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Biomedical subjects

A L Bleyaert

Publications and source records attributed to A L Bleyaert.

26 records · Page 2Linked to original sources
PubMed1980

[Pathogenesis and treatment of anoxic encephalopathy. Definition and importance of experimental animal models (author's transl)].

A reproducible noninvasive monkey model for global brain ischemia with exact insult (no flow x 16 min) to the brain, with survival and with standardized preischemic, ischemic and postischemic variables is described. This model allowed us to demonstrate for the first time: 1) that a substantial part of brain damage early postischemia is reversible and amenable especially to barbiturate treatment; 2) that the postischemic brain shows increased vulnerability for additional insults. Optimal postischemic intensive monitoring and immobilization for 24-48 hours is important for improved outcome; 3) that immediate postischemic reperfusion pressure (MAP 110-150 mm Hg) significantly improves the outcome; 4) that heparinisation during ischemia has no protective effect and 5) that postischemic heparinisation and intravenous hemodilution does not ameliorate the outcome. The protective effect of trimetaphan against neurogenic pulmonary edema can be explained by the prevention of pulmonary hypertension but its protective effect on the development of secondary cerebral edema has to be elucidated.

Animals↗
PubMed1977

Brain blood flow autoregulation and metabolism during halothane anesthesia in monkeys.

Past studies suggest that halothane causes cerebrovascular dilatation and increased cerebral blood flow (CBF); these properties may be relevant to its use for neurosurgical procedures. We studied CBF autoregulation in monkeys during anesthesia with 66% N2O/33% O2 and with 0.5%, 1.0%, and 2.0% inspired halothane at various cerebral perfusion pressures (CPP) achieved by infusion of trimethaphan camsylate or phenylephrine. CBF was measured by monitoring brain xenon-133 clearance after intra-arterial injection of the isotope in saline. CBF autoregulation was intact during N2O/O2 and during 0.5% halothane/N2O/O2 anesthesia at CPPs ranging from 50 to 100 mmHg, but began to fail at 1.0% halothane. Complete loss of autoregulation occurred during 2% halothane/N2O/O2 anesthesia. Estimated brain O2 consumption fell by 30%, 40%, and 50% during 0.5%, 1.0%, and 2.0% halothane anesthesia, respectively, compared to O2 consumption during N2O/O2 anesthesia (100%).

Anesthesia↗
PubMedDate not supplied

Global brain ischemia: a reproducible monkey model.

We developed a monkey model of 16 minutes global brain ischemia (GBI) resulting in reproducible, severe, permanent functional neurologic deficit with long term (7 days) postischemic (PI) survival made possible by standardized intensive care with 24 hour coverage by trained personnel. Quantitated neurologic deficit (ND) and brain histopathological examinations were developed. Fifteen minutes GBI resulted in rapid recovery within12--24 hours PI without residual neurologic sequelae. Twenty minutes GBI caused severe neurologic deficit and within 4 days PI, a delayed Cushing response eventually leading to cardiac arrest. Sixteen minutes GBI resulted in severe neurologic deficit (monkeys unable to sit, stand, walk, or feed themselves), but with long term survival. Brain histopathological analyses revealed a combination of cortical and brainstem lesions. Severest changes were observed in the occipital (calcarine) cortex with less severe damage in the frontal and temporal regions. Oculomotor nuclei and medial longitudinal fasciculus in the midbrain were regularly affected. With this model we can test the efficacy of promising therapies in terms of clinically relevant variables.

Animals↗
PubMedDate not supplied

Reflex sympathetic dystrophy involving the foot.

Reflex sympathetic dystrophy often presents with the subjective chief symptom of pain. This paper demonstrates that careful study of the subtle and often cyclical objective signs can be used to assess the state of the disease. It may also evaluate progress of treatment.

Autonomic Nerve Block↗
PubMedDate not supplied

Case report: increased myocardial irritability with halothane and aminophylline.

Increased cardiac sensitivity to epinephrine during halothane anesthesia has been well documented; however, there are few reports of increased cardiac irritability due to interaction between halothane anesthesia and aminophylline. The following case report is suggestive of such an interaction resulting in ventricular tachycardia.

Aminophylline↗