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Biomedical subjects

C L Rice

Publications and source records attributed to C L Rice.

101 records · Page 6Linked to original sources
PubMed1978

The effect of complement depletion on bacterial lipopolysaccharide (LPS)-induced hemodynamic and hematologic changes in the Rhesus monkey.

Lipopolysaccharide (LPS) isolated from Salmonella minnesota R595 or from Escherichia coli 0111:B4 induces hypotension in rhesus monkeys with normal complement levels. This hypotension is accompanied by decreased total peripheral resistance. The depletion of C3 and terminal complement components by prior intraperitoneal administration of the anticomplementary protein cobra factor did not alter the hemodynamic changes which occur following the rapid injection of 5 mg/kg of R595 LPS, the infusion of 500 microgram/kg of R595 LPS, or the injection of 500 microgram/kg of 0111:B4 LPS. We conclude that the LPS-induced hemodynamic changes in the subhuman primate are medicated by pathways which do not require the participation of C3. The kinetics and extent of the neutropenia and thrombocytopenia resulting from the injection of 0111:B4 or R595 LPS were not latered by prior depletion of greater than 95% of the plasma C3.

Animals↗
PubMed1976

The management of flail chest. A comparison of ventilatory and nonventilatory treatment.

Retrospective analysis of forty-two consecutive patients with flail chest injuries admitted to the Trauma Research Unit of the Naval Regional Medical Center, San Deigo from June 1972 to July 1975 compared ventilatory and nonventilatory management. The actual need for ventilatory support in these patients was determined by analyzing their records for evidence of significant pulmonary dysfunction. This allowed division of patients into three groups: "appropriately" ventilated; "inappropriately" ventilated; and nonventilated. Admission PO2 in the "appropriately" ventilated patients was significantly lower than in the other two groups because the former were admitted with respiratory distress and hypoxemia. Significantly more complications occurred in the ventilated groups than in the nonventilated. Treatment-associated complications were more frequent in the ventilated groups. Because of these findings, we belive that mechanical ventilation should be used in the treatment of flail chest injuries only for significant pulmonary dysfunction and not for the purpose of stabilizing the chest wall. If respiratory support is required, it should be discontinued when normal gas exchange has been restored.

Adolescent↗
PubMed1976

Onset of succinylcholine-induced hyperkalemia following denervation.

Denervation injuries in baboons were used to define the time course of the hyperkalemic response to succinylcholine. Half-peak increase in serum potassium (2.78 mEq/l) occurred 8.4 days following injury. Peak increase (5.5 mEq/l) appeared 14 days after injury. However, changes in potassium levels begin as early as four days after injury. Succinylcholine or other depolarizing muscle relaxants should not be used after the fourth day following an injury or denervation that involves two or more limbs.

Animals↗
PubMedDate not supplied

Role of protein synthesis and CD11/CD18 adhesion complex in neutrophil emigration into the lung.

The mechanism of neutrophil (PMN) emigration into the lung may be stimulus-dependent. This study examined PMN emigration in the lung induced by intratracheal instillation of lipopolysaccharide (LPS), Streptococcus pneumoniae (S. pneu) organisms, supernatant from S. pneu incubated with alveolar macrophages (AM phi), Escherichia coli (E. coli) organisms, or phorbol myristate acetate (PMA). Rabbits were pretreated with either the CD18 monoclonal antibody (MAb) 60.3, the protein synthesis inhibitor cycloheximide (Cx), or, in one case, both. Animals were then given one of the above stimuli to elicit PMN emigration. Four hours after the stimulus was instilled, animals were killed and total and differential cell counts were performed on bronchoalveolar lavage (BAL) fluid. PMN emigration in response to PMA was virtually abolished by MAb 60.3, but was not significantly inhibited by Cx. Emigration induced by LPS was inhibited by 80% by either MAb 60.3 or Cx, and greater than 94% when MAb 60.3 and Cx were given simultaneously. Emigration in response to E. coli organisms was 80% inhibited by MAb 60.3. Emigration induced by S. pneu was approximately 50% inhibited by MAb 60.3, but was greater than 90% blocked by Cx. The MAb 60.3 had approximately the same effect on PMN emigration toward the supernatant from co-incubation of AM phi with S. pneu as it did toward live S. pneu. It is concluded that the mechanism of PMN emigration into the lung is stimulus-dependent. The CD18-dependent mechanism is responsible for the majority of the emigration in response to PMA, E. coli LPS, and E. coli organisms. S. pneu and supernatant from S. pneu + AM phi produce a CD18-independent pathway. These data suggest the requirement for de novo protein synthesis for PMN emigration in response to LPS and S. pneu, but not for PMA-induced emigration.

Animals↗