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Biomedical subjects

S L Archer

Publications and source records attributed to S L Archer.

88 records · Page 5Linked to original sources
PubMed1989

Hypoxic pulmonary vasoconstriction is unaltered by creatine depletion induced by dietary beta-guanidino propionic acid.

It has been suggested that a specific phosphagen pool might serve a sensor function, allowing direct detection of alveolar hypoxia by the pulmonary vascular smooth muscle. The possibility that phosphocreatine (PCr) levels could serve as such a sensor was assessed in isolated rat lungs. Pulmonary vascular reactivity to angiotensin II and alveolar hypoxia was assessed in lungs from control and PCr-depleted rats. PCr depletion was accomplished by feeding rats a diet containing 2% beta-guanidino propionic acid (beta-GPA), an competitive inhibitor of creatine uptake. Total creatine was depleted in beta-GPA lungs, compared to control lungs (p less than 0.05). Lung PCr levels were undetectable by the available 31P NMR spectroscopy system. PCr and creatine were depleted in hearts from beta-GPA rats relative to control hearts (p less than 0.001). Normoxic pulmonary artery pressure and the pressor responses to angiotensin II and hypoxia were not qualitatively or quantitatively altered by the diet indicating either that PCr is not a critical participant in hypoxic pulmonary vasoconstriction or that the degree of PCr depletion achieved was inadequate to expose its role in the hypoxic pressor response.

Animals↗
PubMed1989

Gender differences in identity development: issues of process, domain and timing.

Adolescence has been designated as the first time in one's life span when the identity concerns of developing one's values, beliefs, and goals become salient (Erikson, 1968). Theorists and empiricists have suggested that males and females may address the identity task differently. In three separate studies conducted with early to late adolescents, gender comparisons were made regarding: (I) the process by which their identities are formed; (2) the domains in which they might define themselves; and (3) the time in which this task might be initiated. It was found that both genders used the identity statuses (process) comparably, except for foreclosure which characterized males significantly more than females. Both genders used the identity process similarly in the domains of vocational choice, religious beliefs, and sex-role orientation. Males were significantly more likely to be foreclosed and females, diffuse, in the area of political ideology. Females were significantly more likely to be in moratorium or identity achieved with regard to family roles. In two of the three studies, no timing differences were found. The findings from a third study may reflect a greater complexity of the identity task for some female high school seniors as they confront intrapersonal and interpersonal goals simultaneously.

Adolescent↗
PubMed1989

The status of identity: reflections on the need for intervention.

The primary purpose of this article is to examine the need for intervention in the context of the information we have gathered to date about identity formation. The research evidence indicates that the identity achievement status is associated with the greatest effectiveness in psychological functioning while the identity diffusion status is related to poorer functioning. The moratorium and foreclosure statuses generally occupy intermediate positions in this regard. The identity activity of adolescents and youth is also reviewed. The complexity of the identity construct is discussed as it relates to domains, developmental patterns, gender, historical and social contexts. The author uses the findings from a longitudinal study to illustrate the need for, and purposes of, intervention while respecting the richness of the identity construct of the individual.

Adolescent↗
PubMed1989

Oxygen radicals and antioxidant enzymes alter pulmonary vascular reactivity in the rat lung.

It has been postulated that changes in the availability of partially reduced O2 species, such as O2 radicals, could serve as a link between PO2 in the alveolus and pulmonary vascular tone (Herz 11: 127-141, 1986). To assess this hypothesis, the hemodynamic effects of acute changes in the balance between the production of O2 radicals and availability of antioxidant enzymes were studied in the isolated perfused rat lung. Intravascular generation of O2 radicals, by administration of xanthine-xanthine oxidase, decreased the pulmonary vascular pressor response to alveolar hypoxia (-55 +/- 5%) and angiotensin II (-58 +/- 10%, P less than 0.01 for each) in isolated perfused rat lungs without increasing the lung wet-to-dry weight ratio. Decreases in pulmonary vascular reactivity were inhibited by pretreatment of the lung with desferrioxamine or a mixture of catalase and superoxide dismutase. Catalase and superoxide dismutase preserved the hypoxic pressor response whether given in liposomes or in dissolved form. Superoxide dismutase administered free in solution, or combined with catalase in liposomes, increased the normoxic pulmonary arterial pressure and enhanced vascular reactivity to angiotensin II and hypoxia. Lungs treated with antioxidant enzymes in liposomes had 50% higher lung catalase levels than control lungs (P less than 0.05). These findings demonstrate that exogenous partially reduced O2 species can decrease pulmonary vascular reactivity and suggest that endogenous radicals, superoxide radical in particular, might be important in modulating pulmonary vascular tone.

Animals↗
PubMed1989

Effect of dietary fish oil on lung lipid profile and hypoxic pulmonary hypertension.

The effects of dietary polyunsaturated fats on chronic hypoxic pulmonary hypertension were assessed in rats fed fish oil, corn oil, or a lower fat, "high-carbohydrate" diet (regular) beginning 1 mo before the start of hypoxia (0.4 atm, n = 30 for each). Mean pulmonary arterial pressures were lower in the chronically hypoxic rats fed fish oil (19.7 +/- 1.8 mm Hg) than in the rats fed corn oil (25.3 +/- 1.6 mm Hg) or regular diets (27.5 +/- 1.5 mm Hg, P less than 0.05). The fish oil diet increased lung eicosapentaenoic acid 50-fold and depleted lung arachidonic acid 60% (P less than 0.0001 for each). Lung thromboxane B2 and 6-ketoprostaglandin F1 alpha levels were lower, and platelet aggregation, in response to collagen, was reduced in rats fed fish oil. Chronically hypoxic rats fed fish oil had lower mortality rates than the other hypoxic rats. They also had lower blood viscosity, as well as less right ventricular hypertrophy and less peripheral extension of vascular smooth muscle to intra-acinar pulmonary arteries (P less than 0.05 for each). The mechanism by which dietary fish oil decreases pulmonary hypertension and vascular remodeling during chronic hypoxia remains uncertain. The finding that a fish oil diet can reduce the hemodynamic and morphological sequelae of chronic hypoxia may have therapeutic significance.

Animals↗
PubMed1989

Simultaneous measurement of O2 radicals and pulmonary vascular reactivity in rat lung.

The role of endogenous radicals in the regulation of pulmonary vascular tone was evaluated by simultaneous measurement of pulmonary artery pressure and lung radical levels during exposure of isolated rat lungs to varying inspired O2 concentrations (0-95%) and angiotensin II. Lung radical levels, measured "on-line" using luminol and lucigenin-enhanced chemiluminescence, decreased in proportion to the degree of alveolar hypoxia. Radical levels fell during hypoxia before the onset of pulmonary vasoconstriction and promptly returned to basal levels with restoration of normoxic ventilation. Mild alveolar hypoxia (10% O2), which failed to decrease chemiluminescence, did not trigger pulmonary vasoconstriction. Although chemiluminescence tended to decrease more as the hypoxic response strengthened, there was not a simple correlation between the magnitude of the change in chemiluminescence induced by hypoxia and the strength of the hypoxic pressor response. Normoxic chemiluminescence was largely inhibited by superoxide dismutase but not catalase. Superoxide dismutase also increased normoxic pulmonary vascular tone and the strength of the pressor response to hypoxia and angiotensin II. Thus the predominant activated O2 species in the lung, during normoxia, was the superoxide anion or a closely related substance. Alteration of endogenous radical levels can result in changes in vascular tone. It remains uncertain whether the decrease in lung radical production during hypoxia caused pulmonary vasoconstriction or was merely associated with hypoxic ventilation.

Acridines↗
PubMed1989

Detection of activated O2 species in vitro and in rat lungs by chemiluminescence.

This study used chemiluminescence, an "on-line" photon-counting technique, to detect and characterize activated O2 species in vitro and in isolated rat lungs. The sensitivity and specificity of enhanced chemiluminescence for superoxide anion (O2-.) and hydrogen peroxide (H2O2) was evaluated in vitro. The effect of media conditions (such as O2 tension, albumin concentration, and sulfhydryl group availability) on luminescence was assessed in vitro. Xanthine-xanthine oxidase (X-XO) primarily produced superoxide anion in vitro. Enhanced chemiluminescence varied directly with the dose of luminescent probe used and the quantity of activated O2 species administered. The strength of the luminescent signal was also dependent on the concentration of albumin and O2 in the media. Lucigenin was more sensitive than luminol to the presence of O2-. and, unlike luminol, lucigenin did not alter radical production by XO. However, neither luminescent probe was specific for O2-., as both detected H2O2 and O2 in vitro. H2O2-induced chemiluminescence was inhibited by catalase but not superoxide dismutase (SOD), while X-XO-induced luminescence was inhibited by SOD but not catalase. SOD-inhibitable chemiluminescence was a sensitive and specific marker for O2-. production in vitro. Once the sensitivity-specificity of enhanced chemiluminescence was defined in vitro, this technique was used to explore the mechanism by which exogenous X-XO reduced hypoxic vasoconstriction in isolated rat lungs. The vascular paresis, caused by administration of X-XO to the rat lung, resulted from a brief burst of O2-. production rather than a sustained alteration of lung radical levels.

Acridines↗
PubMed1986

ZK 36-374, a stable analog of prostacyclin, prevents acute hypoxic pulmonary hypertension in the dog.

Vasodilator therapy in pulmonary hypertension is limited by the lack of an agent selective for the pulmonary circulation. The effects of intravenous prostacyclin and two stable prostaglandin analogs, ZK 36-374 and CL 115,347, were assessed on the preconstricted pulmonary vasculature of the anesthetized dog. During hypoxic vasoconstriction ZK 36-374 (0.4 micrograms/kg per min) markedly reduced pulmonary artery pressure (26 +/- 3 to 13 +/- 1 mm Hg) (p less than 0.05) and pulmonary vascular resistance (6.2 +/- 1.1 to 2.8 +/- 0.2 mm Hg/liter per min) (p less than 0.01). There was no significant effect on cardiac output, aortic pressure or arterial blood gases. Pulmonary vasoconstriction induced by prostaglandin F2 alpha was similarly affected by ZK 36-374, and in this instance the aortic pressure was also reduced (158 +/- 11 to 129 +/- 11 mm Hg) (p less than 0.01). ZK 36-374 (0.2 micrograms/kg per min) was more effective in lowering hypoxic pulmonary vascular resistance (from 6.5 +/- 0.6 to 3.0 +/- 0.3 mm Hg/liter per min) than was prostacyclin (0.75 micrograms/kg per min) (from 6.3 +/- 0.6 to 4.2 +/- 0.4 mm Hg/liter per min) (p less than 0.05) and resulted in a smaller fall in aortic pressure (p less than 0.05). CL 115,347 (1.0 micrograms/kg per min) had no effect on the pulmonary vasculature during normoxia or when preconstricted by prostaglandin F2 alpha or hypoxia, but reduced aortic pressure and total systemic resistance (p less than 0.05). It appears to be a selective systemic vasodilator with no pulmonary vascular activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The effects of substance P on the preconstricted pulmonary vasculature of the anesthetized dog.

Substance P is a vasoactive peptide. Nerve fibers containing substance P are present in the media of pulmonary arteries but the physiologic function of substance P in the pulmonary vasculature is unknown. Several doses of substance P were infused intravenously in the anesthetized dog to ascertain its effects on the pulmonary vasculature, both during normoxia and following preconstriction with hypoxia (F1O2 0.1) or prostaglandin F2 alpha (PGF2 alpha 5 mug/kg/min). Substance P resulted in systemic vasodilation during normoxia but had minimal effect on the pulmonary vasculature. During hypoxia and PGF2 alpha-induced pulmonary vasoconstriction, substance P significantly lowered pulmonary artery pressure, pulmonary vascular resistance, mean aortic pressure, and total systemic resistance. It had no effect on cardiac output, wedge pressure, and arterial blood gases. To investigate possible mechanisms for substance P-induced vasodilation, substance P was studied following pretreatment with N-acetylcysteine (a radical scavenging agent), methylene blue (an inhibitor of guanylate cyclase), meclofenamate (a cyclooxygenase inhibitor), and atropine (a muscarinic receptor antagonist). None of these agents impaired substance P-induced vasodilation. Substance P given intravenously is a nonselective vasodilator in the dog but the mechanism of its action remains uncertain.

Acetylcysteine↗
PubMed1986

Redox status in the control of pulmonary vascular tone.

There is mounting evidence that the tone, and possibly the structure, of the pulmonary vasculature is regulated by the redox status (GSH/GSSG, NADPH/NADP) of the pulmonary vascular smooth muscle cell. This hypothesis may explain some studies which have examined endogenous mediators and inhibitors of oxidative phosphorylation. An analogous model of redox regulation of cellular function and calcium flux is seen in the pancreatic beta-cell. The importance of redox status in the regulation of enzyme reactivity is well recognized. Sulfhydryl redox status may also be involved in the ability of the carotid body to detect changes in oxygen tension. It is likely that sulfhydryl redox status transduces the effect of changing oxygen tension for many physiologic control systems, including the pulmonary vasculature.

Animals↗
PubMed1985

Dysgonic fermenter 2 infection resulting in chronic glomerulonephritis.

Dysgonic fermenter 2 (DF-2) is a fastidious gram-negative pathogen that is capable of causing multiorgan disease in humans. In the case reported here infection resulted in subacute bacterial endocarditis, brain abscess and chronic type 1 membranoproliferative glomerulonephritis, a form of renal disease not previously reported in DF-2 infections. The literature is reviewed, and difficulties in diagnosis and treatment are discussed.

Adult↗
PubMed1985

Comparative effects of nisoldipine, nifedipine and bepridil on experimental pulmonary hypertension.

Calcium channel blockers sometimes reduce pulmonary vascular resistance (PVR) in patients with pulmonary hypertension. This study compares the pulmonary vasodilator effect of two new calcium channel blockers, nisoldipine and bepridil, to that of nifedipine in three groups of anesthetized dogs (n = 8 for each group). In each group the normoxic hemodynamics were recorded before and after low, medium and high doses of the respective agents given i.v. In addition, the effect of these doses on the pulmonary pressor responses to hypoxia and prostaglandin F2 alpha (PGF 2 alpha) was measured. During normoxia all doses of bepridil caused brief increases in cardiac output. However, during the hypoxic and PGF 2 alpha challenges cardiac output fell and PVR rose above predrug responses, rather than being reduced. Nisoldipine produced a sustained increase in cardiac output throughout the experiment. During hypoxia, at high dose, it decreased pulmonary arterial pressure, unlike the two other agents. However, in common with them, nisoldipine also caused systemic hypotension. After medium and high dose nisoldipine and after high dose nifedipine, PVR remained close to normoxic control levels during both hypoxic and PGF 2 alpha challenges. Both medium dose nisoldipine (5 X 10(-8) M/kg) and high dose nifedipine (5 X 10(-7) M/kg) reduced hypoxic PVR by 39% of the untreated hypoxic value. Although nisoldipine is more effective in reducing pulmonary hypertension than nifedipine or bepridil, it also causes marked systemic hypotension. This lack of specificity may limit the therapeutic potential of this agent when given i.v.

Animals↗