Pvc Plasticizer And Biological Inflammation Biology Essay

Published: Last Edited:

This essay has been submitted by a student. This is not an example of the work written by our professional essay writers.

Cardiopulmonary bypass is consistent with larger incorporeal tubes to achieve its rescuer purpose. PVC polyvinylchloride plasticizer occupies about 80 of its mass, emphasis on stores and transfers blood, these materials chosen have the biomaterial which is as similar as to the biological property as possible. The excorporeal parts of the CPB combines with transfusion oxygenator, venous rolling pumps, venous reservoir and catheters. As blood passes through this biomaterial, a physiological innate reaction feed back occurs immediately, inflammatory response involves multiple cells, tissue and proteins, enzymes

Activation by shorter period response and longer response variation depends on the individual's immune system proper abilities. To minimize these unwanted responses, some device strategies up taking by improving the surface coating of the materials in the circuit, use number of pharmacological interventions, tailor to suppress the inflammatory response etc, to control by wash out the surface stimulating polyvinylchloride plasticizers hence reduce the biocompatibility.

In this presentation paper, the following parts will have proper discussion and analysis in the enlarger manner of its original idea.

Part one.

Polyvinyl chloride tubing disturbs biological process hence leads to inflammation.

In 1950s When CPB was first introduced into the medical field, the bypass circuit was attention to the scientists about the polyvinyl chloride properties, it is combined material and flexible to be matched as biomaterials, however, although majority patients tolerated, there are quite a lot patients on site of morbidity and mortality. The effects were noted after post CPB 2~3 days which termed the "Post Perfusion Syndrome", and also know as SIRS which means the systemic inflammation response syndrome.

Biophysical inflammation is a body innate response caused by a foreign attack, injury or destruction of tissue. Once the reaction occurs, there are a series of chain reactions from directly, indirectly and mediators from cellular, tissue organs and vascular circulatory involvement feed back. At the purpose of these movement is to response renew the damaged parts, remote end organ and accurate body immune system.


Due to in the perfusion circuit, the PVC tubing contains a large quantity of plasticizer, and that may be up to 80% of tubing's mass, the di-2-ethyl-hexyl-phthalate (DEHP) was blended in the PVC polymer, to achieve promote its mechanical properties, to be flexible. Although it is a critical material in the perfusion tubing, but the DEHP plasticizer, a liquidity property which tends to migrant to the surface area , and encounters with the blood cells. As DEHP plasticizer occupations large surface area, therefore, there is quite a lot of DEHP on the surface contacting with blood materials, in particular, the inflammation response to postoperative morbidity encountered after cardiac surgery.


When blood comes into contact with the CPB circuit, plasma proteins are absorbed to the surface of the circuit, platelets are absorbed either of the protein layer. The contact results in an activating compliment, coagulation, fibrinolytic systems and the kallikrein-bradykinin cascades.


Reperfusion injury takes on damaged tissue when blood supply return to the tissue after operation, there is a period of tissue ischemia. The absence of oxygen and nutrients from the tissues requires a restoration of circulation which results in inflammatory response and oxygen damage, oxidative damage from normal body function.


When lipopolysaccharide- binding protein with endotoxin, releases of TNF by macrophages, then trigger for the development of the SIRS. During CPB, PVC tubing has a transient endotoxemia. It causes damage to the gastrointestinal mucosa, leading to translocation of endotoxin.


Once these activation factors are involved in to the response then the components of the immune system, coagulation system and endothelium are all activated, the series of the inflammatory response are:


Coagulation and fibrinolysis,

The endothelium,

The cellular immune response

The end results of the inflammation after cessation of CPB to full-blown system inflammatory response syndrome (SIRS), Multiorgan dysfunction (MOD) and failure.


The release of other mediators is important of the interaction between the active complexes and active blood cells. The inflammation effects to the blood-biomaterial interaction.


Cytokines are small secreted proteins and polypeptides that act as paracrine massagers and mediate and regulate immunity, inflammation, and hematopoiseis. They are controlled by the partial immune responded monocytes, tissue macrophages, lymphocytes, endothelial cells, shed blood and significant amount of blood cytokines.


CPB leads up-regulation and release of inducible NO synthase (INOS) from macrophage, the vascular endothelium, smooth muscle. Large amount of Nom products potentially causes CPB vascular dilation, vascular permeable and end organ dysfunction.


The endogenous phospholipids intracellular signaling massager also caused an inflammatory and neurotoxin agent. Platelet aggregation and activation produced by a variety cells and leukocytes and endothelial cells.


Tissue factor as proinflammatory mediate expressed ubiquitously by many cell types. The inflammatory cascade follows up regulation of direction.


The cellular immune response develops when the cardiac disease starts, when muscle, tissue and blood cells are in a dysfunctional condition , the immune response protects the body against any kind of sickle situation, therefore, the immune response starts at very earlier period. Leukocytes are made of granulocytes, monocytes, and lymphocytes. Granulocytes contain neutrophils, eosinophils and basophiles. Monocytes becomes tissue macrophages after migrant into tissue, lymphocytes are consistent of B and T cells and natural killer cells.


When CPB associated with suppression of the adaptive system, a patient immune had insufficiency, and was at risk for infection. This suppression relate to the magnitude and duration of the surgery and the volume of the transfused blood.

Cardiac surgery leads to mergers in both cellular and humeral immune functions response, and lymphocytes develops more and is seen on day 3 versus day 1 for b lymphocytes. Hence, mortality occurs more often within days 2 ~ days 3.


Due to patients who are disease carrier with changed that impair an original biological ability, and possessive to meet , and adaptation the demands on the pathophysiological inside their biological system, therefore, their biological immune system defenses ability is weaker, hence, during CPB, a reaction of the micro-circulation to injury while the operation takes place, there is a movement of fluid and white blood cells into the interstitial space or body cavities, infection definitely occurs, and they on set at different degrees. Degree of inflammation presents at local damage and further more extent intensity of the inflammation depends on the amount of injury, and host response's capacity to response and regulates the wound.


In the early injury stage, oedema fluid and neutrophil polymorphs accumulate in the extracellular space of the damaged tissue area, the presentation of the neutrophil polymorph indicates an acute inflammation on set. On the post operation, the patient's vascular dilation in response to acute inflammation changes the normal function of the capillary bed closed by the precapillary sphincters, and allows the sphincters to open, causing the blood to flow through all the capillaries. Next sign of the inflammation after CPB is that, it changes the normal fluid leaving and entering the vessel equilibrium, presents a net loss of fluid together with plasma protein molecules into the extracellular space, resulting in oedema. Further more, Neurophils migrate into the plasmatic zone, adhere to endothelial cells, and pass between endothelial cells through the basal lamina and migrate into the adventitia. Post operation has local and systemic effects, both of which can be harmful or beneficial. The local inflammation can be destructive to invading micro-organism, somehow, it also services with no obvious function, and positively harmful, ending the battle field.


Part two

Significance Polyvinyl Chloride (PVC) Plasticizer in coding with CPB tubing is trouble marker to the excorporeal. To achieve a better understanding of the blood response to interact with PVC, it is necessary to understanding the significance of the plasticizer.


The pure form of the PVC is a fine grained, white power. Chemical characteristics can have multiple uses. It can be processed as a plastic form and its applications can be rigid, elastic and spongy properties. It can be made as bottles, window frames, pipes, flooring, wallpaper, toys, car seats, guttering, cable insulation, credit cards, and medical products such as blood bags, IV tubing and much more.

The properties of the PVC are resistant to water, acid, bases, some solvents, fats, and oils. It can be heat-sealed between 90-180°C. With market value as food containers, molded articles, and water pipes.


The primary material of the PVC is the substance of diethylhexy phthalate (DEPH), this material has over standing incorporated with the plasticizer, and it has been concerned of being over used .Using X-ray photoelectron spectroscope (XPS) to analyses the surface of PVC tubing, shows that DEPH has leaches into the blood during blood-PVC contact. Moreover, it has been shown that, to removal of DEPH from PVC surface, the blood compatibility would change. The effect of the plasticizer level and plasticizer removal is influenced by the absorption of fibrinogen and albumin. The measurement of the absorbed fibrinogen and albumin are relevant with the rate of the blood- biomaterial interaction.


At 25 degree, result of fibrinogen absorption PVC contains with DEPH and without DEPH are: Fibrinogen absorption was much lower, less than 30% without DEPH in PVC material. The albumin adsorption initially increases sharply before undergoing a slight decrease.


This is clear data compared with two tests, the absence of DEPH, leads to a generally remarked reduction in fibrinogen and albumin adsorption, and it is interesting that the quantity of the fibrinogen and albumin adsorbed by a regenerated cellulose hemodialysis membrane. The result shows that the fibrinogen and albumin adsorption is an index of the reactivity of a surface towards blood components.

DEPH incorporation of PVC into bulk of the polymer is essential for the flexibility of PVC and the extraction of the biomaterial result, However, the level of the DEPH at surface of the PVC blood tubing creates a significant feature of the damages.




The bio-interface between human plasma and a polymer is vital if we are to move biomaterial science into an era where predictable performance is the norm rather than the exception and where there are better processing and selection criteria for a material used in any final clinical product. The recognition of interfacial rather than purely bulk properties as prime determinants of any final outcome for an implant has shifted the focus of research in recent years.1 In particular; there has been a more diverse, expanded effort in understanding physicochemical and cell-mediated processes at artificial surfaces, initially under in vitro conditions, the biocompatibility, the evolution of medical grade polyvinyl chloride (PVC) tubing reflect these insights. Whereas, the mechanical and chemical characteristics of the bulk polymer has been mainly interested in its interfacial interactions. The investigation approaches into the new ameliorate biomaterial. There are three methods being essential: To control plasma protein adsorption by the polymer surface by changing the most commonly used plasticizer, di-(2-ethylhexyl)-phthalate (DEHP).This approach is based on the fact that DEHP migrates from the polymer towards the surface. Device high DEHP concentrations are correlated with enhanced protein adsorption.


Convince the material close to bio-passive and protein-repellent. This is accomplished by the creation of micro-domains, using covalent binding of albumin to the polymer surface or by mimicking the outer surface of a red blood cell by the use of phosphorylcholine groups. Even with the introduction of all these new techniques, a lot of the interfacial reactions between plasma proteins and medical polymers are not completely understood.


With the great diversity of plasma proteins, in order to reduce the complexity and to better understand the adsorption of human plasma proteins at the polymer surfaces, much research has been done and new designs with single protein productions are on the way to be used in the operation procedure essential.