PubMed Health⌕ Search

Biomedical subjects

R L Klein

Publications and source records attributed to R L Klein.

138 records · Page 8Linked to original sources
PubMedDate not supplied

Adrenal enkephalin and catecholamine contents following subarachnoid hemorrhage in cats.

A "closed space" subarachnoid hemorrhage (SAH) was produced experimentally in cats by rupture of the right middle cerebral artery to test the working hypothesis that a stressful event which provokes powerful sympathoadrenal discharge: causes a massive release of co-stored endogenous enkephalins together with catecholamines, induces an increased rate of opioid peptide precursor processing and/or synthesis, and eventually results in markedly elevated tissue levels of enkephalins relative to controls and to co-stored catecholamines. Adrenal medulla and other tissues were analyzed for met- and leu-enkephalins by RIAs and norepinephrine and epinephrine by HPLC-EC at 4 hrs, 3, 10, 16 and 30 days post-SAH. Catecholamines of adrenal medulla were already decreased at 4 hrs and by 3 days post-SAH depletion of epinephrine reached 86% and norepinephrine 53% compared to controls. Concurrently, at 4 hrs and 3 days post-SAH, the adrenal medulla was depleted 47% of met- and 53% of leu-enkephalins. By 10 days post-SAH, when catecholamines had regained control levels, met-enkephalin was elevated to 240% of control and 435% compared to the 3 day depletion; it remained elevated through 30 days post-SAH. In comparison, after 10 days reserpine treatment when catecholamines were markedly depleted, met-enkephalin rose to 970% and leu-enkephalin to 360% relative to controls, confirming recent reports in the literature. The data suggest that release of enkephalins originates primarily from epinephrine-type cells of the adrenal medulla in cat.

Adrenal Medulla↗
PubMedDate not supplied

Are NPY and enkephalins costored in the same noradrenergic neurons and vesicles?

Separate studies show that NPY and enkephalins are widely distributed in peripheral noradrenergic neurons. In the present study, the subcellular costorage and release in response to intense sympathetic stimulation and reserpine at near therapeutic doses (0.05 mg/kg every other day) were examined. In young pig arteries and vas deferens, enkephalin and D beta H immunofluorescence show consistent but not total overlap. Also NPY is colocalized with D beta H in many fibers but with VIP (nonnoradrenergic) in others. Ultrastructural immunogold labeling indicates that individual terminals contain large dense cored vesicles (LDVs) which store either NPY or enkephalins, even though costorage of both peptides occurs. Some LDVs costore NPY and VIP, especially in the middle cerebral artery and in the lamina propria of vas deferens. Acute CNS ischemia depletes enkephalins and norepinephrine in all tissues analyzed without parallel loss of NPY. Reserpine depletes norepinephrine 70-85% but does not deplete NPY or enkephalins. The latter is in contrast to commonly used high doses known to produce nonspecific, detergent-like effects. In fact, low doses of reserpine induce a time-dependent new synthesis and processing of NPY precursor peptides in vas deferns. Contrasting effects of reserpine on NPY and enkephalin contents, new synthesis and apparent processing, and a differential response to acute CNS ischemia were found in every tissue studied. Activation of precursor neuropeptide processing occurred immediately upon intense sympathetic stimulation in most tissues. Dual localization of NPY in noradrenergic and nonnoradrenergic fibers and differences in subcellular LDV storage help explain why enkephalin correlates better than NPY with norepinephrine loss in response to acute CNS ischemia. Furthermore, the costorage of NPY and enkephalins in distinct subpopulations of noradrenergic fibers, which varies according to tissue, is likely to be under separate CNS control.

Animals↗
PubMedDate not supplied

State or regional critical care societies.

The success of the SCCM has spurred other individuals with similar backgrounds (many of them SCCM members) to start state or regional critical care societies. Such societies provide a forum where local recognition and educational needs are met; state health regulations and economic issues can be discussed with a unifying voice. The experiences and organizational steps taken are described. The intent of this article is to provide information to those individuals contemplating starting similar societies.

Critical Care↗
PubMedDate not supplied

Burn wound itch control using H1 and H2 antagonists.

This study investigated the use of a combination of H1 and H2 antagonists and topical medications to control burn wound itch. Graeco-Latin square assignment provided an oral combination of 1) cetirizine and cimetidine or 2) diphenhydramine and placebo in four divided doses. The study protocol lasted 16 days divided into 4-day intervals, scoring itch before the initial dose of medication and at 1-hour, 6-hour, and 12-hour intervals after the first medication. A significant difference between mean itch scores across the four times was observed (Wilks' Lambda F = 26.52, df = 3, P <.0005). A three-way nested repeated measures interaction effect (Wilks' Lambda F = 9.85, df = 9, P <.0005) was observed representing a significantly different pattern on days 1 to 4 of the study compared with the remaining days. Controlling for the effect of topical medications, the cetirizine/cimetidine combination demonstrated a dramatic improvement at 1 and 6 hours, and a moderate improvement at 12 hours after initial medication for the day when compared with the diphenhydramine/placebo combination.

Administration, Cutaneous↗
PubMedDate not supplied

Low density lipoprotein metabolism in human macrophages stimulated with microbial or microbial-related products.

To determine whether stimulation of macrophages with products related to, or released as a consequence of, infectious processes could play a role in inducing the formation of foam cells, we studied the metabolism of native and acetylated low density lipoprotein (LDL) by human macrophages stimulated with lipopolysaccharide (LPS), muramyl dipeptide (MDP), polyinosinic:polycytidilic acid (Poly I:Poly C) and gamma-interferon. Cholesteryl ester (CE) synthesis by macrophages stimulated with LPS, MDP and Poly I:Poly C was markedly increased when the cells were incubated with native LDL (p less than 0.05). When incubated with acetylated LDL, LPS-stimulated macrophages showed a depression in CE synthesis (p less than 0.05). When incubated with acetyl-LDL, macrophages stimulated with Poly I:Poly C and gamma interferon showed a significant increase (p less than 0.05) in CE synthesis. The increase in CE synthesis by LPS-stimulated macrophages exposed to native LDL and by gamma-interferon-stimulated macrophages exposed to acetylated LDL was paralleled by an increase in cholesterol ester mass. The increase in CE synthesis and accumulation observed in LPS-stimulated macrophages incubated with native LDL seems to be due to an increase in the receptor mediated uptake of LDL. LPS inhibited and gamma-interferon activated the expression of the scavenger pathway in human macrophages. This may explain the changes observed in CE synthesis and accumulation when macrophages activated by the above stimuli were incubated with acetylated LDL. In conclusion, activation of human macrophages by some products released during, or as a consequence of, infectious processes led to an increase in CE synthesis and accumulation that may be relevant to the formation of "foam cells".

Acetylmuramyl-Alanyl-Isoglutamine↗