acidosis/edema

Current practice with respect to the use of a dilutional prime for cardiopulmonary bypass (CPB) varies widely, and the safe lower limit of perfusate protein content has not been defined. We studied this question in 75 rabbits subjected to a 1-hour CPB with a perfusate colloid osmotic pressure (COP)

The case of a 45-year-old woman with pheochromocytoma, who presented with severe abdominal pain and headache, diabetes mellitus, lactic acidosis and pulmonary edema, is described and discussed. Spleen infarction, not so far described as an ischemic complication of pheochromocytoma, was seen in

BACKGROUND Glutaraldehyde and quaternary ammonium compounds are widely used as disinfectants and sterilizing agents. Glutaraldehyde is irritating to the eyes and upper respiratory tract, and has been associated with occupational asthma. Acute oral ingestion of a concentrated solution has not been

Massive cyanide poisoning occurred in a 21-year-old man who had ingested 600 mg of potassium cyanide. The clinical course was marked by acute pulmonary edema and lactic acidosis. Because the poison was unidentified until nine hours after ingestion, the patient received only supported treatment which

Compared to littermate controls, unstressed Jimpy mice have higher brain water, sodium, potassium and chloride contents and lower carbonic anhydrase activity. When stressed by CO2 to produce a respiratory acidosis or by injection of distilled water to produce brain edema, the Jimpy mouse brain has

OBJECTIVE Low tidal volume (V(T)) ventilation strategies may be associated with permissive hypercapnia, which has been shown by ex vivo and in vivo studies to have protective effects. We hypothesized that hypercapnic acidosis may be synergistic with low V(T) ventilation; therefore, we studied the

Background: Glutaraldehyde is a commonly used disinfectant in most hospitals. It is known to be an irritating agent to the airway. With the exception of one small-quantity (75 mL) ingestion, no large-volume ingestion has been previously

OBJECTIVE Dysregulation of water homeostasis induces cerebral edema. Edema is a major cause of morbidity and mortality following traumatic brain injury (TBI). Aquaporin-1 (AQP-1), a water channel found in the brain, can function as a transporter for CO2 across the cellular membrane. Additionally,

Pathogenic variants in mitochondrial aminoacyl-tRNA synthetases result in a broad range of mitochondrial respiratory chain disorders despite their shared role in mitochondrial protein synthesis. LARS2 encodes the mitochondrial leucyl-tRNA synthetase, which attaches leucine to its cognate tRNA.

Three, previously healthy, patients developed profuse vomiting. In the further course of the disease there was a marked deterioration in their general condition with massive metabolic acidosis, cerebral symptoms and, finally, deep coma which ended in death, without any evidence of poisoning.