ANALYTICAL & LABORATORY EQUIPMENT
are produced. Te epithelial cells burst and die releasing these millions of virus particles to both bind to more epithelial cells and to be exhaled by the patient to possibly infect other humans. Why is this relevant? ACE is a control mechanism for one of the key activation factors of that little-understood system, the Kinin-Kalikrein, Bradykinin. Bradykinin receptors are also found on lung epithelial cells adjacent to the ACE receptors thus under normal conditions ACE bound to lung receptors markedly inhibits the effect of Bradykinin, with the ACE receptor either bound to a SARS Cov-2 virus or destroyed, patients with Covid-19 have a markedly reduced system for controlling the effects of Bradykinin which has a major impact on the patient and pushes them in to the second condition seen in Covid-19 patients.
The BV1 plasma viscometer
the status quo for the body to continue to function. If the balance of any of these systems is disrupted then there are serious consequences. Haemophilia, an inherited disorder where the coagulation factor, factor 8 (FVIII) is either missing or severely reduced, illustrates this point. FVIII is one of more than 20 identified components involved in the control of blood clotting. Yet untreated haemophiliacs have severe life shortening problems.
What does this mean for Covid-19 patients? Scientists are convinced that SARS Cov-2 infects humans by being pulled into the epithelial cells that line the airways into and including the lungs. Tis happens because the protein coat of the virus happens to have either the same or a similar sequence of amino acids to human Angiotensin Converting Enzyme (ACE). Te epithelial cells have a sequence of amino acids that causes ACE to stick to it, called ACE receptors. When the virus is inhaled if it comes in contact with a free ACE receptor it binds and enters the cell. Once inside the cell the virus takes over the cells’ reproductive capacity and millions of new viral particles
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THE ROLE OF BRADYKININ Bradykinin is a potent activator of several cellular and humoral systems, leading to vasodilation (enlarging of the blood vessels) which causes a drop in blood pressure, porous blood vessels which leads to fluids leaking from the blood into the tissues, including the lungs, activation of the white cells to defend against infection, including monocytes, neutrophils and lymphocytes. How does this create the second
Covid-19 condition? A majority of patients that die from Covid-19 infection do so because of multiple blood clots in various organs including the lung, brain and liver. Tese patients have been shown to have levels of the coagulation factor fibrinogen 10 times normal. Tey have also been found to have increased levels of the clotting marker D-Dimer, which is only raised when a clot has occurred within the body. Bradykinin is produced by the initial activation of the clotting system which can be activated both by the release of a substance called tissue factor, which is found in high concentrations in lung tissue. Release of tissue factor can be expected when lungs are damaged, for example when a virus destroys the cells. Coagulation is also
activated when neutrophils are activated to defend against infections because they contain a procoagulant which is released both upon activation and their destruction. Another interesting fact is that fibrinogen production is stimulated by activated monocytes which are found in the liver tissue where fibrinogen is produced.
Te chemicals that control all these
processes are called cytokines, they are potent activators or inhibitors that are released from various cells when the cell is activated. In Covid-19 patients the balance of cytokine activity is pushed towards activation and the inhibition loops appear either not to be working or overwhelmed by the activation loop. Te activation loop of
Coagulation Kinin-Kallikrein Monocyte activation Increased
Fibrinogen production Cytokine
production appears to have had a major inhibitor removed. Te known inhibitor is Angiotensin Converting Enzyme, which is known to be impaired by Covid-19 infection. Te difference in whether patients develop the second stage of the condition the non-respiratory stage may be down to how many ACE receptors are damaged by the virus before the patient recovers from the first phase.
The BV200 plasma viscometer
Steve Walton is clinical applications manager at Benson Viscometers.
www.bensonviscometers.com
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