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Biomedical subjects

J C Fackler

Publications and source records attributed to J C Fackler.

28 records · Page 2Linked to original sources
PubMed1993

Recovery of cerebral blood flow and energy state in piglets after hypothermic circulatory arrest versus recovery after low-flow bypass.

A miniature piglet model that replicates clinical hypothermic (14 degrees C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per minute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral metabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. Data from five animals that underwent circulatory arrest and five animals that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standard error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. In a parallel study with the same animal model, phosphorus 31 magnetic resonance spectroscopy was used to assess cerebral phosphocreatine, nucleoside triphosphate (adenosine triphosphate), and intracellular pH. Five animals (aged 31.8 +/- 1.1 days) underwent circulatory arrest, and five underwent low-flow bypass. A brief phase of hyperemic carotid blood flow was seen immediately after the onset of reperfusion in the circulatory arrest group but not in the low-flow group. In the circulatory arrest and low-flow bypass groups, cerebral blood flow (percentage of baseline 71.2% +/- 8.3% and 69.1% +/- 5.8%, respectively), cerebral oxygen consumption (45.6% +/- 10.0%, 44.5% +/- 7.6%), and cerebral glucose consumption (31.5% +/- 30.7%, 83.5% +/- 24.2%) remained depressed after 45 minutes of reperfusion and rewarming to normothermia. However, after 3 more hours of pulsatile normothermic reperfusion, cerebral oxygen consumption and cerebral glucose consumption had returned to baseline. Phosphocreatine, adenosine triphosphate, and pH were maintained at or above baseline levels throughout low-flow bypass and throughout 3 hours of normothermic reperfusion. In contrast, both phosphocreatine and adenosine triphosphate became undetectable 32 +/- 3.7 minutes after onset of circulatory arrest. During and early after circulatory arrest, pH decreased to a minimum of 6.506 +/- 0.129 at 40 minutes after reperfusion. After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphate recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respectively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.041). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving baseline levels suggests that the degree of hypothermia used provides adequate protection for acute cerebral recovery after 1 hour of circulatory arrest.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1992

Retinal hemorrhages in newborn piglets following cardiopulmonary resuscitation.

OBJECTIVE: To determine whether conventional cardiopulmonary resuscitation causes retinal hemorrhages in piglets. DESIGN: Nonrandomized observations. SETTING: Animal physiology laboratory. PARTICIPANTS: Six 3.5- to 4.5-kg piglets. INTERVENTIONS: Fifty minutes of conventional, closed chest cardiopulmonary resuscitation. MEASUREMENTS/MAIN RESULTS: Intrathoracic venous pressure (right atrium) and intracranial venous pressure (sagittal sinus) were directly measured. At 5 minutes of cardiopulmonary resuscitation, the mean (+/- SEM) sagittal sinus pressure was 41 +/- 8 mm Hg and the mean right atrial pressure was 58 +/- 9 mm Hg. The pressures were sustained throughout the 50 minutes of cardiopulmonary resuscitation. At autopsy, there was no gross or microscopic evidence of retinal hemorrhages. CONCLUSION: These results support the conclusion that cardiopulmonary resuscitation does not cause retinal hemorrhages.

Animals↗
PubMed1992

Rethinking brain death.

OBJECTIVE: To evaluate whether current criteria for the diagnosis of brain death fulfill the requirement for the "irreversible cessation of all functions of the entire brain, including the brainstem." DATA SOURCES: Clinical, philosophical, legal, and public policy literature on the subject of brain death. DATA EXTRACTION/SYNTHESIS: We advance four arguments to support the view that patients who meet the current clinical criteria for brain death do not necessarily have the irreversible loss of all brain function. First, many clinically brain-dead patients maintain hypothalamic-endocrine function. Second, many maintain cerebral electrical activity. Third, some retain evidence of environmental responsiveness. Fourth, the brain is physiologically defined as the central nervous system, and many clinically brain-dead patients retain central nervous system activity in the form of spinal reflexes. We explore options for resolving these inconsistencies between the conceptual definition and the clinical criteria used to make the diagnosis of brain death. CONCLUSIONS: Brain death is a valid conception of death because it signifies the permanent loss of consciousness. Brain death criteria should therefore be based on the diagnosis of the permanent loss of consciousness rather than that of the loss of vegetative brain functions. Revision of our current "whole brain" definition of brain death to a "higher brain" standard should be considered.

Brain↗
PubMed1988

Age-specific characteristics of brain death in children.

Clinical and neuropathologic characteristics of 45 children who met criteria for brain death were analyzed. Children between 2 months and 1 year of age were compared with children older than 1 year and children older than 5 years. The observation period to fulfill brain death criteria was not different between the age groups. Deep tendon and spinal reflexes were preserved significantly less frequently in children younger than 1 year old. Diabetes insipidus and the necessity of inotropic support were significantly more frequent in children older than 5 years. Fifty-eight percent (26/45) of patients had no cerebral perfusion pressure before death. However, 18% (8/45) of patients never had a cerebral perfusion pressure below 40 mm Hg. No relationships could be shown between the clinical or physiologic factors and neuropathologic findings. We found no support for using different brain-death criteria for children between 2 months and 1 year of age.

Adolescent↗
PubMed1985

Epstein-Barr virus infection in a child with acquired immunodeficiency syndrome.

A 3-year-old girl, born to an intravenous-drug-dependent mother, had protracted diarrhea, failure to thrive, generalized lymphadenopathy, and recurrent fevers during the first six months of life. At 7 months of age, the Epstein-Barr virus (EBV) genome was detected in her saliva by DNA dot-blot hybridization using a cloned EBV probe. Spontaneous EBV+ lymphoblastoid cell lines had repeatedly developed from her peripheral blood lymphocytes over the subsequent 2 1/2 years. At 11 months of age, persistent tachypnea and a diffuse pulmonary infiltrate developed. Lung biopsy demonstrated a florid, peribronchiolar lymphocytic infiltrate and the EBV genome was identified in the lung tissue. Serum anti-EBV antibodies remained undetectable until 14 months of age. She had a T4+/T8+ ratio of less than 0.8 and serum antibody to human T-cell lymphotropic virus type III. The delayed seroresponse of this patient to symptomatic EBV infection suggests that reliance on EBV serology to diagnose EBV infection in immunocompromised hosts may be inappropriate, and other methods such as DNA probes should be used.

Acquired Immunodeficiency Syndrome↗