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Biomedical subjects

L Lichtenstein

Publications and source records attributed to L Lichtenstein.

12 recordsLinked to original sources
PubMed1999

Relationship between histamine and physiological changes during the early response to nasal antigen provocation.

To investigate the temporal relationships of mediator release and physiological changes during the early response to allergen, we challenged allergic individuals intranasally with antigen and followed their responses. This was done by using small filter paper disks to challenge one nostril and collect secretions from both the challenged and the contralateral nostril, thus enabling us to evaluate the nasonasal reflex. There was a significant increase in sneezing after allergen challenge that peaked within 2 min and returned to baseline. The weights of nasal secretions as well as nasal symptoms increased immediately and remained significantly elevated for 20 min in both nostrils. Nasal airway resistance increased slowly, reaching its peak at approximately 6 min after challenge on the ipsilateral side, but it did not change on the contralateral side. Histamine levels peaked 30 s after removal of the allergen disk on the side of challenge, whereas albumin levels peaked after those of histamine. Lactoferrin paralleled the increase in secretion weights and occurred in both nostrils. Increasing doses of antigen produced dose-dependent increases in all parameters, whereas control challenges produced no response. These studies describe a human model for the evaluation of the allergic response that is capable of simultaneously measuring mediator release and the physiological response, including the nasonasal reflex. This model should prove useful in studying the mechanism of allergic rhinitis in humans.

Adult↗
PubMed1995

[Preliminary evaluation of composite materials for the repair of incisional hernias].

Recent investigations have shown that direct exposure of the intestines to currently available absorbable and nonabsorbable biomaterials can result in their adhesion to the bowel. This can then lead to bowel obstruction or migration of the mesh into the intestinal lumen and formation of intestinal fistula. It has been suggested by some authors that an absorbable covering of the peritoneal side of a nonabsorbable mesh would prevent adhesions and biomaterial related intestinal fistula formation. However, the effectiveness of such a combination has not been substantiated by recent experimental and clinical studies. This preliminary report examines the feasibility of combining porous and non-porous biomaterials for the creation of a composite that would incorporate with the abdominal wall without adhering to the intestines.

Animals↗
PubMed1988

In vivo release of inflammatory mediators by hyperosmolar solutions.

Hyperosmolar environments induce histamine release from mast cells and basophils in vitro. To assess whether the same stimulus induces mediator release in vivo, 15 healthy human volunteers underwent nasal challenges with instilled solutions of differing osmolalities: lactated Ringer's solution (257 +/- 3 mOsm/kg), isosmolar mannitol (277 +/- 6 mOsm/kg), and hyperosmolar mannitol (869 +/- 8 mOsm/kg). The effect of these challenges on the volume, osmolality, and inflammatory mediator content of subsequent 5-ml isosmolar lavages was determined. The volumes of lavages returned after hyperosmolar challenges were significantly greater than those after isosmolar challenges (5.5 +/- 0.2 ml versus 4.2 +/- 0.1 ml; p less than 0.01) and these lavage solutions had higher osmolalities. Even when corrected for increased volumes, the lavages after hyperosmolar challenges contained significantly higher quantities of inflammatory mediators such as histamine (29.0 versus 10.1 ng; p less than 0.01), TAME-esterase activity (32.7 versus 11.1 cpm x 10(-3); p less than 0.01), and immunoreactive leukotrienes (9.9 versus 3.4 ng; p less than 0.01). The changes in mediators were dose dependent in that incremental increase in challenge osmolality were associated with incremental increases in histamine release. Therefore, when exposed to hyperosmolar stimuli in vivo, the nasal respiratory airway releases inflammatory mediators and fluid rapidly shifts into the airway lumen. It has been suggested that the mediator release observed on breathing cold and dry air is due to increased osmolality of airway secretions; the present data confirm that osmotic variations at the airway surface can provide an adequate stimulus for cell activation.

Adult↗
PubMed1987

The effect of a topical tricyclic antihistamine on the response of the nasal mucosa to challenge with cold, dry air and histamine.

We have previously demonstrated that azatadine, a tricyclic antihistamine, known also to inhibit mediator release from mast cells and basophils in vitro, inhibits the early release of histamine and other mediators after nasal challenge with antigen. In this article, we studied the effect of azatadine on preventing the release of histamine after nasal challenge with cold, dry air (CDA) and its effect on antagonizing nasal challenge with histamine. With histamine challenge, azatadine inhibited symptoms (sneezing, nasal congestion, and rhinorrhea) and the increase in the level of albumin in nasal secretions (p less than 0.01 all). With challenge with CDA, the drug had no effect on either symptoms or histamine and N-tosyl-L-arginine methyl ester-esterase release. Although the patterns of mediator release after CDA and after the early reaction to antigen are similar, the pharmacologic control differs, suggesting different mechanisms of induction of histamine release from mast cells.

Administration, Topical↗
PubMed1979

In vitro studies of antigen-induced bronchospasm: effect of antihistamine and SRS-A antagonist on response of sensitized guinea pig and human airways to antigen.

Exposure of sensitized guinea pig tracheal rings or human bronchial strips to specific antigen in vitro resulted in a rapidly developing, prolonged contraction that was resistant to washing. Treatment of the tissue with diphenhydramine, a histamine H1 antagonist, before antigen delayed the onset and decreased the amplitude of the initial phase of the contraction but did not reduce the duration. Diphenhydramine treatment after development of the contraction did not relax the airway tissue. Antigen-induced histamine release from guinea pig trachea and from human bronchus was complete within the initial 15% of the duration of the contraction. Treatment of sensitized airway tissue with FPL 55712, a SRS-A antagonist, before antigen selectively inhibited the prolonged phase of the response. FPL 55712 administration after the development of antigen-induced contraction resulted in relaxation. These data suggest that both histamine and SRS-A are involved in the response of sensitized guinea pig and human airway tissue to antigen, with histamine mediating the early phase of the contraction and SRS-A primarily mediating the protracted phase.

Animals↗