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PubMed1988

Periarteriolar and tissue PO2 during sympathetic escape in skeletal muscle.

The purpose of this study was to determine whether vascular escape from sympathetic nerve stimulation in skeletal muscle is caused by a fall in the tissue O2 level. O2 microelectrodes were used to measure PO2 at the wall of arterioles (periarteriolar PO2) and near the venous end of capillary networks (parenchymal tissue PO2) in the exteriorized cat sartorius muscle during sympathetic nerve stimulation. Measurements were made under a low O2 suffusate (equilibrated with 5% CO2-95% N2) and under a high O2 suffusate (10% O2-5% CO2-85% N2). During sympathetic stimulation under low O2, mean diameter of proximal (second-order) arterioles decreased from 55 to 32 micron before returning to 37 micron (sympathetic escape). Mean periarteriolar PO2 fell from 50 to 25 mmHg with no secondary increase. Distal (fifth-order) arterioles initially constricted from 7 to 4 micron before relaxing to 6 micron. Periarteriolar PO2 of these vessels fell from 40 to 13 mmHg with no secondary increase. During stimulation under high O2, periarteriolar PO2 levels of both proximal and distal arterioles were similar to those under low O2, yet escape was substantially reduced. The lack of relationship between periarteriolar PO2 and vascular escape argues against a role of vascular wall PO2 in this behavior. Parenchymal tissue PO2 fell to 9 mmHg during stimulation under low O2 but did not fall below 22 mmHg during stimulation under high O2. The attenuation of escape under conditions where tissue PO2 did not fall is consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO2.

Animals↗
PubMed1975

Norepinephrine vascoconstrictor escape in isolated meseneric arteries.

When isolated superfused cat mesentric arterial rings were exposed to norepinephrine(NE) 10'-6 g/ml, force initially increased but subsequently declined despite continuedadministration of NE. Phasic contractions occurred in 48% of the vessels. Norepinephrine concentrations just above threshold induced tonic contractions without escape. When NE was administered after brief exposure of the arterial rings to low-calcium solutions, peak force development and escape were both reduced and phasic contractions were abolished. Escape did not occur in potassium-depolarized vessels. The peak response was increased and escape was reduced by substituting sodium in the Krebs solution by lithium and by substituting chloride with iodide or perchlorate. Substitution of chloride by isethionate reduced the peak NE resonse and abolished escape. Propanolol was without effect. It is suggested that escape from NE vasoconstriction in mesenteric arteries is due to fading of propagated activity.

Animals↗
PubMed1987

Increased synthesis and release of atrial peptide during DOCA escape in conscious dogs.

The escape from the sodium-retaining effects of prolonged mineralocorticoid treatment in animals and humans was first noted over 40 yr ago, but despite intense study the mechanisms responsible for the escape phenomenon have not been identified. Putative "natriuretic hormones" have been proposed to account for the escape phenomenon. To determine whether atrial natriuretic peptides (ANP) could participate in the escape phenomenon, the mineralocorticoid deoxycorticosterone acetate (DOCA) was administered to conscious dogs for 14 days. Escape was accompanied by a doubling of plasma ANP concentration and four- to sevenfold increases in cardiac ANP messenger RNA. There were also significant increases in mean arterial blood pressure during the last 8 days of DOCA treatment. Thus increases in the synthesis and secretion of ANP and increases in atrial pressure may represent mechanisms that contribute to the escape from mineralocorticoid-induced sodium retention.

Animals↗
PubMedDate not supplied

Chronic flumazenil (Ro 15-1788) facilitates acquisition and retention of a swim-escape response in rats.

Since chronic flumazenil treatment was previously found to stimulate exploratory behavior in rodents, the aim of this study was to test the effect of chronic exposure to flumazenil on acquisition and retention of escape behavior. Adult rats were treated with flumazenil (Ro 15-1788; 4 mg/kg/day in drinking water) for 21 days (experiment 1) and for 17 days (experiment 2). In experiment 1 (a round water tank with one escape rope) conducted 24 h after drug/vehicle withdrawal, the time the animals needed to resolve a swim-escape task was significantly shorter in the drug group, compared to the controls. In the retention trial, 24 h later, the control group matched the performance of the drug group. In experiment 2, a water T-maze was used which was equipped with two ropes, one anchored to the bottom and the other unanchored and therefore was more difficult to climb. On day 14 of flumazenil/vehicle treatment, there were no differences between the groups in the time needed to escape from the maze. However, on day 15 and 16 of drug/vehicle treatment, the drug group made highly significant progress, while the control group showed no improvement of the escape behavior. The possible mechanisms of flumazenil-induced facilitation of escape behavior have been discussed.

Animals↗
PubMed1978

Junctional escape rhythm in the sick sinus syndrome.

In 21 patients with and 31 without junctional escape beats, a comparison of the symptoms, revealed that there were no significant differences (p greater than 0.05) in the symptoms between these two groups manifesting a sick sinus syndrome. Thus, the occurrence of junctional escape beats did not provide the anticipated shortening of the asystolic pauses to prevent the occurrence of symptoms related to the period of electrical silence. In 7 patients with an escape junctional rhythm, the long pause was interrupted by the occurrence of a regular junctional rhythm. The pause was not preceded by a supraventricular tachycardia, ruling out physiologic overdrive suppression of the junctional pacemaker. The period of asystole preceding the junctional rhythm was not multiple of the R-R interval of the junctional rhythm. 4 additional patients demonstrated long periods of asystole, uninterrupted by junctional escape beats and at other times exhibited shorter pauses which were terminated by junctional escape beats. These findings can be explained by the presence of a 'junctional arrest' which is analogous to sinoatrial arrest. The phenomenon of 'junctional arrest' may be one tenable explanation to account for the lack of protection by junctional escape activity against the symptoms associated with the sick sinus syndrome.

Aged↗
PubMed1990

High-dose atrial natriuretic factor enhances albumin escape from the systemic but not the pulmonary circulation.

Atrial natriuretic factor (ANF) causes plasma fluid to shift out of the circulation and enhances the escape of radiolabeled albumin. Examination of the mechanisms by which ANF alters microcirculatory fluid and protein transfer will likely require studies in localized vascular regions. This study was aimed at determining the specific organs in which ANF increases the escape of albumin. Anesthetized, splenectomized rats that had both kidneys removed were infused with vehicle alone or rat ANF-(99-126) at 0.025, 0.05, 0.1, or 0.5 micrograms.min-1.kg-1 for 2 hours (n = 8 per group). Total red cell and plasma volumes were measured with chromium-51-labeled erythrocytes and iodine-125-labeled albumin, respectively. At the end of 2 hours, the rats were frozen in liquid nitrogen, and organ blood volumes and tissue 125I-albumin were determined. ANF decreased plasma volume at infusion rates of 0.1 and 0.5 micrograms.min-1.kg-1. ANF increased the rate at which 125I-albumin escaped from the overall circulation at infusion rates of 0.1 and 0.5 micrograms.min-1.kg-1. At an ANF infusion rate of 0.1 micrograms.min-1.kg-1, the albumin escape rate increased in the gastrointestinal tract, skeletal muscle, heart, and lungs. At an infusion rate of 0.5 micrograms.min-1.kg-1, the albumin escape rate increased in the gastrointestinal tract, muscle, and skin, but not the lungs. These findings suggest that at pathophysiological levels, ANF shifts protein out of the circulation in peripheral vascular beds and the lungs and may contribute to pulmonary edema in states such as congestive heart failure. At pharmacological levels, ANF may be protective of the lungs by preventing increased pulmonary albumin escape.

Animals↗
PubMed1997

Dual role for nitric oxide in the regulation of plasma volume and albumin escape during endotoxin shock in conscious rats.

To assess the role of nitric oxide (NO) produced by the constitutive (cNOS) and inducible NO synthase (iNOS) in the regulation of vascular functions, we compared the effects of aminoguanidine, a relatively selective inhibitor of iNOS, and NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NOS inhibitor on blood pressure, plasma volume, and albumin escape during the early and delayed phases of endotoxin shock in conscious, chronically catheterized rats. Red blood cell volume and plasma volume were determined by using chromium-51-tagged erythrocytes and iodine-125-labeled albumin, respectively. Injection of lipopolysaccharide (LPS) 10 mg/kg i.v. resulted in a fall in blood pressure, hemoconcentration, and increased total-body albumin escape, which is reflected by a 25% reduction in plasma volume. When LPS was injected into animals pretreated with L-NAME (7.4 mumol/kg i.v. 15 minutes before LPS), losses in plasma volume and albumin escape were significantly greater than in rats that received LPS alone, despite that L-NAME attenuated the hypotensive action of LPS. Aminoguanidine pretreatment (162 mumol/kg) had no effect on the early responses to LPS, whereas it was as potent as L-NAME in reversing hypotension when injected 70 minutes after LPS. Aminoguanidine treatment also prevented further losses in plasma volume and markedly attenuated total-body and organ albumin escape rates elicited by LPS. L-NAME produced only a slight attenuation of LPS-induced losses in plasma volume and albumin escape in most organs studied, whereas it potentiated albumin extravasation in the lung. These results demonstrate that inhibition of cNOS potentiates, whereas inhibition of iNOS markedly attenuates, losses in plasma volume and albumin escape elicited by LPS, and suggest that selective inhibitors of iNOS may be more effective than nonselective inhibitors of all forms of NOS in the therapy of septic shock.

Animals↗
PubMed2005

Systems with escapes.

There are two types of escapes in conservative dynamical systems with two degrees of freedom: escapes to infinity and escapes to certain singular points at a finite distance. In both cases the areas on a surface of section are not preserved. We consider the basins of escape to infinity in simple Hamiltonian systems. The initial conditions of orbits escaping after 1, 2, ... intersections with a surface of section form in general spiral fractal sets. Then we consider the sets of escapes into two fixed black holes for various values of the energy. The forms of these sets depend on the unstable periodic orbits and their asymptotic curves. We find the characteristics of the simple periodic orbits and their changes for various values of the energy.

Journal Article↗
PubMed1979

Escape from sodium and potassium retaining actions of aspirin-like drugs used in a patient with Bartter's syndrome.

Escape from sodium and potassium retaining actions of aspirin-like drugs used in a patient with Bartter's syndrome. An analysis was done with regard to the mode of escapes from sodium and potassium retaining actions of aspirin-like drugs in a patient with Bartter's syndrome. In the indomethacin therapy of the syndrome, there was a delay in the initiation of potassium escape as compared to sodium escape, whereas no delay was seen in the ibuprofen therapy. This delay was probably related to the direct or indirect inhibition of sodium-potassium exchange in the distal nephrons. The course of aspirin therapy went midway between the above two. In the spironolactone therapy, the mode of escape was a mirror image of the one in the indomethacin therapy. Also, in a patient with rheumatoid arthritis, but without Bartter's syndrome, the escapes from the effects of indomethacin were seen. In order to understand the effect of these drugs on potassium excretion in Bartter's syndrome, some other intrarenal events, such as the influence on chloride transport in the loop of Henle leading to potassium conservation, may have to be considered.

Adult↗
PubMed2006

Human monoclonal antibody combination against SARS coronavirus: synergy and coverage of escape mutants.

BACKGROUND: Experimental animal data show that protection against severe acute respiratory syndrome coronavirus (SARS-CoV) infection with human monoclonal antibodies (mAbs) is feasible. For an effective immune prophylaxis in humans, broad coverage of different strains of SARS-CoV and control of potential neutralization escape variants will be required. Combinations of virus-neutralizing, noncompeting mAbs may have these properties. METHODS AND FINDINGS: Human mAb CR3014 has been shown to completely prevent lung pathology and abolish pharyngeal shedding of SARS-CoV in infected ferrets. We generated in vitro SARS-CoV variants escaping neutralization by CR3014, which all had a single P462L mutation in the glycoprotein spike (S) of the escape virus. In vitro experiments confirmed that binding of CR3014 to a recombinant S fragment (amino acid residues 318-510) harboring this mutation was abolished. We therefore screened an antibody-phage library derived from blood of a convalescent SARS patient for antibodies complementary to CR3014. A novel mAb, CR3022, was identified that neutralized CR3014 escape viruses, did not compete with CR3014 for binding to recombinant S1 fragments, and bound to S1 fragments derived from the civet cat SARS-CoV-like strain SZ3. No escape variants could be generated with CR3022. The mixture of both mAbs showed neutralization of SARS-CoV in a synergistic fashion by recognizing different epitopes on the receptor-binding domain. Dose reduction indices of 4.5 and 20.5 were observed for CR3014 and CR3022, respectively, at 100% neutralization. Because enhancement of SARS-CoV infection by subneutralizing antibody concentrations is of concern, we show here that anti-SARS-CoV antibodies do not convert the abortive infection of primary human macrophages by SARS-CoV into a productive one. CONCLUSIONS: The combination of two noncompeting human mAbs CR3014 and CR3022 potentially controls immune escape and extends the breadth of protection. At the same time, synergy between CR3014 and CR3022 may allow for a lower total antibody dose to be administered for passive immune prophylaxis of SARS-CoV infection.

Amino Acid Substitution↗
PubMed1982

Mineralocorticoid escape in man: role of renal prostaglandins.

The role of renal prostaglandins (PGE2 and PGF2 alpha) and kallikrein in the renal escape from excess mineralocorticoid has been evaluated in 10 normal volunteers on a high sodium diet. Escape from 9-alpha-fluorohydrocortisone (9-alpha-FF) administered for 12 days (0.6 mg daily) occurred within 4-5 days when 345 +/- 50 mmol sodium had accumulated. Indomethacin, a cyclooxygenase inhibitor, was then administered for 3 days while maintaining 9-alpha-FF. This was followed by a further cumulative gain of 105 +/- 28 mmol sodium after which escape resumed. Potassium balance remained negative throughout the study. Both PGE2 and PGF2 alpha excretion increased significantly under 9-alpha-FF from respective control values of 220 +/- 50 and 818 +/- 86 ng/24 h. to 610 +/- 317 and 1213 +/- 132 ng/24 h at the time of escape. Concomitantly urinary kallikrein increased from 1.1 +/- 0.2 to 2.5 +/- 0.3 units/24 h. Creatinine clearance increased from a mean baseline value of 111 +/- 4 to 123 +/- 4 ml/min during the same period. Indomethacin produced an inhibition of prostaglandin excretion without significant alteration of kallikrein excretion. Overall these results and particularly the transient sodium retention induced by indomethacin at the time of mineralocorticoid escape, suggest that prostaglandins may contribute to the escape phenomenon, whereas the role of kallikrein does not appear to be determinant.

Adult↗
PubMed2004

Parameters affecting cellular invasion and escape from the parasitophorous vacuole by different infective forms of Trypanosoma cruzi.

In this study we have examined certain aspects of the process of cell invasion and parasitophorous vacuole escape by metacyclic trypomastigotes and extracellular amastigote forms of Trypanosoma cruzi (G strain). Using Vero (and HeLa) cells as targets, we detected differences in the kinetics of vacuole escape by the two forms. Alcalinization of intercellular pH influenced both invasion as well as the escape from the parasitophorous vacuole by metacyclic trypomastigotes, but not the escape kinetics of extracellular amastigotes. We used sialic acid mutants as target cells and observed that the deficiency of this molecule facilitated the escape of both infective forms. Hemolysin activity was only detected in extracellular amastigotes and neither form presented detectable transialidase activity. Invasion of extracellular amastigotes and trypomastigotes in Vero cells was affected in different ways by drugs that interfere with host cell Ca2+ mobilization. These results are in line with previous results that indicate that metacyclic trypomastigotes and extracellular amastigote forms utilize mechanisms with particular features to invade host cells and to escape from their parasitophorous vacuoles.

Animals↗
PubMed2003

Evaluation of kill strips on boll weevil (Coleoptera: Curculionidae) mortality in pheromone traps and impact on weevil escape.

A field study examined the temporal patterns of boll weevil mortality provided by two commercially available kill strips, Hercon VaporTape II and Plato Insecticide Strip, and to evaluate the impacts of these devices on weevil escape from traps. Both types of kill strips produced similar levels of weevil mortality with the exception of the last two inspection intervals (30 and 46 h after continual exposure to kill strips). At these intervals, the Plato Strip produced significantly higher mortality than the Hercon strip; however, these differences were numerically small (10 and 6%, respectively). Both types of kill strips produced a high level of weevil mortality in traps (> 90%) after 46 h of exposure. On average, 5-8% of weevils escaped from traps whether a kill strip was present or absent. A strong temporal pattern of escape was observed, with > or = 90% of escape occurring within the first hour after weevils were introduced into traps. Because > or = 90% of escape occurred within the first hour weevils were in the traps and < 3% of weevils died during the first hour of exposure to kill strips in traps, use of kill strips in large-scale boll weevil management programs is not justified on the basis of reduced weevil escape.

Animals↗
PubMed2003

Protection against CTL escape and clinical disease in a murine model of virus persistence.

CTL escape mutations have been identified in several chronic infections, including mice infected with mouse hepatitis virus strain JHM. One outstanding question in understanding CTL escape is whether a CD8 T cell response to two or more immunodominant CTL epitopes would prevent CTL escape. Although CTL escape at multiple epitopes seems intuitively unlikely, CTL escape at multiple CD8 T cell epitopes has been documented in some chronically infected individual animals. To resolve this apparent contradiction, we engineered a recombinant variant of JHM that expressed the well-characterized gp33 epitope of lymphocytic choriomeningitis virus, an epitope with high functional avidity. The results show that the presence of a host response to this second epitope protected mice against CTL escape at the immunodominant JHM-specific CD8 T cell epitope, the persistence of infectious virus, and the development of clinical disease.

Amino Acid Sequence↗
PubMed2003

[Escape of transgenes and its ecological risks].

The rapid development of biotechnology, particularly the transgenic technology, has brought us with tremendous opportunities to solve the world's starvation problems that have been caused by the continued expanding of the global population. However, the application of transgenic biotechnology and the environmental release of transgenic organisms have evoked a series of extraordinary debates on biosafety issues related to the prosperity and the future of transgenic technology. The public and scientific communities are desperately interested in knowing whether the transgenic products would pose negative influences on plants and animals, human life and health, as well as on genetic resources and environment. These concerns have become universal hot topics over the last decade. Among the most debated biosafety issues caused potentially by transgenic products, transgene escape to the environment and its consequent ecological risks become one of the appealing focal points. In this review, a series of biosafety issues concerned by public, including the possibility of transgene escape and its various paths, as well as the potential ecological risks caused by such escape were discussed, and various approaches for controlling for transgene escape and the factors to consider when designing safety isolation distance between transgenic varieties and other concerned plants were also examined. The objective of this review is to allow readers to understand the potential biosafety problems caused by environmental release of transgenic crops and by the escape of foreign transgenes in particular, and to use the effective tools to control and avoid transgene escape.

Animals↗
PubMed1990

[Escape rhythms after ablation of the atrioventricular junction and implantation of a pacemaker].

Escape rhythms characteristics after successful catheter ablation of the atrioventricular junction and intentional complete heart block were compared with those due to others etiologies as well as the advantage of the posterior implantation of a rate responsive pacemaker (VVIR). In 22 patients, 9 men and 13 women, with permanent AV block after fulguration and follow-up periods from 4 to 58 months, escape rhythms data studied during the procedure and at short and long-term periods, showed the following characteristics: 1) Classical parameters of valuation are not as a whole useful to evaluate subsidiary escape rhythms after electrical fulguration of the atrioventricular junction system. 2) The QRS morphology of the escape rhythm exhibited frequently right or left bundle branch block and specially the former. 3) Spontaneous variability of the escape rhythm recovery time makes this parameter unreliable. 4) Electrophysiological parameters previous to the shock and energy delivery do not predict the origin and characteristics of the subsidiary escape rhythms. 5) Active ventricular arrhythmias appearing immediately postshock are unrelated with any subsequent complication. 6) Permanent pacing increases pacemaker dependency at least temporarily. In 15 of 22 patients, a rate responsive multiprogrammable pacemaker controlled by QT interval was implanted. Cardiac performance and life-quality was improved in these patients due to the addition of several factors: 1) Control of the tachyarrhythmias. 2) Elimination of antiarrhythmic drugs and their side-effects on ventricular function. 3) Self-regulation of cardiac rate through permanent stimulation with a QT sensitive rate responsive pacemaker.

Adult↗
PubMed1978

The escape of cyclic AMP from human diploid fibroblasts: general properties.

A variety of human diploid fibroblasts released large amounts of cAMP to the medium in a time-dependent fashion concomitant with stimulation of the cells by agonists of the adenylate cyclase. In WI-38 cells increased medium cAMP levels were detectable as quickly as increased cellular levels. Escape was not secondary to serum deprivation nor cell injury. It occurred in defined media, and was pH and temperature dependent. Elevated rates of escape were maintained for up to 24 hours after stimulation. A variety of PDE inhibitors reduced the rate of escape. A rough proportionality existed between the potencies of the compounds as potentiators of PGE1 increased cellular cAMP levels on the one hand and as inhibitors of escape on the other. In the case of IBMX, the inhibition of escape was transient, the most pronounced effect being during the first 5 minutes of incubation. In addition, a variety of compounds without significant acute effects on cellular cAMP levels inhibited escape.

1-Methyl-3-isobutylxanthine↗
PubMed1983

The reversal effect of antidepressants on the escape deficit induced by inescapable shock in rats.

This experiment investigated the effect of antidepressants on the escape deficit induced by inescapable shock. Following exposure to escapable shock, rats received a single injection of either tricyclic antidepressants (imipramine, desipramine), an atypical antidepressant (nomifensine), or saline. In a subsequent two-way shuttle test, treatments with these antidepressants reversed the escape deficit of the "inescapable-shock" groups without affecting performance of the "escapable-shock" groups. It is suggested that catecholamine re-uptake inhibition of the acute actions of antidepressants contributed to this reversal effect. The findings are discussed in relation to the neurochemical hypothesis of the escape deficit induced by inescapable shock and to an animal model of depression.

Animals↗