PubMed Health⌕ Search

Biomedical subjects

D G Okrent

Publications and source records attributed to D G Okrent.

4 recordsLinked to original sources
PubMed1990

Direct cytotoxicity of polymorphonuclear leukocyte granule proteins to human lung-derived cells and endothelial cells.

Neutrophils, in the course of defending the host against microbial invasion, release a potent arsenal of proteins that can potentially damage host tissues. Defensins are major peptides of human polymorphonuclear leukocyte (PMN) granules and are both broadly microbicidal and cytotoxic to several tumor cell lines. To determine whether these peptides could play a role in neutrophil-mediated lung injury, we examined the cytotoxicity of defensins and other PMN granule proteins in a chromium release assay with human lung-derived cell lines MRC-5 (lung fetal fibroblast), A549 (lung adenocarcinoma with features of alveolar epithelium), and primary cultures of human umbilical vein endothelial cells (HUVEC). Crude fractionation of an acid extract of human PMN granules yielded four fractions A-D. Only fraction D (containing mostly defensins) was significantly cytotoxic to all three target cells. In contrast, fraction A (containing myeloperoxidase and lactoferrin) and fraction C (containing lysozyme) had little effect, and fraction B (containing chiefly cathepsin G and elastase) was only injurious to endothelial cells. The cytotoxicity of whole PMN granule extracts on pulmonary epithelial and fibroblast targets could be completely accounted for by their defensin content. Fraction D- and defensin-mediated cytotoxicity was concentration dependent, required at least 10 to 12 h to become manifest, and was inhibited by serum. The role of these peptides in lung damage during acute and chronic inflammation deserves further study.

Blood Proteins↗
PubMed1987

Cardiorespiratory patterns in viral septicemia.

Viral infections are known to produce hypotension and shock, but the cardiorespiratory patterns associated with viral septic shock have not been described. The clinical course of nine patients who died from overwhelming cytomegalovirus sepsis was reviewed. Viral septicemia was associated with increased cardiac index, decreased systemic vascular resistance index (SVRI), and elevated oxygen delivery. This pattern appeared during early and late stages of shock. In contrast to bacterial sepsis and endotoxemia, the pulmonary vascular resistance index (PVRI) was normal. These results indicate that overwhelming viral infection can produce shock associated with a high cardiac output, low peripheral resistance state similar to that seen with bacterial shock. Relative sparing of the pulmonary circulation in viral shock is consistent with the absence of endotoxemia in these patients.

Adult↗
PubMed1987

Metabolic acidosis not due to lactic acidosis in patients with severe acute asthma.

Asthmatics seeking emergency care for severe acute asthma may show metabolic acidosis. We sought to determine the frequency of metabolic acidosis in such patients and to assess the relative contributions of renal bicarbonate loss and lactic acid accumulation to this acidosis. Twenty-two asthmatics (21-71 yr; four males, and 18 females) who came consecutively to the emergency department with severe acute asthma were studied. Most patients reported that their asthmatic symptoms had begun to worsen greater than or equal to 2 days before the emergency department visit. Within several hours, simultaneous measurements of arterial blood gases, whole blood lactate, and serum electrolytes were made. Ten of 22 patients were found to have metabolic acidosis (base deficit greater than 2 mEq/L). All ten patients had nonanion gap acidosis, while nine of ten had whole blood lactate values in the normal range (0.33 to 2.55 mmol/L). In the one patient with an elevated whole blood lactate level, the concentration of lactate in excess of normal (0.45 mmol/L) could not account for the magnitude of the base deficit (-4.9 mEq/L). We conclude that a) nonanion gap metabolic acidosis is very common in asthmatics with acute severe asthma (prevalence 45% in our series), and b) the mechanism of the base deficit in these patients is excessive renal bicarbonate excretion. We believe that the latter occurs as a renal compensatory response to a preceding period of hypocapnia due to hyperventilation related to worsening asthma.

Acid-Base Equilibrium↗