The effect of plasma colloid osmotic pressure on the body

The effect of plasma colloid osmotic pressure on the body

plasma
As people continue to explore the environment inside the body, it is more deeply found that in the huge system of the human body, the basic unit of each life activity is quite complicated, and the osmotic pressure is an important factor to maintain the stability of the internal environment. Recent studies on osmotic pressure, especially plasma colloid osmotic pressure, are summarized below.

1 concept of osmotic pressure and plasma osmotic pressure
1.1 The concept of osmotic pressure Osmotic pressure refers to the attraction of electrolyte and non-electrolyte solute particles in water through a semi-permeable membrane. The size is determined by the total number of solute particles in the solution, and the type of solute in the solution. Independent of particle size [1].
1.2 The concept of plasma osmotic pressure Plasma osmotic pressure includes plasma crystal osmotic pressure and plasma colloid osmotic pressure. The normal human plasma osmotic pressure is about 300 mmol/L (280-320 mmol/L), which is equivalent to 770 kPa. Plasma crystal osmotic pressure is formed by crystalline substances in plasma, such as Na+, Cl-, glucose, urea, etc., Na+ and Cl- account for 80%; plasma crystal osmotic pressure regulates intracellular and extracellular water balance, maintaining normal red blood cells form. Plasma colloid osmotic pressure (COP) is formed by proteins in plasma, regulates blood balance inside and outside the blood vessels, and maintains blood volume. Since albumin has a small molecular weight (about 66 000 Da) and a large number (albumin > globulin > fibrinogen), it is a major factor in determining plasma COP. Albumin is the only protein of all soluble proteins that does not penetrate the capillary wall. 75% to 80% of plasma COP is maintained by albumin [2]. It is about 1.3 mmol/L, which is equivalent to 3.3 kPa or 25 mmHg [1].

2 physiological role of plasma COP
The cell membrane is a semi-permeable membrane in the body, which separates the intracellular fluid from the extracellular fluid, and the K+, Na+ plasma substances are not easily passed freely. Therefore, the circulation of water inside and outside the cell is affected by the osmotic pressure of the crystal produced by the salt. Crystal osmotic pressure plays an important role in maintaining the relative balance of water inside and outside the cell. Clinically, crystalline substance solutions are commonly used to correct water and salt imbalance caused by certain diseases.

The capillary wall is also a semi-permeable membrane in the body, but it is different from the cell membrane. The capillary wall allows free passage of low molecular weight substances such as water, glucose, urea, hydrogen acids and various ions without allowing the passage of high molecular weight proteins. Therefore, the crystal osmotic pressure does not contribute to maintaining the water-salt balance between the blood and the interstitial fluid. If the protein in the plasma is reduced for some reason, the plasma COP will decrease, and the water in the plasma will increase into the interstitial fluid through the capillary wall, resulting in a decrease in blood volume and an increase in tissue fluid, which is one of the causes of edema formation.

Since the number of crystalline solute in plasma is much larger than the number of colloids, the plasma osmotic pressure is mainly composed of crystal osmotic pressure. Because the crystalline material cannot pass through the cell membrane freely, but can freely pass through the porous capillaries, the crystal osmotic pressure only determines the transfer of water on both sides of the cell membrane; the macromolecular colloidal substances such as proteins cannot pass through the capillaries, and the water inside and outside the blood vessels is determined. Balance. Plasma COP is a kind of pinching force against the migration of water from the blood vessels to the outside of the blood vessels. Under normal physiological conditions, COP plays an important role in stabilizing blood volume and preventing tissue edema [1].

COP is also an important component in the effective filtration pressure (EFP) of tissue fluids, and is the main force that causes interstitial fluid to ooze back into the blood vessels from the capillary vein end. Under normal circumstances, plasma and interstitial fluid are in dynamic equilibrium, EFP = (capillary blood pressure + tissue fluid COP) - (plasma COP + tissue fluid hydrostatic pressure), at the capillary artery end, effective hydrostatic pressure (= capillary artery end Blood pressure-interstitial fluid hydrostatic pressure>Efficient COP (=plasma COP-tissue COP), interstitial fluid is formed here; at the capillary venous end, effective COP>effective hydrostatic pressure, interstitial fluid is returned to the blood . Among the four factors that make up EFP, capillary blood pressure and plasma COP are key factors. Through the formation and reflux of tissue fluid, it participates in the exchange of substances between blood and tissue cells, maintaining the balance of fluid distribution inside and outside the blood vessels and the stability of plasma protein concentration.

Factors affecting the plasma COP of a pathological condition 3
Although plasma COP is small, it plays an important regulatory role in the body.
3.1 Clinically, elevated plasma COP is rare, and most of the increase is not the absolute increase of plasma protein, such as hyperthermia in patients with hyperthermia, or other causes such as burns and severe diarrhea caused by severe water loss caused by plasma concentration; dialysis dehydration When blood is concentrated, serum protein levels are elevated, which in turn causes elevated plasma COP, which plays an important role in plasma reperfusion. The increase in plasma COP and the recovery of circulating blood volume are almost simultaneously stopped while hemodialysis is stable [3]. In most patients with renal failure, blood pressure can be kept stable during hemodialysis, because the circulating blood volume is supplemented by the plasma reperfusion process [4]. Plasma reperfusion refers to the gradual decrease of plasma volume in the body when dialysis is dehydrated, and the serum protein concentration increases (we assume that the amount of serum total protein does not change during hemodialysis), formed by various serum proteins (mainly albumin). The plasma COP is also bound to increase, and plasma COP is the most important factor for the transfer of interstitial fluid into the capillaries. Therefore, elevated plasma COP attracts interstitial fluid to the capillary, which is called plasma reperfusion, which helps to maintain Stable circulating blood volume [5]. Schmid et al [6] studied ex vivo mouse hepatocytes found that elevated plasma COP mainly inhibited plasma protein secretion, rather than albumin synthesis. The study also found that human hepatocytes regulate albumin synthesis through COP and express it through alpha-fetoprotein genes [7].
3.2 Clinically, edema caused by the decrease of plasma protein is more common. The following factors can reduce plasma COP, lead to an increase in EFP, increased tissue fluid production and decreased reflux to produce edema [1]. (1) Some patients with digestive diseases have poor protein digestion and absorption. For example, patients with cirrhosis have excessive portal pressure and congestion of the portal system, resulting in decreased digestion and absorption of protein in the gastrointestinal tract, causing a decrease in plasma COP [ 8]. (2) The liver is the main organ for the synthesis and decomposition of proteins in the human body and an important source of protein in plasma. Plasma albumin is regulated by factors such as liver synthesis, decomposition, and release. Liver dysfunction during cirrhosis, due to the reduction of the total number of effective hepatocytes and the disorder of hepatocyte metabolism, albumin synthesis can be reduced by more than half, resulting in hypoproteinemia, which has a certain role in hepatic edema and ascites formation [ 8]. Human plasma proteins play an important role in maintaining COP, binding to ligands, and transport. In liver failure, the binding ability of endogenous substances and drugs is impaired, and patients with end-stage liver disease not only have low plasma COP, but also have poor protein binding ability [9]. The decrease in plasma COP in patients with cirrhosis is accompanied by a decrease in subcutaneous tissue interstitial fluid, with the result that there is no change in the colloidal osmotic gradient across the capillary wall. Subcutaneous tissue interstitial fluid reduction can be explained by liquid dilution and reduced interstitial protein content. The absorption of interstitial proteins by non-visceral tissue can reduce the tendency of edema and hypovolemia [10]. Therefore, infusion of albumin in patients with cirrhosis and liver failure can treat symptoms of hepatic failure such as hypoproteinemia, hyponatremia, hepatorenal syndrome, etc., and simply infusion of colloidal fluid can not correct these abnormalities [11]. (3) The retention of water and sodium in the plasma reduces the plasma protein to be diluted. Some patients with kidney disease, a large amount of protein excreted from the urine can also lead to hypoproteinemia [1]. Liver cirrhosis with renal hemodynamic changes, effective renal blood flow decline, elevated abdominal pressure, compression of the inferior vena cava, resulting in decreased renal perfusion, affecting glomerular blood flow, reducing glomerular filtration rate, Activation of the renin-angiotensin-aldosterone system promotes the production and secretion of aldosterone, increases the secretion of antidiuretic hormone, and ultimately leads to the retention of sodium and water, thereby promoting and aggravating the formation of ascites [12]. (4) When the permeability of the capillary wall is normal, the plasma protein is restricted from entering the interstitial fluid. Increased capillary wall permeability allows intravascular fluid containing a large amount of protein to penetrate into the interstitial fluid, resulting in a decrease in plasma protein and a decrease in plasma COP. For example, in patients with chronic nephritis, the permeability of glomerular filtration membrane is increased, plasma protein is filtered into the original urine, and the reabsorption of protein by the renal tubule is weakened, so that the plasma protein is excessively lost from the urine [8]. Increased capillary permeability under pathological conditions promotes the transfer of body fluids from the blood vessels to the interstitial space, leading to the occurrence of multiple organ edema, especially pulmonary edema. The study found that rodent hepatocytes damaged by hemorrhagic shock and sepsis caused an increase in interstitial protein and an increase in interstitial COP due to the characteristic cell micropore structure destruction and capillary permeability changes [13].

4 clinical application of plasma COP determination
Plasma COP is commonly used clinically to monitor and evaluate the patient's fluid therapy effect. In particular, liquid therapy in patients with hemorrhagic shock or septic shock is also used to guide the preparation of extracorporeal circulation pre-filling for cardiac surgery, to prevent the occurrence of pulmonary edema or tissue edema. Plasma COP can be used as a predictor of pulmonary edema and mortality from critical illness. Sun Youwen et al [14] showed that there is a correlation between plasma COP and central venous pressure. It is speculated that there is a correlation between plasma COP and volume status, but it is not as direct, objective and accurate as CVP. And it is more helpful in assessing the recovery of circulating blood volume. Kudo et al [15] studied 193 patients with heart disease and found that albumin concentration and plasma COP were significantly lower in patients with ventricular low voltage than in patients without ventricular hypotension, suggesting that albumin concentration and plasma COP are correlated with QRS waves.

We know that plasma COP plays an important role in fluid exchange across the capillary wall, especially in glomerular capillaries, which can be estimated clinically by the quadratic equation for total plasma protein or albumin concentration. Geranton et al [16] found that the use of liver-derived non-albumin proteins to maintain COP, especially in patients with nephrotic syndrome, is highly accurate in assessing plasma COP using fibrinogen levels. However, the above method is difficult to be used as a reference for clinical treatment patients because the measurement results cannot be obtained in time. In recent years, the application of membrane colloid osmometer has been promoted, and the results can be obtained within minutes. It can be used to guide the treatment of critically ill patients and detect the therapeutic effect in time. It also makes COP measurement one of the clinical routine monitoring projects. . The so-called membrane colloid osmometer is measured using a membrane that is selective for protein molecules and a sensitive pressure sensor placed in the osmometer sample cell. The sensor output signal is amplified and directly converted into pressure units, displayed on the LCD. Easy to read on.

The influence of plasma COP changes on the body has been paid more and more attention. Especially the effects of liver diseases on plasma COP are various, such as albumin synthesis, decreased secretion, increased portal pressure, and increased lymphatic fluid leakage. Reduce plasma COP. We need to further study the perioperative plasma COP monitoring during perioperative period of liver disease, especially in liver transplantation, in order to provide a credible clinical basis for maintaining perioperative circulation and internal environment stability in critically ill patients.
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