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Biomedical subjects

L Levine

Publications and source records attributed to L Levine.

At least 127 records · Page 7Linked to original sources
PubMed1984

Varied and repeated atropine dosages and exercise-heat stress.

Comparisons of physiological responses to 0, 0.5, 1, and 2 mg atropine (IM) were made in seven males (X +/- SD: age, 24 +/- 3 years; ht, 174 +/- 12 cm; wt, 76 +/- 3 kg) while they exercised (approximately 390 W) in a hot-dry (40 degrees C, 20% rh) environment. Responses to 4 mg, as well as repeatability of responses to 2 mg, were studied in two and six of these subjects, respectively. On 8 test days an intramuscular injection of atropine or saline control was administered 20 min before subjects walked on a treadmill for two 50-min bouts. Heart rate (HR) during exercise did not change in the control trial but by min 50 increased during all atropine trials (P less than 0.01). Rectal temperature (Tre) increased (P less than 0.01) in all trials by min 50 and continued increasing (P less than 0.01) in the 2-mg trial during the second exercise bout. For the two subjects tested with all dosages (0.5 - 4 mg atropine), the change in HR and Tre between the atropine and control trials at 50 min of exercise was regressed against the various atropine dosages. The relationship (r = 0.92) for HR was curvilinear while the relationship (r = 0.99) for Tre was linear. Mean weighted skin temperature (Tsk) was relatively constant during exercise and was warmer (P less than 0.05) with increasing atropine dosage. In a repeat 2 mg trial, HR was 6 bt . min-1 lower (P less than 0.05) on the second exposure but Tre was the same (P greater than 0.05) on both days. For subjects walking in the heat, three new observations were: 1) 0.5 mg of atropine resulted in increased HR and Tsk compared to control values; 2) HR was elevated but the magnitude of change decreased with increasing dosage, while the elevation in Tre was consistent with increasing dosage; and 3) rectal temperatures (in trials with and without atropine) were unaffected by previous days of atropine administration.

Adult↗
PubMed1984

Lectins modulate prostaglandin E2 production by rat peritoneal macrophages.

The effect of Aloctin A (Alo A), a lectin having anti-inflammatory activities, on prostaglandin (PG) E2 production by activated rat peritoneal macrophages was compared with that of concanavalin A (Con A), wheat germ agglutinin (WGA), plsum sativum agglutinin (PSA) and soybean agglutinin (SBA). Alo A, WGA, Con A and PSA at 10 micrograms per ml inhibited PG E2 production. But SBA, even at a dose of 1 microgram per ml, stimulated PG E2 production. The inhibition by Alo A treatment of the release of radioactivity from (3H)arachidonic acid-labeled macrophages and the stimulation of this release by SBA treatment were observed. The uptake of (51Cr)-labeled sheep red blood cells by the macrophage was inhibited by Alo A, Con A, and PSA, all at 10 micrograms per ml and SBA at 1 microgram per ml, however, WGA at 10 micrograms per ml stimulated the uptake of the sheep red blood cells. The mechanism of the anti-inflammatory properties of Alo A was discussed.

Animals↗
PubMed1984

Eicosapentaenoic acid: its effects on arachidonic acid metabolism by cells in culture.

Some eukaryotic cells in culture synthesize a variety of lipoxygenase and/or cyclooxygenase products when stimulated by appropriate agonists. Under normal nutritional conditions, these products are derived from the polyunsaturated fatty acid (PUFA) 5,8,11,14-eicosatetraenoic acid (ETA), arachidonic acid, which before metabolism must be liberated from cellular lipids by deesterification. If the cellular lipids are preloaded with 5,8,11,14,17-eicosapentaenoic acid (EPA) and cells are then stimulated to metabolize the PUFAs, levels of cyclooxygenase and lipoxygenase products synthesized are altered. Cyclooxygenase products decrease, while lipoxygenase products are not significantly affected and may even increase. The decrease in the production of cyclooxygenase products results from reduced utilization of the substrate (ETA). Decreased prostaglandin production by rat basophil leukemia-1 cells preloaded with EPA and radiolabeled with [3H]ETA and [14C]EPA can also be demonstrated by high-performance liquid chromatographic analyses of [3H]- and [14C] radiolabeled metabolites in culture fluids of cells stimulated to metabolize PUFA by the Ca2+ ionophore A23187.

Animals↗
PubMed1984

Effect of atropine on the exercise-heat performance of man.

This paper summarizes the findings from two recent studies involving the physiological effects of atropine (0 to 4 mg, im) on soldiers performing physical exercise in hot-dry environments. Study I determined the threshold of physiological effects and the gradation of these effects with increasing dosage of atropine. Study II examined the effects of exercise-heat acclimation on the reduced physical exercise performance that occurs following atropine administration. The following new observations were made: (1) a 0.5-mg dose of atropine elevates heart rate, rectal temperature, and mean skin temperature; (2) atropine exerts its peak physiological effects approximately 70 min after intramuscular injection; (3) within the dosage levels tested, the magnitude of the elevated heart rate response is curvilinearly related to atropine dosage, whereas, the magnitude of the elevated rectal temperature response is linearly related to atropine dosage; (4) repeated administration of atropine over a number of days does not alter thermo-regulatory responses; (5) heat acclimation improves exercise-heat performance of individuals under the influence of atropine by enabling a reduced rectal temperature; and (6) heat acclimation increases the sweat output of individuals under the influence of atropine; however, the absolute reduction in sweat output from atropine is the same pre-and post-heat acclimation.

Acclimatization↗
PubMed1984

Stimulation of prostaglandin production in rat glomerular epithelial cells by antidiuretic hormone.

Prostacyclin (PGI2) and prostaglandin E2 (PGE2) production by rat glomerular epithelial cells in culture were stimulated by arginine vasopressin (AVP) over a dose range of 10(-9) to 10(-6) M, but only if the cells were allowed to recover from trypsin treatment. The effect of AVP was related to its pressor activity since the antidiuretic analogue of AVP, 1-deamino-8-D-Arg-vasopressin (dDAVP) had no effect. Angiotensin II and kallidin (lysyl-bradykinin) did not affect prostaglandin production by these cells. The stimulatory effect of AVP on arachidonate metabolism was inhibited by the calcium channel antagonist, nifedipine, in a dose-dependent fashion suggesting that cellular uptake of calcium was required.

Angiotensin II↗
PubMed1984

Type-specific capsular antigen is associated with virulence in late-onset group B Streptococcal type III disease.

Strain differences have been postulated to explain the observation that group B Streptococcus type III (GBS III) late-onset disease occurs in only a fraction of colonized infants. To determine the distribution of type-specific polysaccharide antigen (Ag) in GBS III, Ag was measured by rocket immunoelectrophoresis in both supernatant fluids and EDTA extracts and by radial immunodiffusion in multiple HCl extracts of the pellet from cultures of 10 strains of GBS III. Capsular Ag was defined as the sum of Ag in EDTA extracts + Ag in multiple HCl extracts. Both Ag in EDTA extracts and Ag in supernatant fluids correlated with capsular Ag (r = 0.94). GBS III strains were obtained from the blood of 19 infants with late-onset sepsis, from the cerebrospinal fluid or blood of 22 infants with late-onset meningitis, and from mucosal surfaces of both 18 infants and 12 mothers of infants with low levels of type-specific antibody and asymptomatic colonization. Mean values of Ag in supernatant fluids in strains from infants with late-onset sepsis (1.50 +/- 0.08 micrograms/ml) and late-onset meningitis (1.67 +/- 0.09 micrograms/ml) were significantly greater than those in asymptomatic colonization strains (1.14 +/- 0.05 micrograms/ml; P less than 0.001). The number of organisms required for a 50% lethal dose in the chick embryo, determined in 29 strains, was inversely related to Ag in supernatant fluids (r = -0.60). The demonstration that the quantity of capsular Ag produced by GBS III strains is related to their virulence in chick embryos and to their invasiveness in susceptible infants supports the hypothesis that Ag is a virulence factor in humans.

Animals↗
PubMed1984

Arachidonate metabolites in acute and chronic allergic air pouch inflammation in rats and the anti-inflammatory effects of indomethacin and dexamethasone.

Two types of allergic air pouch inflammation, the acute and the chronic types, were induced in the dorsum of rats. 1, 8, and 24 h after the immunologic challenge injection, the exudate contents of cyclooxygenase products, prostaglandin (PG)E2, 13,14-dihydro-15-keto-PGE2, PGI2 (measured as 6-keto-PGF1 alpha) and PGD2, and the lipoxygenase products, hydroxyeicosatetraenoic acids (HETEs) and 6-sulfido-peptide-containing leukotrienes (SRS) were measured by radioimmunoassay. The effects of locally injected indomethacin or dexamethasone on the exudate volumes and the number of cells in the exudates in both types of allergic inflammation and the effects of these drugs on the contents of the cyclooxygenase and lipoxygenase products in the exudates 8 h after the challenge injection were examined.

Animals↗
PubMed1984

Dietary menhaden oil lowers plasma prostaglandins and calcium in mice bearing the prostaglandin-producing HSDM1 fibrosarcoma.

The omega 3 class of polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA, 20:5), has been shown to alter the patterns of arachidonic acid (20:4) metabolism in both in vitro and in vivo systems. To examine further the role of arachidonic acid conversion to prostaglandins (PG) in hypercalcemic mice bearing the PG-producing HSDM1 fibrosarcoma, we have performed experiments in which control and tumor-bearing animals were fed diets either low (0.1-0.2% of total fatty acid) or high (17%) in EPA. In all five experiments performed, tumor-bearing mice eating control diets had markedly elevated (average sixfold above control) plasma concentrations of 13,14-dihydro-15-keto-PGE2 (PGE2-M), while in mice bearing HSDM1 tumors and eating the EPA-enriched menhaden oil diet, the elevation was reduced to only twice control values. The increase in plasma calcium concentration (approximately 2.5 mg/dl above control) in tumor-bearing animals was also reduced significantly (P less than 0.05) to only 1.3 mg/dl above control in mice eating the diet enriched in EPA. Plasma immunoreactive hydroxy fatty acids (i12-HETE) and sulfidopeptide leukotrienes (iSRS) were not elevated in tumor-bearing mice and were unaffected by diet. The contents of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were lower in tumor tissue from animals eating the diet high in EPA, whereas the tissue contents of i12-HETE and iSRS were not altered by diet. Fatty acid analysis of liver and tumor tissue revealed marked increases in certain omega 3 fatty acids (20:5, 22:5, and 22:6) from animals eating the enriched diet. Body weights, tumor weights, and tumor histology were not significantly altered by diet. To determine whether dietary calcium played a role in the elevation of plasma calcium in mice bearing the HSDM1 tumor and the reduction of plasma calcium in animals fed EPA, we compared results in mice fed diets containing 0.80% (normal) and 0.015% (deficient) calcium. The increases in plasma calcium and PGE2-M observed in tumor-bearing mice were the same on both normal and very low calcium intakes. We conclude, in mice of the Swiss albino strain bearing the HSDM1 fibrosarcoma, that consumption of a diet enriched in EPA reduces the production of cyclooxygenase products of arachidonic acid metabolism and thereby reduces the elevation of plasma calcium concentration. Dietary enrichment with EPA did not alter the production of serologically determined lipoxygenase products of arachidonic acid.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1984

Arachidonic acid metabolism by rat liver cells (the C-9 cell line).

Rat liver cells (the C-9 cell line) are capable of producing, from endogenously liberated arachidonic acid, prostaglandins I2, E2 and F2 alpha. Greater than 95% of these cyclooxygenase products is prostaglandin I2. Arachidonic acid metabolism is stimulated by treatment of the C-9 cells with epidermal growth factor, vasopressin, angiotensin II or thrombin. Stimulation by combined treatments with vasopressin, angiotensin II or thrombin is additive; but each stimulation, when incubated in the presence of epidermal growth factor, is synergistic. These stimulations are dependent on Ca++. They are inhibited by indomethacin and dexamethasone. The cells exhibit homologous, but not heterologous, desensitization to vasopressin and thrombin. The synergistic stimulation by epidermal growth factor and vasopressin is inhibited by prior treatment of the cells with epidermal growth factor.

Angiotensin II↗
PubMed1984

Effects of heat acclimation on atropine-impaired thermoregulation.

The effects of saline or atropine injection (2 mg, im) on eccrine sweating and performance time in seven healthy male subjects were evaluated during treadmill walking (1.34 m X s-1) in a hot-dry environment (Ta = 49 degrees C, Tdp = 20.5 degrees C) before and after heat acclimation (HA). Mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were continuously measured. Sweat loss from the skin (Msw) was calculated by changes in body weight. HA resulted in decreased (p less than 0.05) Tre (0.4 degrees C) and HR (17 b X min-1), and increased (p less than 0.05) Msw (16 g X m-2 X h-1) during the saline experiments. Pre-acclimation, Msw was reduced (p less than 0.01) 65% (151 g X m-2 X h-1) with atropine, which resulted in higher (p less than 0.01) Tre (0.4 degrees C) and Tsk (2.8 degrees C). HR was increased 48% (53 b X min-1) by atropine pre-acclimation (p less than 0.01). Post-acclimation, atropine reduced (p less than 0.01) Msw 33% (100 g X m-2 X h-1) and increased (p less than 0.01) HR 63% (62 b X min-1) compared to saline exposures. The change in Tre X min-1 (delta Tre/delta t) was lower (p less than 0.05) in atropine-injected subjects following heat acclimation, and their worktime was improved by an average of 23.5 min (p = 0.08). These data demonstrate that heat acclimation improves the endurance time of atropine-treated subjects in a hot-dry environment. This improvement was, in part, due to the potentiation of sweat gland activity enabling greater evaporative cooling for the same dose of atropine.

Acclimatization↗
PubMed1984

Inhibition of stimulated prostaglandin biosynthesis by retinoic acid in smooth muscle cells.

Bovine aorta smooth muscle cells (SMC) incubated with a tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), released increased levels of prostaglandin I2 [measured as its stable hydrolytic product, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha)], and this response was inhibited by all-trans-retinoic acid (RA) at concentrations as low as 17 nM. Retinol and retinyl acetate, at concentrations as high as 1.7 and 1.5 microM, respectively, did not inhibit the TPA-stimulated 6-keto-PGF1 alpha production. RA was not cytotoxic at 1.7 microM, as assayed by exclusion of trypan blue dye. Inhibition by RA was increased after preincubation of the SMC with RA prior to TPA stimulation. The inhibition of arachidonic acid (AA) metabolism by RA was not specific for TPA stimulation; RA inhibited prostaglandin production after SMCs were stimulated by serotonin; melittin; the Ca2+ ionophore, A23187; and fetal calf serum. RA had no effect on phorbol ester binding to SMC, nor did it inhibit increased 6-keto-PGF1 alpha production in SMC treated with exogenous AA. While RA inhibited TPA-stimulated production of 14C-labeled 6-keto-PGF1 alpha from [14C]AA-labeled cells, it did not inhibit the accumulation of [14C]AA in the culture medium. The data suggest that RA inhibits stimulated, rather than basal, levels of prostaglandin production. RA does not seem to act by inhibiting the deacylation of AA from cellular phospholipid pools, insofar as this is reflected in the accumulation of AA in the media, but may inhibit reactions at, or after, the generation of endoperoxides by cyclooxygenase.

Animals↗
PubMed1983

Inhibition of the A-23187-stimulated leukotriene and prostaglandin biosynthesis of rat basophil leukemia (RBL-1) cells by nonsteroidal anti-inflammatory drugs, antioxidants, and calcium channel blockers.

Rat basophil leukemia cells (RBL-1), when grown in monolayer, synthesize from endogenous substrates the prostaglandins (PG) E2, F2 alpha, and I2 (measured as 6-keto-PGF1 alpha) and 6-sulfidopeptide-containing leukotrienes (SRS), as well as materials that react serologically with anti-12-hydroxyeicosatetraenoic acid (HETE). The non-steroidal anti-inflammatory drugs indomethacin and aspirin inhibited PGE2 synthesis by RBL-1 cells, which had been stimulated with the calcium ionophore A-23187, in a dose-dependent manner with an IC50 of 0.7 and 7.8 microM respectively. Indomethacin, when used at higher concentrations, also inhibited iSRS synthesis with an IC50 of 230 microM. Benoxaprofen, also a non-steroidal anti-inflammatory drug, inhibited both PGE2 and iSRS production in a dose-dependent manner, but inhibition of the iSRS biosynthesis was three times more effective than inhibition of PGE2 production. The anti-oxidants gossypol, butylated hydroxyanisole (BHA), nordihydroguariatic acid (NDGA), and 3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline (BW755c) also inhibited iSRS synthesis more effectively than PGE2 biosynthesis. The IC50 values for inhibition of iSRS production were 0.2 microM (gossypol), 0.5 microM (BW755c), 0.6 microM (BHA), and 0.6 microM (NDGA) compared to 2.8 microM (gossypol), 2.0 microM (BW755c), 4.8 microM (BHA) and 2.6 microM (NDGA) for inhibition of PGE2 synthesis. Gossypol, BW755C, BHA, and NDGA, as well as benoxaprofen, inhibited i12-HETE-biosynthesis (IC50 for gossypol, 0.32 microM; and for benoxaprofen, 0.5 microM). Two calcium channel blockers, verapamil and nifedipine, inhibited PGE2, iSRS and i12-HETE synthesis in a dose-dependent manner. The calcium channel blockers inhibited iSRS synthesis ten times more effectively than PGE2 production.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Human salivary eicosanoids: circadian variation.

A circadian rhythm in the concentrations of prostaglandins (PG) E2, PGF2, PGI2 (measured as 6-keto-PGF1 alpha), immunoreactive h hydroxyeicosatetraenoic acids and immunoreactive 6-sulfidopeptide containing leukotrienes in human mixed saliva was observed. The rhythm reflected changes in the absolute amounts of these compounds in saliva. Under usual sleep-wake cycles a single peak occurred during sleep with maximal levels at 5:00 AM; the amplitude of the peak varied for each product. The rhythm was sleep-dependent and a shift occurred when the sleep-wake cycles were displaced. Basal levels of these eicosanoids were maintained even without sleep.

Adult↗
PubMed1983

Arachidonic acid metabolism by erythrocytes.

Rabbit, chicken, rat, and dog erythrocytes (10(9) cells/ml) synthesized immunologically active 12-hydroxyeicosatetraenoic acid (12-HETE) when stimulated by the Ca2+ ionophore, A-23187. The levels of immunologically active hydroxyeicosatetraenoic acid were independent of the number of white blood cells and platelets in the erythrocyte suspensions. Two products were resolved by high performance liquid chromatography; one product was identified as 12-HETE, while a second product appeared to be a dihydroxyeicosatetraenoic acid. Radiolabeled arachidonic acid was incorporated into phospholipids. Phosphatidylcholine and phosphatidylethanolamine were primary sources of the 12-HETE and dihydroxyeicosatetraenoic acid, all of which were released from the cells.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Identification and quantitation of arachidonic-acid metabolic products in rabbit, rat and human saliva.

Arachidonic-acid metabolites were identified in salivary secretions of rabbits, rats and man and in homogenates of rabbit parotid and submandibular glands. The following levels were determined in mixed saliva of healthy volunteers: PGE2, 0.65 +/- 0.8 ng/ml; PGF2 alpha, 0.41 +/- 0.06 ng/ml; serologically active hydroxyeicosatetraenoic acids (HETE) 319.6 +/- 36.6 ng/ml; serologically active 6-sulphidopeptide-containing leukotrienes 1.72 +/- 0.21 ng/ml (all values mean +/- SEM). In all instances, HETE markedly predominated over all other arachidonic-acid metabolites.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗