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S F Perry

Publications and source records attributed to S F Perry.

At least 109 records · Page 6Linked to original sources
PubMed1990

Morphometric study of the role of pulmonary arterial flow in fetal lung growth in sheep.

Pulmonary hypoplasia has been associated with absent or hypoplastic pulmonary artery in four cases in humans. Despite these reports, the effects of decreased pulmonary arterial flow on fetal lung growth have not been adequately studied. This study defines the effects of left pulmonary artery (LPA) ligation on fetal lung growth in sheep by comparing morphometrically determined pulmonary volumes from LPA-ligated, sham-operated, and un-operated control fetuses. LPA ligation (n = 5) or sham operation (n = 4) was performed at 105- to 114-d gestation. lungs were intratracheally fixed for light microscopy. At 112 d (n = 4) and at 140 d (n = 4), unoperated control fetuses were similarly delivered. Absolute pulmonary volumes were then measured using standard stereologic methods. Normal growth of the left lung from 112 to 140 d resulted in significant increases in wet and dry wt, displacement volume, and volumes of future airspace and capillary contents. LPA ligation caused significant decreases in left lung wet and dry wt, displacement volume, and in absolute volumes of fine nonparenchymal, future airspace, parenchymal tissue, and capillary contents compared to sham-operated and 140-d controls. Parenchymal tissue volume was also less than in 112-d controls. In addition, lung wt, displacement volume, and future airspace volume were significantly decreased in sham-operated fetuses compared to 140-d controls. The effects of LPA ligation on bronchial collateral circulation and factors known to affect lung growth (i.e. lung fluid volume) remain to be determined. Clearly, during the canalicular and alveolar stage of fetal lung development, pulmonary arterial flow is necessary for normal lung growth.

Animals↗
PubMed1990

Characterization of red blood cell metabolism in rainbow trout.

Red blood cell metabolism was studied in vitro using whole blood obtained by catheter from resting rainbow trout (Oncorhynchus mykiss). Preparations were viable as shown by stable NTP, metabolite and catecholamine levels and acid-base status, all of which remained at in vivo levels over the 2 h incubation period. Enzymes diagnostic of glycolysis, the tricarboxylic acid (TCA) cycle and phosphagen metabolism were all present in significant amounts in red blood cells. In direct comparisons of 14C-labelled substrates at normal resting plasma concentrations, rates of CO2 production were in the order: glucose greater than lactate greater than alanine greater than oleate. Total CO2 production rates from these four oxidative substrates did not equal directly measured O2 consumption rates, indicating that other substrates may also be important in vivo. Oxidative pathway Km values for glucose (8.4 mmol l-1), lactate (3.3 mmol l-1) and alanine (0.8 mmol l-1) were well within the normal physiological ranges of plasma concentrations. Glucose concentration did not affect lactate oxidation rates, but there was some inhibition (27%) of glucose oxidation by high lactate concentrations (20 mmol l-1). The observed Km values and competitive interactions suggest that changes in plasma concentrations associated with environmental stresses can considerably alter the relative rates of oxidation of glucose and lactate in vivo. Considerable pentose-phosphate shunt activity was detected in red cells, as indicated by high activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase and high CO2 production rates from (1-14C)-labelled glucose. Even in the presence of normal O2 levels, a significant percentage (28%) of glucose metabolism was directed to lactate production. Taken together, these results demonstrate that rainbow trout whole blood incubated in vitro constitutes a dynamic and viable system for metabolic studies at the pathway level.

Alanine↗
PubMed1990

Control of red blood cell metabolism in rainbow trout after exhaustive exercise.

Metabolic responses (rates of CO2 production from 14C-labelled glucose or lactate, and total O2 consumption) of red blood cells were monitored in rainbow trout (Oncorhynchus mykiss) at rest and during 12 h of recovery from exhaustive exercise. Extracellular acid-base status, red blood cell intracellular pH (pHi), and plasma metabolite and catecholamine levels were recorded simultaneously. Despite a post-exercise rise in plasma glucose level, glucose oxidation was depressed, at least partly because of a rise in plasma lactate level. However, lactate oxidation was stimulated markedly, especially at 0-2 h post-exercise. Subsequent multifactorial experiments in vitro demonstrated that augmentation of lactate oxidation was due partly to increased plasma lactate, and partly to separate stimulatory effects of elevated PCO2 and catecholamine levels. Changes in pH and HCO3- level were not directly involved, but the stimulatory effects of catecholamines occurred only under acidotic conditions. Total red cell O2 consumption (MO2) remained generally stable after exercise. Similar multifactorial experiments in vitro demonstrated that respiratory, metabolic and mixed acidoses all inhibited MO2, an effect largely attributable to the lowered pH. This inhibition was reversed by typical post-exercise levels of epinephrine and norepinephrine; again, catecholamines had no effect under control conditions. Red cell pHi regulation was achieved without an increase in MO2 above resting levels. Our results indicate a complex sensitivity of red cell metabolism to acid-base status and a shift in substrate preference for oxidation after strenuous exercise. The mobilization of catecholamines plays an important coordinating role and helps sustain normal rates of oxidative metabolism by red cells in the face of post-exercise blood acidosis.

Acid-Base Equilibrium↗
PubMed1989

Urea excretion as a strategy for survival in a fish living in a very alkaline environment.

Ammonia is toxic to all vertebrates. It can be converted to the less toxic urea, but this is a metabolically expensive process found only in terrestrial vertebrates that cannot readily excrete ammonia and marine fish that use urea as an osmotic filler. Freshwater fish mostly excrete ammonia with only a small quantity of urea. It seems the ornithine cycle for urea production has been suppressed in all freshwater teleosts except for some airbreathers which, when exposed to air, increase urea synthesis via the cycle. Here we show that the tilapia fish Oreochromis alcalicus grahami, the only fish living in Lake Magadi, an alkaline soda lake (pH = 9.6-10) in the Kenyan Rift Valley, excretes exclusively urea and has ornithine-urea cycle enzymes in its liver. A closely related species that lives in water at pH 7.1 lacks these enzymes and excretes mainly ammonia with small amounts of urea produced via uricolysis. It dies within 60 min when placed in water from Lake Magadi. We suggest that urea production via the ornithine-urea cycle permits O. a. grahami to survive the very alkaline conditions in Lake Magadi.

Acclimatization↗
PubMed1989

Lungs of the gecko Rhacodactylus leachianus (Reptilia: Gekkonidae): a correlative gross anatomical and light and electron microscopic study.

The lungs of the New Caldeonian gecko Rhacodactylus leachianus were examined by means of gross dissection and light and electron microscopy. This tropical species, which is the largest living gecko, possesses two simple, single-chambered lungs. Right and left lungs are of similar size and shape. The lung volume (27.2 ml.100 g-1) is similar to that of the tokay (Gekko gecko) but differs in that the gas exchange tissue is approximately homogeneously distributed, and the parenchymal units (ediculae) are very large, approximately 2 mm in diameter. The parenchymal depth varies according to the location in the lung, being deepest near the middle of the lung and shallowest caudally. Scanning and transmission electron microscopy reveal an unusual distribution of ciliated cells in patches on the edicular walls as well as on the trabeculae. Secretory cells are very numerous, particularly in the bronchial epithelium, where they greatly outnumber the ciliated cells. The secretory cells form a morphological continuum characterized by small secretory droplets apically and large vacuoles basally. This continuum includes cells resembling type II pneumocytes but which are devoid of lamellar bodies. Type I pneumocytes similar to those of other reptiles cover the respiratory capillaries, where they form a thin, air-blood barrier together with the capillary endothelial cells and the fused basement laminae. The innervation, musculature, and vascular distribution in R. leachianus are also characterized. Apparent simplification of the lungs in this taxon may be related to features of its sluggish habits, whereas peculiarities of cell and tissue composition may reflect demands of its mesic habitat.

Animals↗
PubMed1989

Ammonia and urea dynamics in the Lake Magadi tilapia, a ureotelic teleost fish adapted to an extremely alkaline environment.

The tilapia Oreochromis alcalicus grahami, which thrives under harshly alkaline conditions in Lake Magadi, Kenya, was studied in its natural environment (pH = 10, total CO2 = 180 mmol/L, osmolality = 525 mOsm/kg, 30-36.5 degrees C). At rest, this species excretes all nitrogenous waste as urea. This is the first known instance of complete ureotelism in an entirely aquatic teleost fish. Very small 'apparent' ammonia excretion (less than 5% of overall N excretion) was attributable to faecal/bacterial production. Ammonia excretion could not be induced by feeding, reduced temperature, or exposure to pH 7. Exhaustive exercise induced only a small efflux of ammonia. Urea output was inhibited completely by pH 7 water and partly by exhaustive exercise, and greatly stimulated by exposure to 500 mumol/L NH3 (at pH 10). A related species, nominally Oreochromis nilotica, which lives in freshwater at circumneutral pH in the same geographic region, excretes 85% ammonia-N and 15% urea-N at pH 7 in the standard teleost fashion. Urea-N efflux increased to 33% upon transfer of O. nilotica to pH 10 in freshwater. Urea output in this species was only marginally stimulated by exposure to 500 mumol/L NH3 (at pH 7). Plasma and white muscle urea levels were 4- to 5-fold higher in O. a. grahami than in O. nilotica, and plasma levels increased between caudal and cardiac sampling sites, indicating hepatic ureagenesis. Blood pH and PNH3 levels, when corrected for sampling artifact, were unusually high in O. a. grahami. We hypothesize that complete ureotelism in O. a. grahami is an evolutionary response to the problems of excreting ammonia into highly buffered water at pH 10 and/or acid-base balance in this extreme environment.

Acid-Base Equilibrium↗
PubMed1989

Evidence that hypoxemia promotes catecholamine release during hypercapnic acidosis in rainbow trout (Salmo gairdneri).

The concentrations of plasma catecholamines, epinephrine and norepinephrine, were monitored in rainbow trout (Salmo gairdneri) after acute (30 min) exposure to various levels of external hypercapnia (water PCO2 (PwCO2) = 0-11.3 Torr) under normoxic (water PO2 (PwO2) = 153 +/- 1.1 Torr) or hyperoxic (PwO2 = 653 +/- 27.0 Torr) conditions. Whole blood pH decreased to a similar extent as a function of external carbon dioxide tensions in both the normoxic and hyperoxic hypercapnic groups. Arterial oxygen content, however, declined only during normoxic hypercapnia. Similarly, plasma catecholamines (primarily epinephrine) increased only during normoxic hypercapnia in proportion to the severity of the whole blood acidosis. Epinephrine levels were elevated 10-fold from 0.70 +/- 0.06 nM to 7.06 +/- 3.7 nM at the highest concentration of external CO2 (11.3 Torr) whereas norepinephrine increased 3-fold from 0.56 +/- 0.07 nM to 1.62 +/- 0.40 nM. The absence of catecholamine release into the circulation during hyperoxic hypercapnia was not due to inhibition of the 'catecholamine-releasing process' by abnormally elevated arterial oxygen tensions (PaO2 = approximately 400 Torr) because acutely anaemic and thus hypoxemic fish (haematocrit = 4.9 +/- 0.7%) displayed identical elevations of plasma catecholamines under both normoxic and hyperoxic conditions. The results of these experiments demonstrate that arterial hypoxemia, rather than blood acidosis per se, is the proximate stimulus causing catecholamine mobilization in rainbow trout during short-term environmental hypercapnia.

Acidosis↗
PubMed1989

The role of catecholamines in regulating arterial oxygen content during acute hypercapnic acidosis in rainbow trout (Salmo gairdneri).

The involvement of catecholamines in regulating arterial oxygen content (CaO2) during hypercapnic acidosis in rainbow trout (Salmo gairdneri) was investigated by comparing physiological responses during acute normoxic hypercapnia (a condition in which plasma epinephrine is elevated) and acute hyperoxic hypercapnia (a condition in which plasma epinephrine is not elevated). Red blood cell pH (rbc pH) was maintained significantly higher in the normoxic hypercapnic fish despite similar reductions in whole blood pH (pHe) in both groups. Elevation of rbc pH in the normoxic hypercapnic fish was abolished by pre-treatment with the beta-adrenoceptor antagonist, propranolol, whereas injection of epinephrine into hyperoxic hypercapnic fish significantly raised rbc pH. Arterial blood oxygen carrying capacity increased only in the normoxic hypercapnic fish due to significant increases in blood haemoglobin (Hb) levels. The ability of trout to elevate blood Hb was abolished by pre-treatment with the alpha-adrenoceptor antagonist, phentolamine. Injections of epinephrine into normocapnic fish caused increases in blood Hb and concomitant decreases in spleen wet weight and Hb content. Adrenergic elevation of blood Hb was not observed in splenectomized fish. CaO2, although depressed during normoxic hypercapnia, was indeed regulated when compared to CaO2 values predicted from the in vitro Root effect. Pre-treatment with phentolamine, but not propranolol, abolished the ability of trout to regulate CaO2.

Acidosis↗
PubMed1989

Mycology quality assessment: United Kingdom national scheme.

A mycology quality assessment scheme introduced in 1986 was assessed: 289 laboratories participated in the scheme, and six distributions, each containing four specimens, were made. Levels of performance varied considerably among participating laboratories: performance was highest with the commoner organisms distributed, but some laboratories, encouragingly, achieved a consistently high level of species identification. A questionnaire distributed to participants showed that a wide range of methods are commonly used, some of which are contrary to good practice. As the scheme continues, selection of organisms considered to be relevant and of use to participants will become difficult.

Arthrodermataceae↗
PubMed1989

Metabolism of isolated fish gill cells: contribution of epithelial chloride cells.

Gill cell suspensions from freshwater (FW)- and seawater (SW)-adapted teleosts were obtained by density gradient centrifugation. The proportion of chloride cells (CCs) in the mixed cell suspensions was estimated using the fluorescent mitochondrial stain, DASPMEI, and ranged from less than 1% (FW-adapted tilapia) to approximately 13% (SW-adapted toadfish). The gill cells displayed relatively high viability based on Trypan Blue exclusion (greater than 75%), lactate dehydrogenase leakage (less than 6.5% h-1), oxygen consumption rates (5-15 mumol g-1 cell wet mass h-1) and ATP levels (1-3 mumol g-1 cell wet mass). There were no obvious differences between the viability of CCs and the other cell types present. An initial comparison of gill oxidative metabolism in SW-adapted tilapia (Oreochromis mossambicus) and toadfish (Opsanus beta) demonstrated that both species oxidized glucose and lactate at substantially greater rates than alanine or oleate. Metabolic rates were significantly higher in toadfish cell suspensions. Kinetic experiments revealed that toadfish gill cells displayed lower values of Km and higher values of Vm for both lactate and glucose, in comparison to tilapia. The elevated metabolism in toadfish gill cells was correlated with increased activities of the oxidative enzyme citrate synthase and Na+/K+-ATPase. The toadfish cell suspensions had a greater proportion of CCs and it is likely that the difference in CC numbers between the two species is the basis for the observed differences in enzyme activities and rates of oxidative metabolism. This idea is supported by the highly significant correlation between Na+/K+-ATPase activity (or CC numbers) and rates of lactate oxidation in gill cell suspensions from FW- and SW-adapted tilapia and toadfish, as well as SW-adapted tilapia chronically treated with cortisol to elevate CC numbers. Although it has been assumed widely that the high metabolic rate of gill tissue reflects, in part, the oxidative demands of the chloride cell, the results of this study provide the first experimental, albeit indirect, evidence for differential rates of metabolism in the various cell types that comprise the gill.

Alanine↗
PubMed1989

Regulation of hepatic gluconeogenesis and glycogenolysis by catecholamines in rainbow trout during environmental hypoxia.

This study tests the hypothesis that catecholamines regulate glucose availability during hypoxia in the rainbow trout by activating glycogen phosphorylase (GPase) while inhibiting pyruvate kinase (PK) in the liver. The net result would be an increase in liver glycogenolysis and a reduction of glycolysis and/or enhancement of gluconeogenesis. We used the criteria of Stalmans & Hers (1975) and report much lower resting percent GPase a (active) values (20-30%) than those previously published. Dorsal aortic injections of epinephrine or norepinephrine increased plasma glucose (16-46%), had no effect on liver or muscle glycogen levels, decreased the activity of PK, and increased total and percent GPase a activities. Pre-treatment with the beta-adrenoreceptor antagonist propranolol eliminated these effects. During moderate hypoxia, plasma glucose remained unchanged, while lactate levels increased fourfold. When fish were pre-treated with propranolol, hypoxia depressed plasma glucose levels (-26%), total and percent GPase a, and increased PK activity, suggesting that hypoxia mediated the dephosphorylation of these enzymes. We conclude that catecholamines stimulate hepatic beta-adrenoreceptors during hypoxia and sustain plasma glucose levels by nullifying the deleterious effects of hypoxia on metabolic function. The specific metabolic consequences of these catecholamine-mediated effects are an increase in the activity of the active form of GPase and a reduction in PK activity, which suggests an activation of glycogenolysis and an inhibition of glycolysis and/or activation of gluconeogenesis, respectively.

Animals↗
PubMed1989

Cortisol stimulates whole body calcium uptake and the branchial calcium pump in freshwater rainbow trout.

Exposure of rainbow trout to a reduced ambient calcium level (from 490 to 25 mumol Ca2+/l) caused hypocalcaemia and induced a rapid increase (within 1 h) in systemic cortisol levels. Under conditions of low environmental calcium concentrations, cortisol levels remained increased for at least 8 days. After this time the in-vitro Ca2+-transport capacity of branchial basolateral membrane vesicles was increased due to stimulation of Ca2+-ATPase activity, presumably as a result of chloride cell proliferation. Pituitary prolactin cells were unaffected by low ambient calcium levels. Fish kept in water containing 490 mumol Ca2+/l and treated with cortisol for 7 days displayed an increase in whole body calcium uptake and an enhancement of the branchial calcium transport capacity; concomitantly, hypercalcaemia was observed. We conclude that, in the rainbow trout, cortisol exerts hypercalcaemic effects by stimulating Ca2+ uptake from the water and that this effect forms an intrinsic part of the established mineralocorticoid action of cortisol in fish.

Adenosine Triphosphatases↗
PubMed1988

Effects of epinephrine on branchial and renal calcium handling in the rainbow trout.

Acute exposure of rainbow trout (Salmo gairdneri) to low external calcium (25 microM) caused an immediate but transient increase in plasma epinephrine concentration that may have been related to a concomitant depression of blood pH. Intra-arterial infusion of epinephrine at normal ambient calcium levels (0.35 mM) for 4 h caused circulating levels of epinephrine to rise from 2.9 X 10(-9) to 8.0 X 10(-8) M but did not affect norepinephrine levels, or branchial unidirectional calcium fluxes. Active (ATP-dependent) calcium transport across basolateral plasma membranes prepared from gill epithelial cells was not affected by pretreatment of fish with epinephrine or by direct application of epinephrine or cAMP, in vitro. Epinephrine infusion elevated urine flow rate, decreased urine pH, and increased urine phosphate levels significantly. Net renal calcium efflux increased significantly as a result of the increased urine flow rate. It is concluded that epinephrine does not stimulate branchial calcium uptake or renal conservation of calcium in rainbow trout at normal external calcium levels and therefore we cautiously suggest that epinephrine is unlikely to be involved in calcium balance during periods of exposure to low external calcium. Instead, epinephrine may play a role in compensating the acid-base disturbances and the increased branchial water influx that are associated with exposure to low ambient calcium.

Animals↗
PubMed1988

Metabolic consequences of hypercapnia in the rainbow trout, Salmo gairdneri: beta-adrenergic effects.

The metabolic consequences of external hypercapnia (1% CO2) were assessed in rainbow trout (Salmo gairdneri) in the presence or absence of circulating levels of the beta adrenoceptor antagonist, propranolol. External hypercapnia caused a severe extracellular respiratory acidosis and a less pronounced reduction of hepatic intracellular pH (pHi). pHi was restored to prehypercapnic values after 48 hr of continuous hypercapnia due to elevation of bicarbonate levels. In the presence of propranolol, hypercapnia elicited a pronounced activation of pyruvate kinase (PyK) (measured at both low and high phosphoenolpyruvate (PEP) concentrations) and inactivation of both total glycogen phosphorylase (GPase) and glycogen phosphorylase a (GPase a). In the absence of propranolol, the changes in enzyme activities were significantly reduced (low PEP PyK activity) or totally absent (GPase inactivation). These results suggest that beta adrenoceptor-mediated phenomena offset disruptive effects of hypercapnia on PyK and GPase activities and may be important in the control of gluconeogenesis and glycogenolysis during this acid-base disturbance. The adrenergic effects were not related to modification of hepatic intracellular acid-base status. Hypercapnia induced a rapid depletion of liver glycogen and concomitant hyperglycemia. These effects were not prevented by pretreating fish with propranolol and appeared to be unrelated to changes in GPase a activity. These results suggest that factors other than adrenergic activation of GPase a are involved in the enhancement of liver glycogenolysis.

Acid-Base Equilibrium↗
PubMed1988

Interactive effects of catecholamines and hypercapnia on glucose production in isolated trout hepatocytes.

In response to added catecholamines, isolated trout (Salmo gairdneri) hepatocytes substantially increase the output of glucose into the surrounding medium. This effect is due to activation of glycogen breakdown concomitant with increases in gluconeogenesis and cell respiration. Each metabolic parameter is activated to a similar extent. In hormone-treated and untreated cells, glycogenolysis accounts for more than 97% of glucose production. Activation of glycogen phosphorylase is implicated in the degradation of cell glycogen, while increased flux through the gluconeogenic pathway from lactate is associated with inactivation of pyruvate kinase, possibly through enzyme phosphorylation as indicated by the activity ratio measured at low and saturating concentrations of phosphoenolpyruvate. From studies with specific adrenergic agonists and antagonists, we conclude that stimulation of glycogenolysis and gluconeogenesis in trout hepatocytes is consistent with a beta-adrenergic effect. Results are inconclusive with respect to catecholamine-mediated activation of cell respiration. None of the monitored cell acid-base variables (pH, PCO2, [HCO3-]) are implicated in the catecholamine-dependent changes in metabolic output of hepatocytes. Imposed hypercapnic conditions (increased medium PCO2 and decreased medium pH), which cause changes in cell acid-base parameters, result in a depression of lactate oxidation and gluconeogenesis, while the rate of glycogenolysis is not affected. In addition, the total amounts of glycogen phosphorylase and pyruvate kinase assayable are negatively affected by hypercapnic treatment of hepatocytes. Under hypercapnic conditions, cells are highly responsive to adrenergic agonists. It appears that--especially in the long term--the catecholamine-dependent activation of gluconeogenesis may compensate for the acid-base-dependent shortfall in glucose output by the liver.

Animals↗
PubMed1988

Experimental hypercalcemia induces hypocalcin release and inhibits branchial Ca2+ influx in freshwater trout.

Intravascular CaCl2 infusion in freshwater rainbow trout (Salmo gairdneri) causes a significant degranulation of the corpuscles of Stannius (CS). Concurrently, there is a specific and acute inhibition of whole body Ca2+ influx; Ca2+ efflux is not effected. The material released from the CS after CaCl2 injection consists primarily of a 28-kDa product which we identified as hypocalcin. Electron microscope observations of the CS reveal that type 1 and type 2 cells are degranulated to a similar extent. We conclude that hypocalcin is directly involved in hypocalcemic control in freshwater fish via inhibition of branchial Ca2+ influx, thereby promoting a net loss of Ca2+ across the gill.

Animals↗
PubMed1988

Antimicrobial susceptibility testing of Streptococcus pneumoniae: quality assessment results.

Six strains of Streptococcus pneumoniae were distributed to 405 United Kingdom laboratories who were asked to test the susceptibility of the strains to penicillin, tetracycline, chloramphenicol and erythromycin and to provide details of methodology to test the standards of susceptibility testing. High error rates were seen only in failure to detect moderate resistance to penicillin (12%) and resistance to chloramphenicol (16%). Increased error rates were associated with several methods or practices. These included the use of certain culture media; failure to standardise the inoculum; inoculation by loop rather than by swab; failure to use control organisms; failure to measure zone sizes; the use of discs containing a high content of penicillin to test susceptibility to penicillin, and the use of high content discs for testing erythromycin, tetracycline, and chloramphenicol.

Chloramphenicol↗