Thursday, January 21, 2021

Surface Tension and Pulmonary Surfactant - What you need to know

 

Respiratory | Surface Tension & Surfactant in Alveoli


 

https://www.google.com/search?q=ACE-2+sars+surfactant&rlz=1C1CHBD_enUS903US903&oq=ACE-2+sars+surfactant&aqs=chrome..69i57.8991j0j7&sourceid=chrome&ie=UTF-8

https://www.sciencedirect.com/science/article/abs/pii/S0306987720310732#:~:text=Severe%20acute%20respiratory%20syndrome%20coronavirus,ACE2)%20receptor%20and%20causes%20pneumonia.&text=Pulmonary%20surfactant%20is%20believed%20to,surface%20tension%20in%20mammalian%20lungs.


https://www.sciencedirect.com/science/article/abs/pii/S0306987720310732#:~:text=Severe%20acute%20respiratory%20syndrome%20coronavirus,ACE2)%20receptor%20and%20causes%20pneumonia.&text=Pulmonary%20surfactant%20is%20believed%20to,surface%20tension%20in%20mammalian%20lungs.


Pulmonary surfactant itself must be a strong defender against SARS-CoV-2

Abstract

Pulmonary surfactant is considered to be one of the soaps. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the other enveloped viruses become very weak against surfactant. The SARS virus binds to angiotensin-converting enzyme (ACE2) receptor and causes pneumonia. In the lung, the ACE2 receptor sits on the top of lung cells known as alveolar epithelial type II (AE2) cells. These cells play an important role in producing surfactant. Pulmonary surfactant is believed to regulate the alveolar surface tension in mammalian lungs. To our knowledge, AE2 cells are believed to act as immunoregulatory cells; however, pulmonary surfactant itself has not been believed to act as a defender against the enveloped viruses. This study hypothesises that pulmonary surfactant may be a strong defender of enveloped viruses. Therefore, old coronaviruses merely cause pneumonia. On the contrary, new SARS-CoV-2 can suppress the production of surfactant that binds to the ACE2 of AE2 cells. The coronavirus can survive in the lung tissue because of the exhaustion of pulmonary surfactant.

Keywords

SARS-CoV-2
Pulmonary surfactant
ACE2
Alveolar epithelial type II cell

Research data for this article

Data not available / No data was used for the research described in the article
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Purines, such as adenosine triphosphate are potent stimulators of surfactant secretion and may be important for its secretion at birth. Mechanical stretch such as lung distension and hyperventilation, have also been found to be involved in stimulating surfactant secretion.Feb 4, 2009
What exactly are purines?
Purines are substances in animal and plant foods that your body converts to uric acid. If you can't flush the uric acid out through your kidneys, it can build up in the bloodstream and be deposited as needle-shaped crystals in your joints.




https://clinicaltrials.gov/ct2/show/NCT04362059

Brief Summary:
Lung surfactant is present in the lungs. It covers the alveolar surface where it reduces the work of breathing and prevents the lungs from collapsing. In some respiratory diseases and in patients that require ventilation this substance does not function normally. This study will introduce surfactant to the patients lungs via the COVSurf Drug Delivery System


Detailed Description:

The hypothesis behind the proposed trial of surfactant therapy for COVID-19 infected patients requiring ventilator support is that endogenous surfactant is dysfunctional. This could be due to decreased concentration of surfactant phospholipid and protein, altered surfactant phospholipid composition, surfactant protein proteolysis and/or oedema protein inhibition of surfactant surface tension function and/or oxidative inactivation of surfactant proteins. Variations of these dysfunctional mechanisms have been reported in a range of lung diseases, including cystic fibrosis and severe asthma, and in child and adult patients with ARDS. Our studies of surfactant metabolism in adult ARDS patients showed altered percentage composition of surfactant PC, with decreased DPPC and increased surface tension-inactive unsaturated species, and decreased concentrations of both total PC and phosphatidylglycerol (PG)

The SARS-CoV-2 virus binds to the angiotensin converting enzyme-2 (ACE2) receptor, which is preferentially expressed in the peripheral lung ATII cells. Consequent viral infection of ATII cells could reduce cell number and impair the capacity of the lungs to synthesise and secrete surfactant. This, however, has not yet been demonstrated empirically in COVID-19 patients. If this is the case, then exogenous surfactant administration to the lungs is potential one treatment option to mitigate disease severity in these patients.




https://go.drugbank.com/drugs/DB11098

Potassium bicarbonate

IDENTIFICATION

Name
Potassium bicarbonate
Accession Number
DB11098
Description

Potassium bicarbonate is a white, crystalline, slightly alkaline and salty substance. It is produced by the passage of carbon dioxide through an aqueous potassium carbonate solution. It is used in medicine as an antacid.3 It is registered in the FDA under the section of suitable, safe and effective ingredients for OTC antacids.7 This FDA denomination classifies potassium bicarbonate as a GRAS ingredient.8

Type
Small Molecule
Groups
Approved
Structure
Thumb
Weight
Average: 100.1151
Monoisotopic: 99.956275759
Chemical Formula
CHKO3


Pharmacodynamics

Potassium is the principal intracellular cation in most body tissues. The concentration of potassium ions is essential to conduct nerve impulses in specialized tissues like brain, heart and skeletal muscle, as well as to maintain normal renal function, acid-base balance, and cellular metabolic functions.9 The use of compounds containing bicarbonate is showed to produce the release of CO2. This effect has been one of the problems of the use of potassium bicarbonate as it can cause eructation.5

Mechanism of action

The antacid potential of potassium bicarbonate is attained by increasing the gastrointestinal pH by neutralizing hydrochloric acid.6 The increase in pH results in suppression of the action of pepsin which is the enzyme that exacerbates ulceration due to the presence of acid.5


What makes pulmonary surfactant?
Pulmonary surfactant is a mixture of lipids and proteins which is secreted by the epithelial type II cells into the alveolar space. Its main function is to reduce the surface tension at the air/liquid interface in the lung.


How does surfactant increase lung compliance?
Pulmonary surfactant thus greatly reduces surface tension, increasing compliance allowing the lung to inflate much more easily, thereby reducing the work of breathing. It reduces the pressure difference needed to allow the lung to inflate.


What stimulates the production of surfactant?
Surfactant secretion can be stimulated by a number of mechanisms. Type II cells have beta-adrenergic receptors and respond to beta-agonists with increased surfactant secretion [40]. Purines, such as adenosine triphosphate are potent stimulators of surfactant secretion and may be important for its secretion at birth.Feb 4, 2009


Interfacial properties of therapeutic pulmonary surfactants studied by thin liquid films

Dotchi Exerowa, ... Dimo Platikanov, in Colloid and Interface Science in Pharmaceutical Research and Development, 2014

Abstract

The pulmonary surfactants are considered predominantly from the perspective of surfactant insufficiency in preterm newborns developing respiratory distress syndrome (RDS). Currently, lung extracts of animal origin, known as therapeutic pulmonary surfactants, are largely used in RDS treatment. We introduced a new in vitro method for the study of therapeutic pulmonary surfactants based on the model black foam film, including bilayer film. Microscopic foam films from aqueous surfactant solutions are explored by means of interferometric technique which provides for introducing new parameters and measuring new dependences characterising interfacial properties of therapeutic pulmonary surfactants. Film thickness, probability of black film formation and disjoining pressure are measured. The wetting properties of surfactant solutions are studied. Interfacial characteristics such as minimal surfactant concentration to obtain black film and concentration at which a black film is 100% obtained are determined. The following therapeutic pulmonary surfactants are studied: Curosurf, Infasurf, Survanta, Alveofac and Exosurf.

Conversion of α-Helical Proteins into an Alternative β-Amyloid Fibril Conformation

Jason C. Collins, Lesley H. Greene, in Bio-nanoimaging, 2014

Lung Surfactant Protein C

LSP-C (Fig. 43.3C) plays a role in the very rare pulmonary alveolar proteinosis in which accumulation of surfactant protein amyloid-like fibrils impairs respiration [47]. The etiology of this rare disease has been associated with improper clearance of aberrant surfactant proteins by macrophages [47]. LSP-C is one of the most hydrophobic peptides known to exist naturally, and it functions in concert with a complex mixture of proteins and phospholipids in the lungs to reduce surface tension at the alveoli interface [48]. This small protein is believed to be post-translationally cleaved from a larger precursor protein upon insertion into a lipid bilayer [48,49]. Hydrogen/deuterium exchange experiments show that the transition of α to β occurs through a short lived and almost completely unfolded intermediate [48]. Despite destabilizing conditions, this transition is relatively slow due to a significant energy barrier associated with the nature of LSP-C’s rigid α-helical structure [49]. It is interesting to think about how nature has dealt with the polyvaline sequence in LSP-C which is prone to β-sheet formation [48,50]. Even though the structure of LSP-C is very stable it is of importance to note that the precursor form may be more stable when not embedded in the lipid bilayer, and this may indicate an evolutionary adaptation to prevent the aggregation of the active protein until cleavage of the precursor protein occurs [48,49]. Also, palmitoylation of two N-terminal cysteines may also indicate further evolutionary selection for native structure stability because depalmitoylation of LSP-C reduces the stability of the α-helical structure, decreases the energy barrier for unfolding, and increases the fibrillation rate of LSP-C [47–49]. It appears that nature has evolved this highly conserved small peptide in many facets most likely due to its high importance in proper lung function.

Interstitial Lung Disease

Mark P. Steele, ... Paul W. Noble, in Genomic and Personalized Medicine (Second Edition), 2013

Pulmonary Surfactant

Pulmonary surfactant is a complex mixture of phospholipids and proteins that functions to reduce surface tension at the alveolar air interface preventing atelectasis. Deficiency of pulmonary surfactant is the principal cause of respiratory distress syndrome in premature infants (Whitsett and Weaver, 2002). Four surfactant-associated proteins, surfactant proteins A, B, C, and D, have been described, and deficiency of surfactant proteins B and C has been associated with respiratory distress in newborns. Surfactant protein C (SP-C) is a highly hydrophobic protein that enhances the surface tension-lowering properties of pulmonary surfactant. Familial cases of neonatal respiratory distress have been associated with surfactant protein B deficiency, but respiratory distress of neonates is not considered to be a form of DPLD/ILD (Nogee et al., 2000). Genetic variants of SP-A and SP-C have been associated with increased risk of idiopathic pulmonary fibrosis (IPF) (Lawson et al., 2004).

Lung Growth and Maturation

Richard Harding, ... Stuart B. Hooper, in Fetal Medicine (Third Edition), 2020

Pulmonary Surfactant

Pulmonary surfactant is essential for postnatal lung function because it stabilises alveoli, making the lung easier to expand, thereby decreasing the work of breathing and enhancing gas exchange. Pulmonary surfactant is a complex, surface active mixture of phospholipids and proteins (∼90% lipid and 10% protein) that is synthesised within type II epithelial cells.106 After being secreted, surfactant forms a monolayer of tightly packed lipid molecules at the air–liquid interface of the liquid film that lines the alveoli. This monolayer displaces water molecules from the interface, thereby greatly lowering the surface tension. Surfactant deficiency is common in preterm infants because of immaturity and reduced numbers of type II alveolar epithelial cells. The lack of surfactant can lead to RDS (or hyaline membrane disease), which is characterised by laboured breathing and progressive cyanosis because of inadequate gas exchange.107,108 In preterm infants, the effects of surfactant deficiency may be exacerbated by structural immaturity of the lungs. Antenatal glucocorticoid treatment enhances surfactant synthesis and structural maturation of the lungs,109 both of which are essential for normal lung function after birth.

ACUTE RESPIRATORY DISTRESS SYNDROME

G.J. Bellingan, S.J. Finney, in Encyclopedia of Respiratory Medicine, 2006

Surfactant administration

Alveolar surfactant is lost early in ARDS. The administration of exogenous surfactant either via a bronchoscope or nebulizer may reduce surface tension within alveoli and prevent cyclical collapse, improving oxygenation, and ameliorating VILI. Multiple administrations appear necessary due to the neutralization of surfactant by edema fluid. Despite improvements in oxygenation and phase I/II survival benefits, no large studies of surfactant have demonstrated any mortality advantage and thus it is not administered to patients with ARDS. However, there are many outstanding questions regarding the optimal formulation, patient selection, and dosing regimen.

Relation of foam stability to solution and surface properties of gemini cationic surfactants derived from arginine

Authors:

Abstract

The dynamic surface tensions, under constant area and pulsating area are reported for one cationic monomeric surfactant LAM (Nα-lauroyl arginine methyl ester) and three related bicationic gemini surfactants Cn(LA)2, or bis (Args), with a spacer chain of n=3, 6, or 9 methylene groups. The tension equilibrates faster the higher the concentration, even beyond the cmc, indicating a substantial micellar contribution to tension dynamics. Both LAM and the gemini surfactants form more stable foams at 25°C as the concentration increases up to about half the cmc of LAM or half the second cmc of the geminis. The geminis are about twenty times more efficient foam stabilizers than LAM. The foam stability correlates strongly with tension equilibration time. The logarithm of the time t50f, for the initial foam height to drop by 50%, is a linear function of t50γ, which is the time for the tension to drop 50% of its equilibrium change. At comparable concentrations, the gemini surfactant with the shorter spacer chain (n=3 or 6) equilibrate faster and form more stable foams than the one with n=9.


Article

Abstract

Aspiration is the inhalation of solid or liquid materials into the airways. It occurs when solids or liquids are introduced into the supraglottic area rapidly or in large volumes or when airway defences are diminished by structural abnormalities or neurological impairment. Aspiration may cause no complications or may result in a range of complications from paroxysms of coughing to respiratory failure and death [1, 2]. Tracheobronchial aspiration syndromes are usually defined by the aspirated material and, in some instances, by the mechanism or sequelae of aspiration: foreign body aspiration (FBA), aspiration of oropharyngeal or gastric content (aspiration pneumonia and aspiration pneumonitis), aspiration of hydrocarbons or lipids (lipoid pneumonia) and near-drowning. Foreign body aspiration The aspiration of a foreign body is an important clinical event requiring immediate recognition and treatment to minimise complications [1–3]. The majority (y80%) of recognised cases occur in patients agedv15 yrs [2]. However, multiple retrospective case series of paediatric FBA suggest that most events occur in patients aged v3 yrs, with males affected more frequently than females [3–7]. In the USA in 2001, w17,000 children aged ƒ14 yrs were treated in emergency departments for choking, and w100 emergency room visits occurred for every choking-related death [8, 9]. Children agedv1 yr and adults agedw75 yrs are at an increased risk of death following FBA [10]. Across all age groups, suffocation due to FBA is the fifth most common cause of death by unintentional injury in the USA [8, 9].


Health effects of dietary phospholipids


Pulmonary surfactant is composed of approximately 90% lipids and 10% proteins. The main phospholipid in surfactant is dipalmitoylphosphatidylcholine (DPPC), also known as lecithin. It is surface active because of its hydrophilic head and hydrophobic tails (Fig. 46.7).




Improvement of pulmonary surfactant activity by introducing D-amino acids into highly hydrophobic amphiphilic α-peptide Hel 13-5

Abstract

The high costs of artificial pulmonary surfactants, ranging in hundreds per kilogram of body weight, used for treating the respiratory distress syndrome (RDS) premature babies have limited their applications. We have extensively studied soy lecithins and higher alcohols as lipid alternatives to expensive phospholipids such as DPPC and PG. As a substitute for the proteins, we have synthesized the peptide Hel 13-5D3 by introducing D-amino acids into a highly lipid-soluble, basic amphiphilic peptide, Hel 13-5, composed of 18 amino acid residues. Analysis of the surfactant activities of lipid-amphiphilic artificial peptide mixtures using lung-irrigated rat models revealed that a mixture (Murosurf SLPD3) of dehydrogenated soy lecithin, fractionated soy lecithin, palmitic acid (PA), and peptide Hel 13-5D3 (40:40:17.5:2.5, by weight) superior pulmonary surfactant activity than a commercially available pulmonary surfactant (beractant, Surfacten®). Experiments using ovalbumin-sensitized model animals revealed that the lipid-amphiphilic artificial peptide mixtures provided significant control over an increase in the pulmonary resistance induced by premature allergy reaction and reduced the number of acidocytes and neutrophils in lung-irrigated solution. The newly developed low-cost pulmonary surfactant system may be used for treatment of a wide variety of respiratory diseases.

1. Introduction

The pulmonary surfactant is a lipid–protein complex secreted from the alveolar cells and plays an essential role in the pulmonary function by reducing the surface tension [1], [2], [3]. The pulmonary surfactant contains phospholipid and neutral fat such as cholesterol and triglycerol. Phospholipids such as dipalmitoylphosphatidylcholine (DPPC) and phosphatidylglycerol (PG) are considered to be essential to the surfactant activity [2]. In addition, surfactant proteins (SPs) SP-A, SP-B, SP-C and SP-D account for approximately 5% of the total pulmonary surfactants [1]. Among these surfactant proteins, SP-B and SP-C are important and induce surfactant activities for pulmonary respiration [4], [5]. Since SP-B localized to the surface of the cell membrane and SP-C is membrane resident, their activities in the pulmonary surfactant differ from their action modes. Their roles in the pulmonary surfactant activities remain largely unknown. It is thought that the proteins catalyze the migration of lipids from the monolayer membrane to the bilayer membrane occurring at the air–liquid interface of the lung surface at the time of respiration [4], [5]. A recent study found that the interaction between the basic properties of PG and SP is of significance [6].



What does amphiphilic mean in chemistry?
Illustrated Glossary of Organic Chemistry - Amphiphilic. Amphiphilic (amphiphatic): A molecule having both hydrophobic (nonpolar) and hydrophilic (polar) regions. ... That phospholipids form a bilayer for a cell membrane via the hydrophobic effect is due to the phospholipid's amphiphilic character.






Surfactant dysfunction

Surfactant dysfunction is a lung disorder that causes breathing problems. This condition results from abnormalities in the composition or function of surfactant, a mixture of certain fats (called phospholipids) and proteins that lines the lung tissue and makes breathing easy. Without normal surfactant, the tissue surrounding the air sacs in the lungs (the alveoli) sticks together (because of a force called surface tension) after exhalation, causing the alveoli to collapse. As a result, filling the lungs with air on each breath becomes very difficult, and the delivery of oxygen to the body is impaired.

The signs and symptoms of surfactant dysfunction can vary in severity. The most severe form of this condition causes respiratory distress syndrome in newborns. Affected babies have extreme difficulty breathing and are unable to get enough oxygen. The lack of oxygen can damage the baby's brain and other organs. This syndrome leads to respiratory failure, and most babies with this form of the condition do not survive more than a few months.

Less severe forms of surfactant dysfunction cause gradual onset of breathing problems in children or adults. Signs and symptoms of these milder forms are abnormally rapid breathing (tachypnea); low concentrations of oxygen in the blood (hypoxemia); and an inability to grow or gain weight at the expected rate (failure to thrive).

There are several types of surfactant dysfunction, which are identified by the genetic cause of the condition. One type, called SP-B deficiency, causes respiratory distress syndrome in newborns. Other types, known as SP-C dysfunction and ABCA3 deficiency, have signs and symptoms that range from mild to severe.



https://ghr.nlm.nih.gov/condition/surfactant-dysfunction


May 9, 2009 - 6. An Alka-Seltzer is then dropped into the middle of the beaker. When the Alka- Seltzer hits the oil/water barrier it breaks the surface tension and the ink mixes with the water. Once the Alka-Seltzer is in the water it begins to react and release gas triggering the convection process.

Unheated Convection Procedure1 : 1. Fill the beaker with 600ml of Vegetable Oil. 2. Fill the graduated cylinder with 90ml of water. 3. Mix the water with the vegetable oil in the beaker and allow the water to settle to the bottom 4. Fill the graduated cylinder with 10ml of ink and then mix that with the oil/water mixture. 5. The ink droplets then settle down on top of the oil/water barrier but won’t break through due to the surface tension caused by the hydrophobic barrier. 6. An Alka-Seltzer is then dropped into the middle of the beaker. When the AlkaSeltzer hits the oil/water barrier it breaks the surface tension and the ink mixes with the water. Once the Alka-Seltzer is in the water it begins to react and release gas triggering the convection process.


 

https://repository.arizona.edu/bitstream/handle/10150/278414/azu_td_1357290_sip1_m.pdf;jsessionid=2F01F5000E2D3CE0B95EB17EA5BAD33F?sequence=1

Arterial hypoxemia (Pa02<60 mmHg) is the earliest, most dramatic and most consistent clinical response seen, within minutes, after inhalation of acidic gastric fluid. Hypoxemia has a myriad of causes. First, reflex airway closure (bronchospasm) occurs in response to the aspiration of fluid. Second, surfactant activity decreases when surfactant is diluted, altered or destroyed by acid leading to alveolar instability and atelectasis. Third, the outpouring of protein and fluid into damaged lung tissues causes interstitial and alveolar noncardiogenic pulmonary edema 

resulting in further airway closure and atelectasis. Fourth, alveolar hemorrhage and consolidation occurs, followed by hyaline membrane formation (cause of respiratory distress syndrome) (Ganong, 1987). All of these conditions contribute to the large alveolar-arterial oxygen differences as well as the significant increase in venous admixture (Wynne & Moddell, 1977; Schwartz, Wynne, Gibbs, Hood & Kuck, 1980; Stoelting & Miller, 1989). 


Pulmonary vasculature is also effected by acid aspiration. At the onset, pulmonary artery pressure may rise rapidly; however, it declines quickly in association with decreased cardiac output resulting from loss of intravascular volume (Greenfield et al., 1969). As a result, pulmonary artery pressure is usually low or normal. Pulmonary vascular resistance is elevated due to hypoxic vasoconstriction or anatomic obstruction causing pulmonary hypertension (Greenfield et al., 1969; Miller, 1990). Figure 3 illustrates the theoretical basis of the study in relation to the impact of gastric acid aspiration on lung tissue. 


Conceptual Model The conceptual model (Figure 4) illustrate the Construct, Concept and Operational Level investigated within this research. Gastric acidity, the overall construct, has been depicted at < 2.5, the known pH of gastric contents prior to neutralization. Neutralization of gastric acidity, the concept, was accomplished by the administration of two different nonparticulate antacids. Finally, at the operational level, gastric pH levels were measured at 30 and 60 minutes post-ingestion of one or the other antacids.


CHAPTER 1 INTRODUCTION The severe pulmonary complications associated with gastric acid aspiration were first described by Hall (1940) and Mendelson (1946) and included "massive atelectasis with the classical picture of cyanosis, tachycardia, dyspnea, mediastinal shift, and signs of consolidation over the collapsed area." 








Is Surfactant a phospholipid?
Pulmonary surfactant contains several classes of lipids, including phospholipids, triglycerides, cholesterol, and fatty acids. Surfactant also contains the key surfactant proteins A, B, C, and D (SP-A, SP-B, SP-C, and SP-D) (Fig 1). The phospholipid composition of surfactant is highly conserved among mammals [7, 8].Sep 29, 2012



Development of low cost pulmonary surfactants composed of a mixture of lipids or lipids-peptides using higher aliphatic alcohol or soy lecithin

Authors:

Abstract

The artificial pulmonary surfactant composition in the present study is characterized by a lipid mixture system composed of higher aliphatic alcohol, egg yolk phosphatidylcholine (egg PC), soy lecithin and higher aliphatic acid as the major components or a peptide-lipid mixture system composed of a combination of the lipid mixture system to which a peptide is added. Three peptides with amphiphilic surface-staying, membrane spanning, and both properties were designed and synthesized. The evaluation of pulmonary surfactant assay was performed by a hysteresis curve drawn upon the measurement for the surface tension-area curve with the Wilhelmy surface tensometer in vitro and the recovery of lung compliance for the pulmonary surfactant-deficient rat models in vivo. Lipid-mixture systems composed of octadecanol or soy lecithins containing no peptide were favorable hysteresis curves as compared with commercially available Surfacten, but were not prominent. The peptide-lipid mixture systems composed of a combination of the lipid mixture of alkyl alcohol or soy lecithin to which peptides designed were added were desirable hysteresis curves similar to Surfacten and amphiphilic Hel 13-5 peptide-lipids mixture systems were much more effective than the lipid mixture system. Particularly, the recovery of lung compliance treated with hydrogenated soy lecithin-fractionated soy lecithin PC70-palmitic acid-peptide Hel 13-5 (40:40:17.5:2.5, w/w) was comparable to that with Surfacten. Because the artificial pulmonary surfactant compositions of this study can be prepared at lower costs, they are useful for the treatment of respiratory distress syndrome and acute respiratory distress syndrome as well as for inflammatory pulmonary diseases, dyspnea caused by asthma, etc.


Surfacten

Surfacten may be available in the countries listed below.

Ingredient matches for Surfacten

Beractant

Beractant is reported as an ingredient of Surfacten in the following countries:

  • Japan


Surprising Ways to Use Alka-Seltzer Every Day

alka seltzer

Alka-Seltzer can feel like a lifesaver when you’ve over-indulged in food or drink, but did you know they can do a lot more than deal with a hangover or upset stomach?

The simple but effective mix of ingredients in Alka-Seltzer effervescent tablets makes them useful  for everything from cleaning and deodorizing to brightening your whites! Here, I’ll share a few brilliant ideas you might not have heard about before.

Related: 9 Unexpected (But Useful) Things You Can Do With Windex

What is Alka-Seltzer?

If you’re not already familiar with it, Alka-Seltzer is an effervescent antacid and pain reliever.

As well as Alka-Seltzer original tablets, you can also buy Alka-Seltzer Extra Strength, which contains a larger dose of aspirin. Or, if you have cold or flu symptoms, Alka-Seltzer Plus has the same ingredients as the original effervescent tablets, but with an added antihistamine and decongestant.

While Alka-Seltzer is the brand name most people are familiar with, there are other products on the market with very similar ingredients, including Medi-Seltzer and Neutralin.

alka seltzerWhat’s in an Alka-Seltzer Tablet?

Alka-Seltzer is a brand name used to describe a combination of generic medicines. Each tablet contains:

  • Aspirin (325mg)
  • Anhydrous citric acid (1000mg)
  • Sodium bicarbonate (1916mg)

Aspirin or acetylsalicylic acid (ASA) is a nonsteroidal anti-inflammatory drug (NSAID). It provides pain-relief by blocking the production of a substance in your body that causes swelling and inflammation.

Sodium bicarbonate neutralizes the excess acid in your stomach, helping to relieve indigestion and heartburn. Sodium bicarbonate also reacts with the anhydrous citric acid in Alka-Seltzer to dissolve the tablets and make a fizzy drink.


https://www.onegoodthingbyjillee.com/uses-for-alka-seltzer/

What is Alka-Seltzer Mainly Used For?

In the US alone, Bayer produces and sells around 2.5 billion tablets each year. Almost all of those will be taken by people hoping to ease acid indigestion or heartburn, relieve minor body aches, or treat headaches.
Alka-Seltzer is a nonprescription medication, but that doesn’t mean health professionals don’t occasionally prescribe it for certain conditions. The aspirin in an Alka-Seltzer is sometimes recommended at a low dose to help prevent heart attacks and strokes in high-risk individuals.

Of course, if you plan to use it for any medical reason, you should always check the product guidelines and follow the advice of your physician.

Surprisingly Useful Ways to Use Alka Seltzer

Now we know a little more about how it is used medically, we can move on to the less conventional uses!

alka seltzerUnclogging a Drain

If you’ve got a slow draining sink or basin, the sodium bicarbonate and citric acid in Alka-Seltzer can help!

The fizz that’s created when you drop two tablets into water is even more powerful when mixed with another mild acid. In fact, it’s powerful enough to breakdown the greasy build-up that’s often responsible for blocking plumbing completely.

Drop four tablets into your drain, followed by a cup of white vinegar. Wait for about ten minutes, then flush the pipes with a pot of boiling water. Nasty clogs will be washed away, and the reaction will help the drain smell better too!


Treat Urinary Tract Infections (UTIs)

Around six million people suffer from a UTI each year. If you’ve ever had one, you’ll know just how distracting and painful they can be.

https://www.onegoodthingbyjillee.com/uses-for-alka-seltzer/


Although it’s not one of its more common uses, Alka-Seltzer can offer quick relief if you take two chewable Alka Seltzer tablets in a glass of water as soon as you notice any symptoms.

It’s important to remember that Alka-Seltzer comes with a few warnings. For example, you shouldn’t use it if you’re breastfeeding, in the final three months of pregnancy, or have high blood pressure.

https://1md.org/article/probiotics-alkaline-body-1md

How Your Probiotic Therapy Helps Alkalize Your Body

8 minute read


Your digestive system is the one place in your body that requires acid in order to function properly. The gut, therefore, can play an important role in maintaining a pH balance to reduce any Candida overgrowth.

Since your diet can cause too much alkalinity, there is a special diet you can follow to restore digestive acids. The right diet and a high potency, multi strain probiotic supplement can ensure that Candida does not get a chance to take over.


Acid-producing probiotics, such as acidophilus, are able to slow and reverse the overgrowth of Candida. Our digestive systems have naturally evolved to be acidic as a way to prevent this and protect us from pathogens.




















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