Nasal inspiratory peak flow rates after cold stimulation of the feet in allergic rhinitis and normals

2002 ◽  
Vol 109 (1) ◽  
pp. S97-S97
Author(s):  
Renata Witkowska ◽  
Alan Wolff ◽  
Kumar Patel ◽  
Stanley Weiss ◽  
Leonard Bielory
Keyword(s):  
Allergic Rhinitis ◽  
Peak Flow ◽  
Cold Stimulation ◽  
Flow Rates ◽  
Nasal Inspiratory Peak Flow ◽  
Stimulation Of

scholarly journals The benefits of planar circular mouths on suction feeding performance

2012 ◽  
Vol 9 (73) ◽  
pp. 1767-1773 ◽  
Author(s):  
Tyler Skorczewski ◽  
Angela Cheer ◽  
Peter C. Wainwright
Keyword(s):  
Prey Capture ◽  
Peak Flow ◽  
Mouth Opening ◽  
Suction Feeding ◽  
Flow Rates ◽  
Computational Fluid Dynamics Simulations ◽  
Enhance Efficiency ◽  
And Performance ◽  
Dynamics Simulations ◽  
Hydrodynamic Effects

Suction feeding is the most common form of prey capture across aquatic feeding vertebrates and many adaptations that enhance efficiency and performance are expected. Many suction feeders have mechanisms that allow the mouth to form a planar and near-circular opening that is believed to have beneficial hydrodynamic effects. We explore the effects of the flattened and circular mouth opening through computational fluid dynamics simulations that allow comparisons with other mouth profiles. Compared to mouths with lateral notches, we find that the planar mouth opening results in higher flow rates into the mouth and a region of highest flow that is positioned at the centre of the mouth aperture. Planar mouths provide not only for better total fluid flow rates through the mouth but also through the centre of the mouth near where suction feeders position their prey. Circular mouths are shown to provide the quickest capture times for spherical and elliptical prey because they expose the prey item to a large region of high flow. Planar and circular mouths result in higher flow velocities with peak flow located at the centre of the mouth opening and they maximize the capacity of the suction feeders to exert hydrodynamic forces on the prey.

Inhibition of milk ejection in cows by oxytocin receptor blockade, α-adrenergic receptor stimulation and in unfamiliar surroundings

1997 ◽  
Vol 64 (3) ◽  
pp. 315-325 ◽  
Author(s):  
RUPERT M. BRUCKMAIER ◽  
OLGA WELLNITZ ◽  
JÜRG W. BLUM
Keyword(s):  
Adrenergic Receptor ◽  
Peak Flow ◽  
Oxytocin Receptor ◽  
Receptor Blockade ◽  
Milk Ejection ◽  
Receptor Stimulation ◽  
Flow Rates ◽  
Milk Flow ◽  
Drug Treatments ◽  
Similar Peak

Inhibition of milk ejection in cows by oxytocin receptor blockade (Atosiban) and α-adrenergic receptor stimulation (phenylephrine) prior to prestimulation was compared with inhibition of milk ejection in unfamiliar surroundings. In addition, Atosiban and phenylephrine were administered after a 1 min prestimulation or 1 min after the start of milking. Oxytocin concentrations increased during milking in all treatments. The spontaneously removed milk fraction (before oxytocin was injected) was similar for Atosiban and phenylephrine treatments and in unfamiliar surroundings, but lower than in controls. Peak flow rates were similar in all treatments, but reduced as compared with controls when phenylephrine and Atosiban were administered before prestimulation. Peripheral (Atosiban, phenylephrine) and central (unfamiliar surroundings) inhibition of milk ejection reduced the amount of available milk similarly. Drug treatments resulted in similar peak flow rates; however, teats were contracted after phenylephrine administration but not after Atosiban. The inhibition induced by Atosiban could be abolished by oxytocin injection, but not that induced by phenylephrine, which was antagonized by α-adrenergic receptor blockade. These results indicate that inhibition of milk ejection through activation of α-adrenergic receptors is based on blockade of milk flow into the cistern, but not through the teats.

The effect of facial cold stimulation on airway conductance in healthy man

1969 ◽  
Vol 47 (5) ◽  
pp. 453-457 ◽  
Author(s):  
W. T. Josenhans ◽  
G. N. Melville ◽  
W. T. Ulmer
Keyword(s):  
Airway Resistance ◽  
Facial Skin ◽  
Air Trapping ◽  
Cold Stimulation ◽  
Resistance Increase ◽  
Cold Receptors ◽  
Residual Capacity ◽  
Young Subjects ◽  
Airway Conductance ◽  
Stimulation Of

The effect on airway conductance (Gaw) and functional residual capacity (FRC) of stimulation of cold receptors in facial skin was studied in 12 healthy young subjects, with a body plethysmograph. Mean Gaw decreased significantly, from 0.44 to 0.38 liter s−1 cm−1 H2O, in 10 subjects. FRC was only slightly affected, probably because the experiment was too brief to allow air-trapping. It is concluded that the Gaw decrease during exposure to cold results from bronchoconstriction due to (a) stimulation of trigeminal nerve cold receptors and to (b) pharyngeal and glottal airway resistance increase resulting from frequent involuntary 'dry' swallowing.

Aminophylline Therapy Does Not Improve Outcome and Increases Adverse Effects in Children Hospitalized With Acute Asthmatic Exacerbations

PEDIATRICS ◽  
1994 ◽  
Vol 93 (2) ◽  
pp. 205-210
Author(s):  
Raphael E. Strauss ◽  
David L. Wertheim ◽  
Vincent R. Bonagura ◽  
David J. Valacer
Keyword(s):  
New York ◽  
Adverse Effects ◽  
Hospital Admissions ◽  
Peak Flow ◽  
Controlled Trial ◽  
Tertiary Care ◽  
Time Interval ◽  
Double Blind ◽  
Flow Rates ◽  
Duration Of Hospitalization

Objective. To evaluate the effects of aminophylline (Am) in children hospitalized with asthma. Methods. Prospective, randomized, double-blind, placebo-controlled trial. Subjects were children between the ages of 5 and 18 years admitted for asthma exacerbation to either a tertiary care children's hospital or an innercity general hospital in New York. Exclusion criteria were admission to the intensive care unit, initial theophylline level > 5 µg/dL, or the presence of other systemic disorders. All patients received nebulized albuterol therapy and intravenous glucocorticosteroids in standardized doses. Thirty-one patients were randomized to receive either an Am bolus followed by continuous Am infusion or placebo (P) bolus and infusion. The outcome variables were: duration of hospitalization, percent of predicted peak expiratory flow rates recorded at 12-hour intervals, number of albuterol treatments required, and adverse effects. Results. There were no significant differences at study entry in age, sex, race, number of previous hospital admissions, prior medications used, clinical symptom scores, or initial peak flow rates for the two groups. For 26 patients who completed this study, 15 patients in the P group were hospitalized for a mean duration of 2.33 ± 1.3 days, whereas 11 patients in the Am group required 2.58 ± 1.5 days. There were no significant differences between the two groups for hospital days, peak flow rates at any time interval, or amount of albuterol therapy required (P > .2). In the Am group, 6 of the 14 patients who entered the study experienced significant adverse effects consisting of nausea, emesis, headache, abdominal pain, and palpitations. Only 1 of 17 patients in the P group had an adverse effect (P <. 05). Conclusions. There is no benefit and considerable risk of adverse effects associated with the use of Am in hospitalized asthmatic children.

Stimulation of oxygen uptake by glucagon is oxygen dependent in perfused rat liver

1989 ◽  
Vol 256 (2) ◽  
pp. G369-G376
Author(s):  
Z. Kizaki ◽  
R. G. Thurman
Keyword(s):  
Intracellular Calcium ◽  
High Flow ◽  
Perfused Liver ◽  
Normal Flow ◽  
Sprague Dawley ◽  
O2 Uptake ◽  
Intact Cells ◽  
Flow Rates ◽  
Isolated Mitochondria ◽  
Stimulation Of

Livers from well-fed female Sprague-Dawley rats (100-150 g) were perfused at flow rates of 4 or 8 ml.g liver-1.min-1 to deliver O2 to the organ at various rates. During perfusion at normal flow rates (4 ml.g-1.min-1), glucagon (10 nM) increased O2 uptake in perfused liver by approximately 40 mumol.g-1.h-1. In contrast, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 when livers were perfused at high flow rates. Increase in O2 uptake was directly proportional to flow rate and was blocked partially by infusion of phorbol myristate acetate (100 nM) before glucagon. Increase in O2 uptake due to elevated flow was not due to enhanced glucagon delivery, since infusion of 120 nM glucagon at normal flow rates only increased O2 uptake by approximately 40 mumol.g-1.h-1. On the other hand, when O2 tension in the perfusate was manipulated at normal flow rates, the stimulation of O2 uptake by glucagon increased proportional to the average O2 tension in the liver. Infusion of 8-bromo-adenosine 3',5'-cyclic monophosphate (BrcAMP; 25 microM) also increased O2 uptake more than twice as much at high compared with normal flow rates. In the presence of angiotensin II (5 nM), a hormone that increases intracellular calcium, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 at normal flow rates. Infusion of glucagon or BrcAMP into livers perfused at normal flow rates increased state 3 rates of O2 uptake of subsequently isolated mitochondria significantly by approximately 25%. In contrast, perfusion with glucagon or BrcAMP at high flow rates increased mitochondrial respiration by 50-60%. Glucagon addition acutely to suspensions of mitochondria, however, had no effect on O2 uptake. These data are consistent with reports that glucagon administration in vivo or treatment of intact cells with glucagon increases O2 uptake of subsequently isolated mitochondria, a phenomenon that can account for the observed increase in O2 uptake in livers perfused at high flow rates with glucagon. Furthermore, these results are consistent with the hypothesis that the effect of glucagon on mitochondria is O2 dependent in the perfused liver. This is most likely due to an effect of intracellular calcium on a mechanism mediated via cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of unilateral nasal inspiratory peak flow in nasal obstruction—A study of 70 patients undergoing septorhinoplasty surgery

2019 ◽  
Vol 44 (3) ◽  
pp. 427-430
Author(s):  
Anika Kaura ◽  
Jagdeep S. Virk ◽  
Jonathan Joseph ◽  
Catherine Rennie ◽  
Prem Singh Randhawa ◽  
...  
Keyword(s):  
Nasal Obstruction ◽  
Peak Flow ◽  
Nasal Inspiratory Peak Flow

scholarly journals Mechanoregulation of BK channel activity in the mammalian cortical collecting duct: role of protein kinases A and C

2009 ◽  
Vol 297 (4) ◽  
pp. F904-F915 ◽  
Author(s):  
Wen Liu ◽  
Yuan Wei ◽  
Peng Sun ◽  
Wen-Hui Wang ◽  
Thomas R. Kleyman ◽  
...  
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Bk Channel ◽  
Slow Flow ◽  
Cortical Collecting Duct ◽  
Flow Rates ◽  
Calphostin C ◽  
Flow Stimulation ◽  
Slow Flow Rate ◽  
Stimulation Of

Flow-stimulated net K secretion ( JK) in the cortical collecting duct (CCD) is mediated by an iberiotoxin (IBX)-sensitive BK channel, and requires an increase in intracellular Ca2+ concentration ([Ca2+]i). The α-subunit of the reconstituted BK channel is phosphorylated by PKA and PKC. To test whether the BK channel in the native CCD is regulated by these kinases, JK and net Na absorption ( JNa) were measured at slow (∼1) and fast (∼5 nl·min−1·mm−1) flow rates in rabbit CCDs microperfused in the presence of mPKI, an inhibitor of PKA; calphostin C, which inhibits diacylglycerol binding proteins, including PKC; or bisindolylmaleimide (BIM) and Gö6976, inhibitors of classic and novel PKC isoforms, added to luminal (L) and/or basolateral (B) solutions. L but not B mPKI increased JK in CCDs perfused at a slow flow rate; a subsequent increase in flow rate augmented JK modestly. B mPKI alone or with L inhibitor abolished flow stimulation of JK. Similarly, L calphostin C increased JK in CCDs perfused at slow flow rates, as did calphostin C in both L and B solutions. The observation that IBX inhibited the L mPKI- and calphostin C-mediated increases in JK at slow flow rates implicated the BK channel in this K flux, a notion suggested by patch-clamp analysis of principal cells. The kinase inhibited by calphostin C was not PKC as L and/or B BIM and Gö6976 failed to enhance JK at the slow flow rate. However, addition of these PKC inhibitors to the B solution alone or with L inhibitor blocked flow stimulation of JK. Interpretation of these results in light of the effects of these inhibitors on the flow-induced elevation of [Ca2+]i suggests that the principal cell apical BK channel is tonically inhibited by PKA and that flow stimulation of JK in the CCD is PKA and PKC dependent. The specific targets of the kinases remain to be identified.

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