40 min following injury, and at sacrifice (72 h). All nerves subjected to ocular displacements greater than 6 mm demonstrated axonal swellings and retraction bulbs, while nerves subjected to displacements below 4 mm did not show any signs of morphological injury. Planned comparisons of latency shifts of the N35 peak in the VEPs showed that ocular displacements greater than 5 mm produced electrophysiological impairment that was significantly different from sham animals. Logit analysis demonstrated that less stretch was required to elicit electrophysiological changes (5.5 mm) than morphological signs of damage (6.8 mm). Moreover, Student t tests indicated that the mean latency shift measured in animals exhibiting morphological injury was significantly greater than that calculated from animals lacking morphological injury (p < 0.01). These data show that distinct mechanical thresholds exist for both morphological and electrophysiological damage to the white matter. In a larger context, the distinct injury thresholds presented in the report will aid in the biomechanical assessment of animate models of head injury, as well as assist in extending these findings to predict the conditions that cause white matter injury in humans.

Animals↗

PubMed2000

Tissue-level thresholds for axonal damage in an experimental model of central nervous system white matter injury.

In vivo, tissue-level, mechanical thresholds for axonal injury were determined by comparing morphological injury and electrophysiological impairment to estimated tissue strain in an in vivo model of axonal injury. Axonal injury was produced by dynamically stretching the right optic nerve of an adult male guinea pig to one of seven levels of ocular displacement (Nlevel = 10; Ntotal = 70). Morphological injury was detected with neurofilament immunohistochemical staining (NF68, SM132). Simultaneously, functional injury was determined by the magnitude of the latency shift of the N35 peak of the visual evoked potentials (VEPs) recorded before and after stretch. A companion set of in situ experiments (Nlevel = 5) was used to determine the empirical relationship between the applied ocular displacement and the magnitude of optic nerve stretch. Logistic regression analysis, combined with sensitivity and specificity measures and receiver operating characteristic (ROC) curves were used to predict strain thresholds for axonal injury. From this analysis, we determined three Lagrangian strain-based thresholds for morphological damage to white matter. The liberal threshold, intended to minimize the detection of false positives, was a strain of 0.34, and the conservative threshold strain that minimized the false negative rate was 0.14. The optimal threshold strain criterion that balanced the specificity and sensitivity measures was 0.21. Similar comparisons for electrophysiological impairment produced liberal, conservative, and optimal strain thresholds of 0.28, 0.13, and 0.18, respectively. With these threshold data, it is now possible to predict more accurately the conditions that cause axonal injury in human white matter.

Analysis of Variance↗

PubMed1999

Experimental investigation of cerebral contusion: histopathological and immunohistochemical evaluation of dynamic cortical deformation.

We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral contusions. DCD produces experimental contusion by rapidly deforming the cerebral cortex with a transient, nonablative vacuum pulse of short duration (25 milliseconds) to mimic the circumstances of traumatic injury. A neuropathological evaluation was performed on brain tissue from adult rats sacrificed 3 days following induction of either moderate (4 psi, n = 6) or high (8 psi, n = 6) severity DCD. In all animals, DCD produced focal hemorrhagic lesions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss in the cortex at the injury site, with the volume of cell loss dependent upon the mechanical loading (p < 0.001). Axonal pathology shown with neurofilament immunostaining (SMI-31 and SMI-32) was observed in the subcortical white matter inferior to the injury site and in the ipsilateral internal capsule. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining revealed widespread reactive astrocytosis surrounding the necrotic region in the ipsilateral cortex. This analysis confirms that rapid mechanical deformation of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that massive release of neurotoxic substances from a contusion may cause damage throughout the brain, these data emphasize the importance of combined injury mechanisms, e.g. mechanical distortion and excitatory amino acid mediated damage, that underlie the complex pathology patterns observed in traumatic brain injury.

Animals↗

PubMed1995

Biomechanical analysis of experimental diffuse axonal injury.

The purpose of this paper is to present results from methodologies used in our laboratory that are targeted toward identifying specific brain injury thresholds. Results from studying one form of brain injury, diffuse axonal injury, are presented in this report. Physical models, or surrogates, of the skull-brain complex are used to estimate the relationship between inertial loading and brain deformation. A porcine model of diffuse axonal injury, developed with information from these physical models and earlier in vitro tissue modeling studies, is used to correlate histologic and radiologic evidence of axonal injury to predicted regions of injury from the experimental and theoretical analysis. These results form the basis for developing improved diffuse brain injury tolerance levels, as well as identifying new means of diagnostic and treatment techniques for diffuse axonal injury.

Animals↗