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Biomedical subjects

A H Schultheis

Publications and source records attributed to A H Schultheis.

6 recordsLinked to original sources
PubMed1994

Guinea pig lung inflammatory cell changes following acute ozone exposure.

The time course of inflammatory cell infiltration into guinea pig lungs following a single 4 h exposure to 2 ppm O3 was established by measuring the changing cell populations recovered by both bronchoalveolar lavage (BAL) and collagenase tissue digestion. Analysis of BAL-recovered albumin was used as an indicator of permeability damage and demonstrated an increase immediately following ozone exposure, reaching a maximum within 24 h, but returning to air-control levels by 7 days post-ozone exposure. A twofold enhancement in macrophages was observed in the lavage-recovered cell population after 2 days, returning to air-control numbers by 7 days. Collagenase digest-recovered monocytes and macrophages, identified by nonspecific esterase staining, were found to be elevated between 2 and 14 days following O3 exposure. Immediately following O3 exposure, a 4.5-fold increase in collagenase digest-recovered neutrophils was observed, with a subsequent decline to air-exposed lung levels during the next 12 h. In contrast, BAL-recovered neutrophils were observed to be increased immediately following O3 exposure at a level that was sustained for up to 3 days. The tissue accumulation of neutrophils was not associated with their subsequent appearance in the lavageable spaces. Although significant increases in collagenase digest-recovered eosinophils could not be detected, lavage-recovered eosinophil numbers were transiently increased by threefold after 3 days. By employing both BAL and collagenase digestion to evaluate this model of reversible lung injury, this study demonstrated that the use of BAL-recovered cell measurements alone does not adequately reflect the early inflammatory cell changes taking place within oxidant-exposed lungs.

Animals↗
PubMed1994

Ozone-induced airway hyperresponsiveness and loss of neuronal M2 muscarinic receptor function.

The effect of acute ozone exposure on the function of efferent parasympathetic nerves, M3 muscarinic receptors on airway smooth muscle, and inhibitory M2 muscarinic receptors on the parasympathetic nerves was studied. Immediately after exposure to 2.0 ppm ozone for 4 h, guinea pigs became hyperresponsive to electrical stimulation of the vagus nerves. The normal airway response to intravenous cholinergic agonists at this time demonstrates normal M3 receptor function. M2 muscarinic receptors on the nerves, which normally inhibit release of acetylcholine, were dysfunctional after ozone exposure, as demonstrated by the failure of the muscarinic agonist pilocarpine to inhibit, and the failure of the M2 antagonist gallamine to potentiate, vagally mediated bronchoconstriction. Thus, loss of inhibitory M2 muscarinic receptor function after ozone exposure potentiates release of acetylcholine from the vagus nerves, increasing vagally mediated bronchoconstriction. By 14 days, postozone responses to vagal nerve stimulation were not different from those of air-exposed animals and the function of the neuronal M2 muscarinic receptor was normal, confirming that ozone-induced hyperresponsiveness is reversible.

Acetylcholine↗
PubMed1991

Inflammatory cell influx into ozone-exposed guinea pig lung interstitial and airways spaces.

As a model of non-immunological lung inflammation, guinea pigs were exposed to 2.0 ppm ozone for 4 hours. Polymorphonuclear leukocytes (PMNs) rapidly accumulated in lung interstitium but declined from 147 +/- 34 million cells to control values (33 +/- 6 million cells) within the first 24 hours. Bronchoalveolar lavage (BAL) recovered PMNs were maximal by 3-6 hours (4 +/- 1 million cells) and remained elevated for 3 days. Macrophage numbers were doubled in lavageable spaces but those in interstitium increased by only a third at 2 days post-exposure. By 7 days post-exposure BAL macrophages had declined to control values of 12 +/- 2 million cells while those in interstitium remained elevated through 14 days. These data demonstrate that BAL does not necessarily reflect cellular changes in lung interstitium.

Animals↗
PubMed1990

Hypercholesterolemia: prevention, detection and management.

High serum cholesterol, leading to atherosclerosis, heart attack and stroke, is a major health problem in the United States and other Western countries. Hypercholesterolemia is amenable to dietary and other lifestyle changes that are brought about through education and supportive counseling. Dietary modification includes weight control, lowered intake of fats and cholesterol, and increased ingestion of water-soluble fiber. This article explores cholesterol metabolism and the mechanisms of factors lowering serum cholesterol in the body. The actions of chylomicrons, very low density lipoproteins, low density lipoproteins and high density lipoproteins are reviewed. Detection and evaluation of serum total and low density lipoproteins, and pharmacological therapy for hypercholesterolemia are discussed. Specific techniques for the health care provider to use in educating and counseling clients are emphasized.

Counseling↗