HBOT hyperbaric chambers Mild HBO Hyperbaric Chamber ST901 for sport use 1.3ATA HBOT
Macypan Hyperbaric Oxygen Chamber for sale
| MACY-PAN ST901 OXYGEN CHAMBER | |||
| Size | 90cmx225cm (36x89inch) | Net Wight | 14kg |
| Pressure | 1.3ATA (30kPa) | Type | Lying |
| Air Compressor | |||
| Size | 39x24x26cm (16x10x11inch) | Power | 550W |
| Flow | 70L/Minute | Weight | 18Kg |
| Oxygen Concentrator | |||
| Size | 65x40x37cm (25.60x15.75x14.37inch) | Flow | 0-5L/Minute~0-10L/Minute adjustable |
| Oxyen Purity | 93%±3 | Weight | 30Kg |
| Cooling System | |||
| Size |
18x12x27cm (7x5x11inch) |
Powder | 220W |
| Capability | 150L/min | Weight | 5KG |
Shanghai Baobang Medical Equipment Co.,Ltd is located in Shanghai, China. We specialize in manufacturing portable hyperbaric chambers, home oxygen concentrators, etc. Our chambers are certified with ISO13485 and CE certification, and we also hold a PATENT REGISTRATION for our chambers. In the past 7 years, our chambers are sold over 35 countries in which Japan is our main market. We present the strong quality commitment and we have gone through hard work to be able to offer this health equipment at an accessible price for the first time in the world, We are proud to be the top Chinese factory doing this chambers and be able to give an opportunity to people that need HBOT in their life .A lot of professional sport players have started to use this chambers and the health benefits this offers are scientifically backed up. We are happy to be the most reliable provider in the world, we can design the chamber with customer’s logo with no MOQ. We welcome not only family buyers, but also sales companies by providing you with tailored OEM products. With confident and enthusiastic service, we expects our cooperation with products of sound quality and affordable price.
MACY-PAN:
---- Professional Manufacturer of Portable Hyperbaric Chamber in China for 8 years.
-----Most affordable and Competitive Price on global market.
-----Accept Custom Made(OEM & ODM) for your requests.
-----Fast Delivery Time.
-----All the chambers have been carefully tested.
-----Warranty 1 year.
Lyme Disease Hyperbaric Oxygen Chamber
Lyme disease, an illness that can start mild and quickly progress to something far more debilitating, is a very scary and life changing disease to get. Many people do not understand Lyme disease and therefore do not know what symptoms to look for after possibly being infected with the disease.
People with cognitive damage from Lyme disease often experience restored cognitive function; since cognitive disorders are one of the gravest side effects of Lyme disease, this may be the number one benefit of hyperbaric oxygen therapy for Lyme disease patients.
Fortunately, there’s a treatment option for Lyme disease patients that has few to no side effects, a high rate of efficacy, but it can be quite expensive. It is one of the more expensive treatments you can have, ranging from 100-500.00 a session if you go to a clinic. As many as 40-1000 treatment may be needed. The patient may need to do it for the rest of their life. This is why it makes sense to look into purchasing an affordable home hyperbaric chamber. Once you figure out if Hyperbaric oxygen therapy is right for you. Hyperbaric oxygen therapy has been used all over the country for Lyme disease patients with great success.
There are many benefits to using hyperbaric oxygen therapy as a primary therapy for Lyme disease. Many patients report a return in their energy level, which often dips after Lyme disease sets in. Pain relief is another great benefit. People with cognitive damage from Lyme disease often experience restored cognitive function; since cognitive disorders are one of the gravest side effects of Lyme disease, this may be the number one benefit of hyperbaric oxygen therapy for Lyme disease patients[3].
One woman with lymes that I spoke with informed me that she almost gave up on hbot after doing it with her home hyperbaric chamber for 5 months. Then, the magic happened. After lymes ruining her life for almost 10 years, taking every supplement and doing every she read about , she regained her energy, vitality, clarity of mind and was able to live life normally again. When, I talked to her last she had been doing her chamber for a year straight not missing one day.
There is one side effect that Lyme disease patients should anticipate when pursuing hyperbaric oxygen therapy. If you do not know about it, it may seem like a negative side effect. However, it is a positive side effect that indicates that the therapy is working. Symptoms may flare up or seem even worse after the initial HBOT session. This is because the bacteria that cause Lyme disease are dying, and they release endotoxins as they die. However, as all of the bacteria die off, patients will feel an immediate improvement in their health and well-being.
POTENTIAL MECHANISMS OF HBOT
Researches on HBOT in experimental TBI studies have clarified diverse mechanisms leading to neuroprotection. Many of the pathways work parallel, or together, to induce neuroprotection in the brain. These mechanisms include: 1) increasing tissue oxygenation; 2) reducing inflammation; 3) decreasing apoptosis; 4) reducing ICP; 5) promoting neurogenesis and angiogenesis. For the purpose of this review, a brief summary of the recent discoveries in the mechanism of HBOT will be discussed. Table 1 lists most recent exciting discoveries in animal models, and Figure 1 summarizes the potential mechanisms involved in HBOT.
HBOT increases tissue oxygenation
Henry's law states that the amount of gas dissolved in a liquid or tissue is proportional to the partial pressure of that gas in contact with the liquid or tissue. This is the basis for increased tissue oxygen tensions with HBO treatment. In physiological condition, most oxygen carried in the blood is bound to hemoglobin, which is 97% saturated at atmospheric pressure. The other oxygen is carried in solution, and this portion is increased with the pressure due to Henry's Law. When breathing normobaric air, arterial oxygen tension is approximately 100 mmHg, and tissue oxygen tension approximately 55 mmHg. However, 100% oxygen at 3 ATA can increase arterial oxygen tensions to 2,000 mmHg, and tissue oxygen tensions to around 500 mmHg (Ratzenhofer-Komenda et al., 2006). The marked increased oxygen tension gradient from the blood to metabolizing cells is a key mechanism by which hyperoxygenation of arterial blood can improve effective cellular oxygenation even at low rates of tissue blood flow (Thom, 2011). And as the oxygen is in solution, it can reach physically obstructed areas where red blood cells cannot pass. HBO (1.5 ATA for 60 minutes) significantly increases brain tissue oxygen pressure (pO2) in both injured and sham-injured rats (Daugherty et al., 2004; Niklas et al., 2004). Results of several studies suggest that increasing brain tissue oxygenation contributed to reduced mortality and improved outcome of TBI patients (Rockswold et al., 2010, 2013).
HBOT suppresses inflammation
The acute inflammatory response plays an important role in secondary brain damage after TBI, which is characterized by cytokine release, neutrophil activation and microvascular adherence. Reducing inflammation is essential for the treatment of TBI. HBO has been shown to suppress inflammation in many studies (Vlodavsky et al., 2006; Lin et al., 2012; Zhang et al., 2014a; Meng et al., 2016a, b). When healthy humans are exposed to HBO at 2.8 to 3.0 ATA for at least 45 minutes, the ability of circulating neutrophils to adhere to target tissues is temporarily inhibited (Kalns et al., 2002). In a blast-induced traumatic brain injury model in rabbits, HBOT (2 ATA for 60 minutes) administrated at 12 hours after injury reduced the RNA and protein levels of caspase-3, interleukin-8 and tumor necrosis factor-α (Zhang et al., 2014a). In the early stage of TBI in rats, HBOT improved outcomes and reduced inflammation by increasing anti-inflammatory cytokine interleukin-10 (Lin et al., 2012; Chen et al., 2014), attenuating microgliosis and decreasing the level of tumor necrosis factor-α (Lim et al., 2013), and decreasing the expression of matrix metalloproteinase-9 (Vlodavsky et al., 2006). Recently, Meng et al. (2016a) showed HBOT significantly increased the expression of nuclear factor (erythroid-derived 2)-like 2 and heme oxygenase-1, and inhibited the expression of Toll-like receptor 4 and nuclear factor-kappaB in a rat TBI model (Meng et al., 2016b). The inhibitory effect of HBOT on inflammation closely associated with the decreased brain edema, blood-brain barrier leakage, cell apoptosis and improved neurological disorders after TBI.
HBOT decreases apoptosis
Apoptosis occurred in the brain tissues from the first few hours to weeks after TBI (Rink et al., 1995). The growth and progression of TBI lesions depend significantly on the developments in traumatic penumbra area and perilesional region, where neuronal apoptosis occurs. Inhibition of apoptosis becomes a therapeutic strategy to preserve brain tissues and promote functional recovery. In previous studies, HBOT reduced brain infarction and improved neurological deficits by preventing neuron apoptosis in ischemic stroke (Zhou et al., 2000; Yin et al., 2003; Li et al., 2005; Lou et al., 2006; Peng et al., 2009) and hypoxia-ischemia (Calvert et al., 2002, 2003; Liu et al., 2013) animal models. The neuroprotective, anti-apoptotic effects of HBOT in the development of secondary brain damage after TBI have been extensively investigated. Palzur et al. (2004, 2008) proved that HBOT reduced apoptosis in dynamic cortical deformation rats. HBOT suppressed the activation of the mitochondrial mediated apoptotic pathway by inducing the expression of Bcl-2 and preserving mitochondrial integrity (Palzur et al., 2008). The same mechanism was observed that HBOT increased expression of anti-apoptotic proteins (Bcl-2 and Bcl-xl) and decreased apoptosis in rat models of TBI (Vlodavsky et al., 2005; Liu et al., 2006; Xu et al., 2012). These results suggest that the neuroprotective effects of HBO are at least partially mediated by the reduction of apoptosis.
HBOT reduces ICP
Critical elevation of ICP represents the leading cause of morbidity and mortality in patients suffering from severe TBI (Horn et al., 1999). One of the important mechanisms of HBOT for severe brain injury is to lower ICP. Brown et al. (1998) first reported that HBO at 2 ATA for 60 minutes lowered ICP during the first 15 minutes of therapy in head-injured patients, however, rebound elevation were seen during or after therapy (Brown et al., 1988). A definite positive effect of HBOT on ICP was achieved by Rogatsky et al. (2005). HBOT (2.5 ATA for 60 minutes) applied within 24 hours ameliorated the outcome and reduced ICP by decreasing endothelin, improving the blood velocity of middle cerebral artery and decreasing cerebral vascular resistance in severe TBI patients (Ren et al., 2001b). Mechanisms of HBOT reducing ICP can also be related to the subsequent sustained improvement in tissue metabolism of the traumatized brain, as shown by Rockswold et al. (2001). The same conclusion was drawn when applied HBO to rats after severe fluid percussion brain injury. HBOT significantly diminished ICP elevation rate and decreased mortality when HBO was administrated within 2 hours after severe trauma (Rogatsky et al., 2005).
HBOT promotes neurogenesis and angiogenesis
Many studies have reported that multiple HBOT could improve neurological deficits and cognitive impairments at the acute stage (Lin et al., 2012) and at late chronic stages, months to years after TBI (Brown et al., 1988; Contreras et al., 1988; Horn et al., 1999; Ren et al., 2001b; Daugherty et al., 2004; Harch et al., 2007, 2009, 2012; Kernie and Parent, 2010; Brkic et al., 2012; Xu et al., 2012; Boussi-Gross et al., 2013). The therapeutic effects of long-term HBOT may be associated with multifaceted repair, including activation of angiogenesis and triggering of neuroplasticity, and induce proliferation and differentiation of neuronal stem cells. When HBO (2 ATA for 60 minutes twice a day for 3 consecutive days) was given within 3 hours after injury in fluid percussion model of TBI in rats, there was a significant increase in newborn endothelia cells, neurons and glial cells at 4 days after TBI (Lin et al., 2012). Ten exposures of HBO (2.5 ATA for 60 minutes for 10 days) can intensify neuroplastic responses by promoting axonal sprouting and synapse remodeling, which contributes to the recovery of locomotor performances in TBI rats (Brkic et al., 2012); 40-day series of 80 HBOTs (1.5 ATA for 90 minutes each time) caused an increase in contused hippocampus vascular density and an associated improvement in cognitive function (Harch et al., 2007). Activation of several signaling pathways and transcription factors have been suggested to play an important role in HBOT-induced neurogenesis, including Wnt, hypoxia-inducible factors and cAMP response element-binding (Mu et al., 2011).
Well, we are a leading manufacturing company selling hbot chamber for ten years in China and our quality can be competitive to the top world brand.
Our strength as below:
1.Durable, Customizable, Flexible
2.Perfect after-sales service system
3.Complete certificates
4.Many verieties to choose
5.Approved by the customer
6.Safe material
Our chambers enjoy good fame in the world and our brand MACY-PAN will bring the health and beauty to more and more areas.
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Alertness.
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Improves metabolism and aids digestion.
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Reduces fatigue and improves sleeping patterns. |
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