Biomedical subjects

J S Gibson

Publications and source records attributed to J S Gibson.

At least 19 recordsLinked to original sources

PubMed2006

The effect of O2 tension on pH homeostasis in equine articular chondrocytes.

OBJECTIVE: To determine the effects of varying O(2) on pH homeostasis, based on the hypothesis that the function of articular chondrocytes is best understood at realistic O(2) tensions. METHODS: Cartilage from equine metacarpophalangeal/tarsophalangeal joints was digested with collagenase to isolate chondrocytes, and then loaded with the pH-sensitive fluorophore 2',7'-bis-2-(carboxyethyl)-5(6)-carboxylfluorescein. The radioisotope(22)Na(+) was used to determine the kinetics of Na(+)/H(+) exchange (NHE) and the activity of the Na(+)/K(+) pump, and ATP levels were assessed with luciferin assays. Levels of reactive oxygen species (ROS) were determined using 2',7'-dichlorofluorescein diacetate. RESULTS: The pH homeostasis was unaffected when comparing tissue maintained at 20% O(2) (the level in water-saturated air at 37 degrees C) with that at 5% O(2) (which approximates the normal level in healthy cartilage); however, an O(2) tension of <5% caused a fall in intracellular pH (pH(i)) and slowed pH(i) recovery following acidification, an effect mediated via inhibition of NHE activity (likely through acid extrusion by NHE isoform 1). The Na(+)/K(+) pump activity and intracellular ATP concentration were unaffected by hypoxia, but the levels of ROS were reduced. Hypoxic inhibition of NHE activity and the reduction in ROS levels were reversed by treatment with H(2)O(2), Co(2+), or antimycin A. Treatment with calyculin A also prevented hypoxic inhibition of NHE activity. CONCLUSION: The ability of articular chondrocytes to carry out pH homeostasis is compromised when O(2) tensions fall below those normally experienced, via inhibition of NHE. The putative signal is a reduction in levels of ROS derived from mitochondria, acting via altered protein phosphorylation. This effect is relevant to both physiologic and pathologic states of lowered O(2), such as in chronic inflammation.

Adenosine Triphosphate↗

PubMed2006

Haematology and biochemistry in healthy young pheasants and red-legged partridges and effects of spironucleosis on these parameters.

Plasma biochemical and haematological parameters were examined in 4-week-old to 12-week-old game birds. Healthy, uninfected pheasants and partridges had similar levels of total protein, albumin, osmolality, Na+, Cl-, K+, Mg2+ and glucose. Triglyceride, globulin and Ca2+ were significantly higher and PO43- was lower in the partridges. Pheasants carrying a light to moderate infection with Spironucleus had significantly lower total protein, albumin, osmolality, Na+, Cl-, Ca2+ and PO43-. In severely affected pheasants, the osmolality, Na+ and Cl- fell further. Triglyceride and glucose were significantly lower than in healthy birds, and Mg2+ was higher. Similar data were obtained from infected partridges. Red cell parameters rose significantly in pheasants severely affected by spironucleosis, and the percent of heterophils was significantly higher and lymphocytes and basophils lower in their blood smears. The breast and leg muscle wet weight from severely affected pheasants was 22.2 and 37.7% that of uninfected birds, although the water content of the breast muscle was significantly higher.

Animals↗

PubMed2005

Fluid absorption in the small intestine of healthy game birds and those infected with Spironucleus spp.

Absorption of fluid by the small intestine of 4-week-old to 12-week-old farmed pheasants and partridges has been studied using an inverted sac technique. The mean rate of absorption was 54 +/- 4 (mean +/- standard error of the mean) microl/g dry tissue/min in pheasants and 49 +/- 3 microl/g dry tissue/min in partridges. Use of inhibitors and ion substitution suggested transepithelial transport driven by baso-lateral Na+/K+ pumps, in combination with mucosal Na+-coupled transporters, including Cl(-)-coupled transporters. Absorption was more than halved to 17 +/- 2 microl/g dry tissue/min (P < 0.001) in birds that were very heavily infected with Spironucleus spp. in their small intestine and showing a syndrome of diarrhoea, depression and loss of weight to severe emaciation. Birds carrying light to moderate levels of infection with Spironucleus had very variable rates of absorption that were statistically similar to the controls. Doubling the glucose concentration in the buffer to 40 mM significantly enhanced absorption.

Animals↗

PubMed2003

Effect of 1-chloro-2,4-dinitrobenzene on K+ transport in normal and sickle human red blood cells.

1-Chloro-2,4-dinitrobenzene (CDNB), which causes oxidative stress through depletion of reduced glutathione (GSH), increases the passive K+ permeability of red cells. In this paper, we investigated the effects of CDNB (1 mM) on the activities of the K+-Cl- cotransporter (KCC; measured as Cl--dependent K+ influx) and the Gardos channel (taken as clotrimazole-sensitive K+ influx, 5 microM) in human red cells, using 86Rb+ as a K+ congener. 45Ca2+ was used to study passive Ca2+ entry and active Ca2+ efflux via the plasma membrane Ca2+ pump. Both the Gardos channel and KCC were stimulated in both normal and sickle red cells. In sickle cells, stimulation of KCC was similar in oxygenated and deoxygenated cells; that of the Gardos channel was greater in deoxygenated cells. In normal red cells, stimulation of both pathways was greater in oxygenated cells (by 4 +/- 1-fold; all means +/- S.E.M., n = 3). The effects on the Gardos channel were dependent on extracellular Ca2+ and were associated with inhibition of the plasma membrane Ca2+ pump (by 29 +/- 3 %, P < 0.01) and increased Ca2+ sensitivity of the channel (EC50 for [Ca2+]i reduced from 260 +/- 26 to 175 +/- 15 nM; P < 0.05). Cell volume, pHi, ATP levels and passive Ca2+ entry were not affected by CDNB. The effects on KCC were inhibited (93 +/- 6 %) by prior treatment with the protein phosphatase inhibitor calyculin A (100 nM) and were not additive with stimulation by N-ethylmaleimide (1 mM), regardless of the order of addition. These findings are therefore consistent with inhibition of a regulatory protein kinase, although stimulation of the conjugate protein phosphatase(s) may also occur. KCC stimulation was also Ca2+ dependent. These findings are important for understanding how GSH depletion alters membrane permeability and how to protect against red cell dehydration.

Anemia, Sickle Cell↗

PubMed2003

Homeostasis of intracellular Ca2+ in equine chondrocytes: response to hypotonic shock.

REASONS FOR PERFORMING STUDY: Ca2+ homeostasis in articular chondrocytes affects synthesis and degradation of the cartilage matrix, as well as other cellular functions, thereby contributing to joint integrity. Although it will be affected by mechanical loading, the sensitivity of intracellular Ca2+ concentration ([Ca2+]i) in equine articular chondrocytes to many stimuli remains unknown. HYPOTHESIS: An improved understanding of Ca2+ homeostasis in equine articular chondrocytes, and how it is altered during joint loading and pathology, will be important in understanding how joints respond to mechanical loads. METHODS: [Ca2+]i was determined using the fluorophore fura-2. We examined the effects of hypotonic shock, a perturbation experienced in vivo during mechanical loading cycles. We used inhibitors of Ca2+ transporters to ascertain the important factors in Ca2+ homeostasis. RESULTS: Under isotonic conditions, [Ca2+]i was 148 +/- 23 nmol/l, increasing by 216 +/- 66 nmol/l in response to reduction in extracellular osmolality of 50%. Resting [Ca2+]i, and the increase following hypotonic shock, were decreased by Ca2+ removal; they were both elevated when extracellular [Ca2+] ([Ca2+]o) was raised or following Na+ removal. The hypotonicity-induced rise in [Ca2+]i was inhibited by exposure of cells to gadolinium (Gd3+; 10 micromol/l), an inhibitor of mechanosensitive channels. [Ca2+]i was also elevated following treatment of cells with thapsigargin (10 micromol/l), an inhibitor of the Ca2+ pump of intracellular stores. CONCLUSIONS: A model is presented which interprets these findings in relation to Ca2+ homeostasis in equine articular chondrocytes, including the presence of mechanosensitive channels allowing Ca2+ entry, a Na+/Ca2+ exchanger for removal of intracellular Ca2+ and intracellular stores sensitive to thapsigargin. POTENTIAL RELEVANCE: A more complete understanding of Ca2+ homeostasis in equine chondrocytes may allow development of future therapeutic regimes to ameliorate joint disease.

Animals↗

PubMed2001

K(+) transport in red blood cells from human umbilical cord.

The current study was designed to characterise K(+) transport in human fetal red blood cells, containing mainly haemoglobin F (HbF, and termed HbF cells), isolated from umbilical cords following normal parturition. Na(+)/K(+) pump activity was comparable to that in normal adult human red cells (which contain HbA, and are termed HbA cells). Passive (ouabain-resistant) K(+) transport was dominated by a bumetanide (10 microM)-resistant component, inhibited by [(dihydroxyindenyl)oxy]alkanoic acid (100 microM), calyculin A (100 nM) and Cl(-) removal, and stimulated by N-ethylmaleimide (1 mM) and staurosporine (2 microM) - all consistent with mediation via the K(+)-Cl(-) cotransporter (KCC). KCC activity in HbF cells was also O(2)-dependent and stimulated by swelling and urea, and showed a biphasic response to changes in external pH. Peak activity of KCC in HbF cells was about 3-fold that in HbA cells. These characteristics are qualitatively similar to those observed in HbA cells, notwithstanding the different conditions experienced by HbF cells in vivo, and the presence of HbF rather than HbA. KCC in HbF cells has a higher total capacity, but when measured at the ambient PO(2) of fetal blood it would be similar in magnitude to that in fully oxygenated HbA cells, and about that required to balance K(+) accumulation via the Na(+)/K(+) pump. These findings are relevant to the mechanism by which O(2) regulates membrane transporters in red blood cells, and to the strategy of promoting HbF synthesis as a therapy for patients with sickle cell disease.

Acetates↗

PubMed2001

O2 dependence of K+ transport in sickle cells: the effect of different cell populations and the substituted benzaldehyde 12C79.

The molecular basis of sickle cell disease (SCD) is well known but the pathophysiology is poorly understood. It remains intractable to therapy. Hyperactivity of several membrane transport systems, including the K+-Cl- cotransporter (termed KCC), cause HbS-containing red cells (termed HbS cells) to dehydrate and sickle, leading to the development of sickle cell crises (SCCs). Contrary to normal red cells (HbA cells), KCC in HbS cells is active at low O2 tensions (PO2s), remaining responsive to low pH or urea. Since these stimuli are usually encountered in hypoxic regions, the abnormal O2 dependence increases the contribution of KCC to dehydration, and hence development of SCCs. These differences with HbA cells may be due to the younger population of cells or to polymerization of HbS. We used 86Rb+ as a K+ congener to investigate the activity of KCC at different PO2s, and density gradient separation to investigate different red cell fractions. We found no correlation of O2 dependence with cell fractions. We also used the substituted benzaldehyde 12C79 to increase the O2 affinity of HbS and found that its effect on HbS O2 saturation and cell sickling correlated with that on both Cl--independent and Cl--dependent K+ transport, implying that, at low PO2s, KCC activity correlated with HbS polymerization. The importance of these results to understanding the pathophysiology of SCD, and for the design of chemotherapeutic agents to ameliorate or prevent SCC, is discussed.

Antisickling Agents↗

PubMed2000

Effect of dimethyl adipimidate on K+ transport and shape change in red blood cells from sickle cell patients.

Dimethyl adipimidate (DMA) reduces K+ loss from, and dehydration of, red cells containing haemoglobin S (HbS cells). Three membrane transporters may contribute to these processes: the deoxygenation-induced cation-selective channel (Psickle), the Ca2+-activated K+ channel (or Gardos channel) and the K+-CI- cotransporter (KCC). We show that DMA inhibited all three pathways in deoxygenated HbS cells. The Gardos channel could be activated following Ca2+ loading. Considerable KCC activity was present in oxygenated HbS cells, showing a selective action of DMA on the transporter in deoxygenated cells. Inhibition of sickling correlated strongly with that of Psickle and moderately with that of KCC activity. We conclude that DMA does not inhibit the K+ pathways directly, but acts mainly by preventing HbS polymerisation and sickling. These findings are relevant to the development of novel chemotherapeutic agents for amelioration of sickle cell disease.

Anemia, Sickle Cell↗

PubMed2000

Hydrocephalus in the H-Tx rat: a monogenic disease?

The H-Tx rat is a genetic model of hydrocephalus for which thereis a poor understanding of the mode of inheritance. Previous studies suggested a polygenicmode of inheritance but the breeding data to supportthis hypothesis have not been reported. In an attempt to clarify the hereditary mode we have analyzed the data from eight generations of H-Tx rats and four generations of cross-matings between H-Tx rats and Sprague-Dawley (SD) rats. In the H-Tx rat colony 113 of 129 random brother-sister matings (87.60%) produced hydrocephalic offspring, with males and females being equally affected. The overall incidence varied greatly with an average of 30. 35%. In matings with more than three litters, all mating pairs yielded hydrocephalic pups. In cross-matings both hydrocephalic and normal H-Tx rats were mated with normal SD rats. No hydrocephalus was observed in the first generation of 124 pups (F1). Subsequent brother-sister matings of F1 animals generated hydrocephalic pups in the F2 generation with a lower incidence (4.67% in hydrocephalic HTx/SD matings and 5.11% in normal HTx/SD matings, respectively) than in the H-Tx rat colony (30.35%). Back-cross-matings between F2 rats and normal H-Tx rats yielded an incidence of hydrocephalus higher than that of the cross-matings but lower than that of the H-Tx colony. These data strongly suggest that the H-Tx rat is a homozygous carrier of an autosomal recessive hydrocephalus gene with incomplete penetrance. Furthermore, the data clearly rule out sex-linked and polygenic modes of inheritance and provide further insight with respect to genetic inheritance of hydrocephalus.

Animals↗

PubMed2000

A mathematical model of the stress induced during avascular tumour growth.

In this paper a mathematical model is developed to describe the effect of nonuniform growth on the mechanical stress experienced by cells within an avascular tumour. The constitutive law combines the stress-strain relation of linear elasticity with a growth term that is derived by analogy with thermal expansion. To accommodate the continuous nature of the growth process, the law relates the rate of change of the stress tensor to the rate of change of the strain (rather than relating the stress to the strain directly). By studying three model problems which differ in detail, certain characteristic features are identified. First, cells near the tumour boundary, where nutrient levels and cell proliferation rates are high, are under compression. By contrast, cells towards the centre of the tumour, where nutrient levels are low and cell death dominant, are under tension. The implications of these results and possible model developments are also discussed.

Humans↗

PubMed2000

Effects of protein kinase and phosphatase inhibitors and anti-L antisera on K+ transport in LK sheep red cells.

We investigated the role of protein phosphorylation in the action of anti-L on low potassium (LK) sheep red cells. Anti-L stimulated the Na/K pump by four- to fivefold, but Na/K pump activity in anti-L-stimulated or in control cells was unaffected by protein kinase/protein phosphatase (PK/PP) inhibitors. KCl co-transport activity was inhibited by anti-L (about 50%). Co-transport was stimulated by staurosporine; and inhibited by calyculin A, okadaic acid, tyrphostin B46 and genistein; with a similar pattem in both control and anti-L-treated cells. O2 sensitivity of KCl co-transport was similar in control and anti-L-treated cells. Neither control nor anti-L-stimulated Na/K pump activities were O2 sensitive. Incubation with urea stimulated KCl co-transport in both control and anti-L-treated cells. Inhibition of co-transport by anti-L was unaffected by low concentrations of urea but was reduced at higher urea concentrations. Na/K pump activity of control cells was unaffected by incubation with urea, but that in cells stimulated by anti-L was reduced, though not significantly. Under high hydrostatic pressure, KCl co-transport was stimulated, and the inhibitory effects of PP inhibition (okadaic acid), anti-L or combinations of the two were reduced. Results suggest that anti-L does not affect K+ transport in LK sheep red cells via protein phosphorylation.

Animals↗

PubMed2000

A comparison in normal individuals and sickle cell patients of reduced glutathione precursors and their transport between plasma and red cells.

INTRODUCTION: Reduced glutathione is an important antioxidant in red cells whose depletion may contribute to the pathophysiology of sickle cell disease. The current study was designed to examine the availability of reduced glutathione precursors (glutamate, cysteine, glycine and possibly glutamine) together with the activity of the main transport pathways for their uptake (system ASC for cysteine and glycine; system gly for glycine). MATERIALS AND METHODS: Blood samples were obtained from normal (HbAA, HbA cells) and sickle cell disease patients (HbSS, HbS cells); amino acids were measured by HPLC; and transporter activity was measured by radioactive tracer fluxes (using serine and glycine for activity of system ASC; and glycine for that of system gly). RESULTS: Plasma concentrations of cysteine and glycine were increased and concentrations of all amino acids were elevated in HbS cells. The activity of system ASC was increased in HbS cells (both transport capacity and affinity were elevated for serine transport; transport capacity only for glycine). Activity of system gly was also increased (twofold increase in V(max) for glycine flux), though not significantly. Oxygenation also increased the activity of both transporters in normal and HbS cells. CO prevented deoxy-inhibition of glycine transport. Staurosporine (5 microM) inhibited O(2)-stimulated glycine transport through system ASC. It also inhibited the absolute magnitude of transport through system gly, but the O(2)-dependent flux was unaffected. CONCLUSION: Low reduced glutathione levels in HbS cells were not due to decreased substrate availability and O(2) stimulated transport of reduced glutathione precursors in both normal and HbS cells, through a mechanism that is likely to involve Hb and possibly protein phosphorylation.

Adult↗

PubMed2000

Oxidants and regulation of K(+)-Cl(-) cotransport in equine red blood cells.

The effect of oxidants on K(+)-Cl(-) cotransport (KCC) was investigated in equine red blood cells. Carbon monoxide mimicked O(2). The substituted benzaldehyde, 12C79 (5 mM), markedly increased O(2) affinity. In N(2), however, O(2) saturation was low (<10%) but KCC remained active. Nitrite (NO(2)(-)) oxidized heme to methemoglobin (metHb). High concentrations of NO(2)(-) (1 and 5 mM vs. 0.5 mM) increased KCC activity above control levels; it became O(2) independent but remained sensitive to other stimuli. 1-Chloro-2, 4-dinitrobenzene (1-3 mM) depleted reduced glutathione (GSH). Prolonged exposure (60-120 min, 1 mM) or high concentrations (3 mM) stimulated an O(2)-independent KCC activity; short exposures and low concentrations (30 min, 0.5 or 1 mM) did not. The effect of these manipulations was correlated with changes in GSH and metHb concentrations. An oxy conformation of Hb was necessary for KCC activation. An increase in its activity over the level found in oxygenated control cells required both accumulation of metHb and depletion of GSH. Findings are relevant to understanding the physiology and pathology of regulation of KCC.

Animals↗

PubMed2000

Oxygen-sensitive membrane transporters in vertebrate red cells.

Oxygen is essential for all higher forms of animal life. It is required for oxidative phosphorylation, which forms the bulk of the energy supply of most animals. In many vertebrates, transport of O(2) from respiratory to other tissues, and of CO(2) in the opposite direction, involves red cells. These are highly specialised, adapted for their respiratory function. Intracellular haemoglobin, carbonic anhydrase and the membrane anion exchanger (AE1) increase the effective O(2)- and CO(2)-carrying capacity of red cells by approximately 100-fold. O(2) also has a pathological role. It is a very reactive species chemically, and oxidation, free radical generation and peroxide formation can be major hazards. Cells that come into contact with potentially damaging levels of O(2) have a variety of systems to protect them against oxidative damage. Those in red cells include catalase, superoxide dismutase and glutathione. In this review, we focus on a third role of O(2), as a regulator of membrane transport systems, a role with important consequences for the homeostasis of the red cell and also the organism as a whole. We show that regulation of red cell transporters by O(2) is widespread throughout the vertebrate kingdom. The effect of O(2) is selective but involves a wide range of transporters, including inorganic and organic systems, and both electroneutral and conductive pathways. Finally, we discuss what is known about the mechanism of the O(2) effect and comment on its physiological and pathological roles.

Animals↗

PubMed1999

Regulation of Na+-K+-2Cl- cotransport in turkey red cells: the role of oxygen tension and protein phosphorylation.

1. Na+-K+-2Cl- cotransport (NKCC) was studied in turkey red cells using Na+ dependence or bumetanide sensitivity of 86Rb+ influx to monitor activity of the transporter. 2. Deoxygenation was the major physiological stimulus for NKCC activity: oxygen tensions (PO2) over the physiological range modulated the transporter, with a PO2 for half-maximal activation of about 41 mmHg (n = 3). In air, activity of NKCC was also stimulated by shrinkage and isoproteronol (isoprenaline, 5 microgr;M). By contrast, in deoxygenated cells, although the transporter activity was markedly elevated, it was no longer sensitive to volume or beta-adrenergic stimulation. 3. Calyculin A, a protein phosphatase inhibitor, stimulated cotransport with a lag of about 5 min. N-Ethylmaleimide (NEM) inhibited cotransport and also blocked the stimulatory effect of calyculin A if administered before calyculin A. Stimulation by calyculin A and deoxygenation were not additive. Staurosporine (2 microM) inhibited deoxygenated-stimulated K+ influxes, but not those stimulated by calyculin A. NEM added during calyculin A stimulation, i.e. during the 5 min lag, caused transport activity to be clamped at levels intermediate between maximal (calyculin A alone) and control. Cells treated with calyculin A alone or with calyculin A followed by NEM were no longer sensitive to volume, isoproteronol or PO2. 4. The results have characterized the interaction between deoxygenation and other stimuli of NKCC activity. They have also shown that it is possible to manipulate the transporter in a reciprocal way to that shown previously for K+-Cl- cotransport.

Adrenergic beta-Agonists↗

PubMed1999

Oxygen-dependent K+ influxes in Mg2+-clamped equine red blood cells.

1. Cl--dependent K+ (86Rb+) influxes were measured in oxygenated and deoxygenated equine red blood cells, whose free [Mg2+]i had been clamped, to examine the effect on O2 dependency of the K+-Cl- cotransporter. 2. Total [Mg2+]i was 2.55 +/- 0.07 mM (mean +/- s.e.m. , n = 6). Free [Mg2+]i was estimated at 0.45 +/- 0.04 and 0.68 +/- 0. 03 mM (mean +/- s.e.m., n = 4) in oxygenated and deoxygenated red cells, respectively. 3. K+-Cl- cotransport was minimal in deoxygenated cells but substantial in oxygenated ones. Cl--dependent K+ influx, inhibited by calyculin A, consistent with mediation via the K+-Cl- cotransporter, was revealed by depleting deoxygenated cells of Mg2+. 4. Decreasing [Mg2+]i stimulated K+ influx, and increasing [Mg2+]i inhibited it, in both oxygenated and deoxygenated red cells. When free [Mg2+]i was clamped, Cl--dependent K+ influxes were always greater in oxygenated cells than in deoxygenated ones, and changes in free [Mg2+]i of the magnitude occurring during oxygenation-deoxygenation cycles had a minimal effect. Physiological fluctuations in free [Mg2+]i are unlikely to provide the primary link coupling activity of the K+-Cl- cotransporter with O2 tension. 5. Volume and H+ ion sensitivity of K+ influx in Mg2+-clamped red cells were increased in O2 compared with those in deoxygenated cells at the same free [Mg2+]i, by about 6- and 2-fold, respectively, but again these features were not responsible for the higher fluxes in oxygenated cells. 6. Regulation of the K+-Cl- cotransporter by O2 is very similar in equine, sheep and in normal human (HbA) red cells, but altered in human sickle cells. Present results imply that, as in sheep red cells, O2 dependence of K+-Cl- cotransport in equine red cells is not mediated via changes in free [Mg2+]i and that cotransport in Mg2+-clamped red cells is still stimulated by O2. This behaviour is contrary to that reported for human sickle (HbS) cells.

Animals↗

PubMed1999

Effect of the substituted benzaldehyde 12C79 on Cl--dependent K+ influx in human red blood cells.

Ouabain- and bumetanide-resistant K+ influx, and haemoglobin (Hb) O2 saturation, were measured in HbA red cells over a range of oxygen tensions (PO2 values) in the presence and absence of 12C79 (5 mM), a substituted benzaldehyde which increases the O2 affinity of Hb. PO2 values for half-maximal O2 saturation declined from 29+/-2 mmHg (mean +/-SEM, n=3) in control cells to 7+/-1 mmHg with 12C79. In control cells, Cl--dependent K+ influx (indicative of KCl cotransport activity) was fully O2 dependent, i.e. inactive at low PO2 values. By contrast, in the presence of 12C79, KCl cotransport was largely resistant to inactivation at low PO2 values. Substantial cotransport activity was still present (>60% of that at high PO2 values) in N2, although O2 saturation was low (about 10%). In all cases, Cl--independent K+ influxes were low [<0.25 mmol (l cells h)-1] and unaffected by PO2 or 12C79. The significance of these results is discussed.

Antisickling Agents↗

PubMed1999

Randomized comparison between low-pressure laparoscopic cholecystectomy and gasless laparoscopic cholecystectomy.

BACKGROUND: Laparoscopic cholecystectomy using low-pressure pneumoperitoneum (8 mmHg) minimizes adverse hemodynamic effects, reduces postoperative pain, and accelerates recovery. Similar claims are made for gasless laparoscopy using abdominal wall lifting. The aim of this study was to compare gasless laparoscopic cholecystectomy to low-pressure cholecystectomy with respect to postoperative pain and recovery. METHODS: Thirty-six patients were randomized to low-pressure or gasless laparoscopic cholecystectomy using a subcutaneous lifting system (Laparotenser). RESULTS: The characteristics of the patients were similar in the two groups. The procedure was completed in all patients in the low-pressure group, but two patients in the gasless group were converted to pneumoperitoneum. There were no significant differences in postoperative pain and analgesic consumption, but patients in the gasless group developed shoulder pain more frequently (50% vs 11%, p < 0.05). Gasless operation took longer to perform (95 vs 72.5 min, p = 0.01). CONCLUSIONS: Gasless and low-pressure laparoscopic cholecystectomy were similar with respect to postoperative pain and recovery. The gasless technique provided inferior exposure and the operation took longer, but the technique may still have value in high-risk patients with cardiorespiratory disease.

Adult↗