Printer Friendly

Bioregulatory basic peptides liberated from gall-bladder inflammatory wall of people who are sick with acute cholecystitis after laparatomy cholecystectomy.

INTRODUCTION

In the middle of 1980s of relic of the past, there was proved the presence of specific information molecule in the cells of the humans' and animals' bodies, which at first had the name of "tetins" [1-2]. Then in physiology there was articulated the model about new peptide class regulators--about cytomedines [3-4]. This word was formed from the words "cytos"--the cell and from the word "mediator". Nowadays, it is thought that cytomedines sends the specified information [5-6] which is written with the help of sequence code of amino acids [7-8]. The biggest effect cytomedines have on the organ, from which they are liberated [9-11].

At the moment cytomedines are liberated from thymus gland [12], bursa of Fabricius [13], spleen [14] placenta [15], heart [16], stomach [17], liver [18], lungs [19], bronchial mucosa [20], bone [21], the bladder mucosa [22], erythrocytes [23], retinal [24], brain [25] and of other organs and tissues.

We believe it is necessary to emphasize that all these bioregulatory peptides are liberated from organs of healthy animals. Naturally, the question arises, whether in pathological conditions, during diseases the transfer of information from one cell to another cell performs the same bioregulatory peptides or the new one can form, which is specific for each pathology bioregulatory peptides. In the regulation of gallbladder there involved gastrin [26], cholecystokini-pancreozymin [27]. However, there is some information in the available literature that in the wall of an inflamed gallbladder, uterine [28-29] there are specific bioregulatory peptides that can affect hemostasis, on the mass content of sex hormones, on the morphology and function of the uterus, tubes and ovaries.

The aim of our study was the liberation of specific peptides by bioregulatory acetate extraction from the wall of the inflamed gallbladder removal of the patients who are sick with acute cholecystitis abscess and the study of their effects on hemostasis on experimental rabbits.

MATERIALS AND METHODS

Technique for separation of peptide fractions:

Carefully removed gallbladders from 130 women were washed from the mucus, blood clots and fibrin deposits and stored in a freezer at temperature (t) - 20[degrees]C. Frozen gallbladder wall washed in cold water and then homogenized. The resulting mass in porcelain mortar and pestle porcelain with finely comminuted glass was homogenized. The resulting raw material was charged into a glass reactor with a 3% solution of acetic acid at room temperature. The reactor contents were stirred with an electromagnetic stirrer regularly. One part of the resulting homogeneous mass of tissue was mixed with five parts of a solution of acetic acid. Extraction was carried out for 72 hours at room temperature with occasional stirring for 1 hour three times a day. In the end of a process, the extract was filtered through 8-10 layers of gauze and passed through ashless filter. Obtained opalescent color extract. Acetone, cooled in a thin stream under constant stirring, the filtered extract was slowly poured into a 1:5 (one part of extract, and 5 parts acetone). Sediment formation continued for at least 3 days at no higher t+10[degrees] C. The precipitate was filtered in vacuum through 2 layers of ashless filter paper and washed 3 times with pure acetone. The resultant precipitate was subjected to vacuum drying (vacuum degree -2 atm at t+25[degrees] C). As a result, there were received 9 peptide fractions: from acute catarrhal -1 of phlegmonous -3, of gangrenous -1 and chronic calculus - 4.

In this paper we studied the effect on hemostasis of the third peptide fraction obtained from the gallbladder wall of patients who are sick with acute cholecystitis phlegmonous ([OFXG.sub.3]) after laparoscopic cholecystectomy.

The peptide fraction is administered intramuscularly to animals at a dose of 1 mg/kg body weight for 15 days at 1 time a day. Before introducing a peptide fraction is then diluted in sterile physiological solution. As a control, 6 animals in the same volume injected sterile of 0.9 % sodium chloride solution in the same terms . Haemostatic system during animal experiments was surveyed to (background), the 15th and on the 10th, 20th and 30th days after the intramuscular injection of fifteen blood obtained from the heart [30].

Methods of characterizing the vascular-platelet hemostasis: counting the number of platelets in platelet-rich plasma; platelet adhesion; aggregation of platelets.

Methods of characterizing the overall activity of the blood coagulation: a method of recording the whole blood coagulation on coagulation analyzer - H-334; whole blood clotting time in a siliconized and non-siliconized dish; plasma coagulability time; kaolin time plasma; kaolin cephalin clotting time; plasma tolerance to heparin (PTH); anticoagulation test (ACT).

Methods of characterizing the individual phases of blood coagulation: prothrombin time; thrombin time; clotting fibrinogen; antithrombin III (AT III), protamine sulfate test, ethanol test.

Methods of characterizing the fibrinolytic activity of blood: total euglobulin fibrinolysis; Hageman-dependent euglobulin fibrinolysis.

The resulting material was processed by methods of variation statistics for Student's related and unrelated observations and calculated confidence score differences (P).

RESULTS AND DISCUSSION

Intramuscular OFXG3 within 15 days in the blood taken from the heart of rabbits (table 1) decreased from 367,8 [+ or -] 10,4x[10.sup.9]/l to 166,0 [+ or -] 8,05x[10.sup.9]/l (P<0.001), platelet count. Also, among these experimental animals with 33,8 [+ or -] 1,7% to 41,0 [+ or -] 2,5% (P<0.01) increased adhesion and aggregation was suppressed, as evidenced by a lengthening of 22,0 [+ or -] 0,7s to 31,0 [+ or -] 3,3s (P<0.05) time aggregation of blood platelets. According to whole blood clotting time Lee-White, electrocoagulograph, ACT in blood taken from the heart of rabbits on the 15th day of administration fraction reverse-phase high performance liquid chromatography identified multidirectional hyper-hypocoagulational changes in hemostasis. Whole blood clotting time in the non-siliconized with 5,1 [+ or -] 0,53 min. to 1,4 [+ or -] 0,08min. (P<0.001) and in siliconized tubes with 7,1 [+ or -] 0,7min. to 1,5 [+ or -] 0,08 min. (P<0.001) shortened. Hypercoagulation on electrocoagulogram manifested with shortening to 483,8 [+ or -] 21,7s to 153,3 [+ or -] 8,8s (P<0.001) and with the beginning of the period 720,1 [+ or -] 21,9s to 433,0 [+ or -] 17,3s to (P<0.001) period closure clotting. However, the duration of the period, on the contrary, to 253,0 [+ or -] 2,8s up to 296,6 [+ or -] 3,5s (P<0.01) lengthened. Increase from 2,6 [+ or -] 0,5uel.u to 1,6 [+ or -] 0,08uel.u (P<0.001), the electrical resistance of blood indicated that the 15day introduction reverse-phase high performance liquid chromatography fraction increases in blood taken from the heart, toughness. Recalcification time by more than a factor of 2 120.0 [+ or -] 2.3s to 60,3 [+ or -] 3,8s (P<0.001) shortened, which also talked about hyper coagulation orientation in hemostasis. Upon activation of Hageman factor kaolin fibrin clot formation time with a 89,3 [+ or -] 1,0s to 39,0 [+ or -] 0,8s (P<0.001). Also, during the experimental conditions there were not detected violations of platelet coagulation activity. If we consider that the animals had severe thrombocytopenia with the activation of adhesion and 4 of the 10 animals were detected positive ethanol and protamine sulfate sample, we can say with confidence that the OFXG3 layer (fraction) in the heart's blood of rabbits during the 15-day of observation causes development of thrombus (TGS) syndrome. Moreover, in his hypercoagulable phase, as evidenced by the kaolin cephalin clotting time (P<0.05) consumed most full functionally active platelets. This mosaic changes hemostasis must be accompanied hyperfibrinogenemia. However, the changes in its level on the 15th day of administration [OFXG.sub.3] layer (fractions) were not significant (P>0.2). This gives us the argument that peptide layer (fractions) obtained from patients who are sick with acute phlegmonous DGP OX after LCE, in its molecular weight close to fibrinogen and fibrinogen camouflage decreases resulting its move to microthread fibrin. This reasoning is confirmed with non-reliable 45,3 [+ or -] 3,5s to 40,3 [+ or -] 2,1s (P>0.2) by decreasing the content of AT III. Also, note that the data on the ACT 6 min (P<0.001) for 8 min (P<0.05) and at 10 min (P<0.01) showed a hypercoagulable state. Anticoagulant system in the blood is taken from the heart of rabbits on the 15-day of administration layer (fraction) [OFXG.sub.3] was depressed. This truncation was shown to 48,0 [+ or -] 1,1s to 24,0 [+ or -] 1,6s (P<0.001) and thrombin time with a tendency to 9,3 [+ or -] 0,3s to 10,0 [+ or -] 1,6s up with increasing content free heparin. Total euglobulin and Hageman -dependent fibrinolysis in these experimental animals was depressed.

10 days after the 15-day intramuscular experienced rabbit layer (fraction) [OFXG.sub.3] (table 2) platelet count dramatically, with 367,8 [+ or -] 10,4x[10.sup.9]/l to 151,6 [+ or -] 3,5x[10.sup.9]/l (P<0.001) fell, but increased to 33,8[+ or -]1,7% to 35,0 [+ or -] 1,4% (P<0.01) and their adhesion with a 22,0 [+ or -] 0,7s to 40,0 [+ or -] 0,7s (P<0.001) lengthens aggregation. In themselves these facts, in our opinion, indicate that thrombocytopenia due to consumption during intravascular coagulation functionally most full of blood platelets. These hemostasiogramm on the 25th day of the experiment indicate divergent shifts in hemostasis. If whole blood clotting time Lee-White with 5,1 [+ or -] 0,5min. to 2,8[+ or -]0,1min. (P<0.001) shortened non-siliconized and 7,1 [+ or -] 0,7min. to 3,1 [+ or -] 0,03min. (P<0.001) in siliconized tubes, the whole blood clotting when recording on electrocoagulograph showed no difference in electrocoagulogram test and control animals (periods beginning P>0.2, the length of P>0.2, closure P>0.2). Plasma recalcification time on the 10th day after the 15-day intramuscular peptide [OFXG.sub.3] from 120,0 [+ or -] 2,3s up to 98,5 [+ or -] 1,07s (P<0.001) shortened, as well as with 89,3 [+ or -] 1,0s to 54,5 [+ or -] 1,1s (P<0.001), plasma kaolin time. That is the fact that this peptide [OFXG.sub.3] term surveys do not inhibit the activity of Hageman factor. However, the coagulation effect of platelets was dramatically reduced, as kaolin cephalin clotting time lengthened from 39,3 [+ or -] 1,2s to 51,8 [+ or -] 0,3s (P<0.001). Shortening of clotting time with a 20,0 [+ or -] 1,2s to 9,3 [+ or -] 0,3s (P<0.001) for 6 min and a 11,0 [+ or -] 1,0s to 8,0[+ or -]0,3c (P<0.05) for 8 min testified hypercoagulable. In general, assessing data of hemostasiogramm, we tend to believe that this period of rabbits in the experimental survey was hyper - TGS hyper-hypocoagulational phase syndrome. And its formation took place amid a sharp oppression of anticoagulant activity, as the level of free heparin sharply with 9,3[+ or -]0,3s to 5,3 [+ or -] 0,3s (P<0.05) fell, while shortening with multidirectional 48,0 [+ or -] 1,1s to 29,8 [+ or -] 0,3s (P<0.001) and the lengthening of thrombin with a 25,3 [+ or -] 1,2s to 35,5 [+ or -] 0,1s (P<0.001), prothrombin time and increase from 14,6 [+ or -] 0,7min. to 1,05 [+ or -] 0,01min (P<0.001) PTH. Note that these changes proceeded in background of hemostasis significant (P<0.01) hyperfibrinogenemia.

On the 35th day of the experiment on rabbits (table 3), which was introduced with a layer (fraction) [OFXG.sub.3] with 367,8 [+ or -] 10,4x[10.sup.9]/l to 159,1 [+ or -] 2,8x[10.sup.9]/l (P<0.001), platelet quantity fell, oppressed with 33,8 [+ or -] 1,7% to 40,3 [+ or -] 0,7% (P<0.001) increased with the aggregation and 22,0 [+ or -] 0,7s to 35,3 [+ or -] 0,7s (P<0.001), the adhesion. Changes in blood clotting time Lee-White in non-siliconized (P<0.001) and siliconized (P<0.001) tubes showed hypercoagulable which was also registered during the recording of clotting on electrocoagulograph. According to the data of electrocoagulogram periods beginning from 483,8 [+ or -] 21,7s to 131,3 [+ or -] 7,1s (P<0.001), with a duration of 253,0 [+ or -] 2,8s to 97,8 [+ or -] 0,8s (P<0.001), graduating with a 720,1 [+ or -] 21,9s to 212,5 [+ or -] 12,0s (P<0.001) shortened. Up to this period the data shortened from 120,0 [+ or -] 2,3s to 67,5 [+ or -] 1,1s (P<0.001), plasma recalcification time, with a 89,3 [+ or -] 1,0s to 23,3 [+ or -] 0,7s (P<0.001) and kaolin with a 39,3 [+ or -] 1,2s to 24,1[+ or -]0,7s (P<0.001) kaolin cephalin clotting time. The processes of prothrombinase formation on the 20th day after the 15-day intramuscular peptide [OFXG.sub.3] were accelerated. Time formation of plasmoid for 6 min with a 20,0 [+ or -] 1,2s to 9,0[+ or -]0,35s (P<0.001) for 8 min with a 11,0 [+ or -] 1,0s to 8,0 [+ or -] 0,35s (P<0.001) and 10 min. with a 7,1 [+ or -] 0,53s to 6,0 [+ or -] 0,35s (P<0.05) has been shortened. At the same time anticoagulant hemostasis was clearly depressed during this term survey since PTH with 14,6 [+ or -] 0,7min to 2,0 [+ or -] 0,01min. (P<0.001) increased, falling from 9,3 [+ or -] 0,3s to 2,8 [+ or -] 0,3s (P<0.001) levels of free heparin, with a 48,0 [+ or -] 1,1s to 27,0 [+ or -] 0,3s (P<0.001) and thrombin time is shortened with a 25,3 [+ or -] 1,2s to 28,3 [+ or -] 0,7s (P<0.05) plasma prothrombin time lengthened. These shifts in hypercoagulable hemostasis are not detected on the background of significant changes of the fibrinogen (P>0.2) and activation 420,0 [+ or -] 0,0min. to 181,6 [+ or -] 3,5min. (P<0.001) and total euglobulin 320,0 [+ or -] 0,0min. to 178,8 [+ or -] 3,5min. (P<0.001) Hageman-dependent fibrinolysis.

Conclusion:

Thus, removal of the inflamed gallbladder phlegmonous of patients who are sick with acute cholecystitis phlegmonous after laparoscopic cholecystectomy by acetic acid extraction there allocated 3 peptide layers (fraction). The third layers (faction) of acute cholecystitis abscess close to the molecular weight of fibrinogen in the blood of patients who are sick with acute cholecystitis phlegmonous and experimental rabbits.

Accumulation and circulation of the third fraction in the blood of experimental rabbits modulates hyperfibrinogenemia, being in patients with acute cholecystitis reliable predictor of laboratory assessment of inflammatory destruction of the gallbladder wall.

Summary:

Thus, the 15-day intramuscular abscess of acute cholecystitis peptide revealed that the level of natural anticoagulant antithrombin III, fibrinogen and fibrinolytic activity of the blood are diagnostic and prognostic indicators to assess the degree of inflammatory destruction of the gallbladder wall.

ARTICLE INFO

Article history:

Received 15 April 2014

Received in revised form 22 May 2014

Accepted 25 May 2014

Available online 15 June 2014

REFERENCES

[1] Gomazkov, O.A., 2000. Current trends in the study Physiologically active peptides. Success of modern biology, 116(1): 60-68.

[2] Adelson, I.W., S.S. Rotham, 1995. Chymodenin, a duodenal peptide: specific stimulation of chromotrypsin secretion. American J. of Physiology, 229: 1680-1686.

[3] Kozhemjakin, A.L., V.G. Morozov, V.H. Havinson, 2002. Participation cyclase system in the molecular mechanisms regulating the differentiation immune competent cells. Biochemistry, 49(4): 658-666.

[4] Johnson, I.R.., M.I. Grossman, 1994. Intestinal hormones as inhibitors of gastric secretion. Gastroentyerology, 60: 120-124.

[5] Filev, L.V., N.S. Petrov, V.H. Havinson, 2000. The role of polypeptide factors of the hypothalamus and pineal gland in the regulation of the functional activity of stem progenitor cells granulopoiesis. Biological and medical experiment, 10: 481-482.

[6] Adrian, T.E., 1990. Pancreatic polypeptide. Journal of clinical pathology, 33(8): 43-50.

[7] Tsepelev, V.L., 2002. Cytomedines of macrophages as regulators of metabolic activity of the RCC. Experimental and Clinical Immunology in the east. Krasnoyarsk, pp: 113-118.

[8] Hibbs, J.B., L. Uavrin, R.R. Tainiop, 2001. L-arginine in required for expression of the activated macrophage effector mechanism causing selective metabolic inhibition in target cells. Journal Immunol. 138: 852-854.

[9] Yakovlev, G.M., V.G. Morozov, V.H. Havinson, 1986. Cytomedines. The function in the body. Use in clinical practice: Sat scientific tr. Tomsk, pp: 9-11.

[10] Kuznik, B.I., V.G. Morozov, V.H. Havinson, 1998. Cytomedines (25 years of experience in experimental and clinical studies). St. Petersburg, Science, pp: 310.

[11] Simbirtsev, A.S., 2006. Clinical use of drugs cytokines. Immunology, 4: 247-251.

[12] Pierpaoli, W., H.O. Beserdoursk, 2000. Role of the thymus in programm ng of neuroendocrine to function. Clin. exp. Immunol., 20: 232-238.

[13] Tsepelev, V.L., 2003. Study of the immunostimulatory activity of peptides isolated from the bursa of Fabricius. Immunology, 24(2): 89-92.

[14] Vedernikova, L.A., A.B. Tcipin, M.V. Velikaya, S.K. Solovyev, 1992. In vitro donor kseno spleen connection in the treatment of systemic lupus erythematosus. Doctor, 3: 24-27.

[15] Athannassiades, A., P.K. Lala, 1998. Role of placenta growth factor (PLGF) in human extravillious trophoblast proliferation, migration and invasiveness. Placenta, 19(7): 465-473.

[16] Tamura, N., Y. Ogawa, A. Yasoda 1996. Two cardiac natriuretic peptide genes (atrial natriuretic peptide and brain natriuretic peptide) are organized in tandem in the mouse and human genomes. Journal Mol Cell Cardiol., 28: 1811-1885.

[17] Bryuant, M.G., S.R. Bloom, 1988. Distribution of the gut hormones in the primate intestinal tract. Gut., 20: 653-659.

[18] Isenberg, 1.1., R. Cano, 1997. Effect of graded amonnts of acid instilled into the duodenum on pancreatic bicarbonate secretion and plasma secretin in duodenal ulcer patients and normal subjects. Gastrienterology, 72: 6-8.

[19] Lichistein, D., D. Rodburd, 2000. A second look at the second mesenger hypothesis. Life sci., 40(21): 2041-2051.

[20] Ivanov, V.T., A.A. Karelin, O.N. Yatskin, 2005. Generation of peptides by human erythrocytes: facts and artifacts. Biopolymers, 80: 332-346.

[21] Vacanti, C.A., 1992. Cell growth on collagen: a review of tissue engineering using scaffolds containing extracellular matrix. Journal Long Term. Eff. Med. Implants, 2(1): 67-80.

[22] Combs, A.J., A.D. Glasberg, D. Gerdes, M. Horowitz, 1998. Biofeedback therapy for children with disfunctional voiding. Journal Urol., 52(2): 312-315.

[23] Sarajevo, N.O., 2006. Use of recombinant erythropoietin in hematological practice. Siberian Journal of Medicine, 64(6): 5-10.

[24] Havinson, V.H., S.V., 1999. Trofimov Application of peptide bioregulators in ophthalmology. Westnik ophthalmology, 5: 42-44.

[25] Schultzenberg, M., C.F. Dreyfus, 1998. VIP-, enkefalin-, substranceP-, and somatostatin-like immunoreactivity in neuron intrinsic to the intestine. Brain Research, 155: 239-248.

[26] Edrinkis, I.S., 1986. The chemical mechanism of gastrin release. Journal of physiology, 34: 133-144.

[27] Iospes, I.E., W. Mutt, K. Toczko, 1998. Further purification of cholecystokinin and pancreozymyn. Acta chemica Scandinavica, 18: 4408-4412.

[28] Kerimaly Kyzy Mairamkan, 2010. The role of peptides myoma tissue of women with uterine fibroids, the formation of gynecological pathology in the experiment. Diss. by SOIS. MD.

[29] Sumannov, E.E., 2012. Effect of peptides myoma tissue of women with uterine cancer on morphology and function of the fallopian tubes and ovaries in the experiment. Abstract. diss. by SOIS. MD.

[30] Baluda, V.P., Z.S. Barkagan, E.D. Goldberg, 1980. Laboratory Methods of the hemostatic system, pp: 310.

Gulbubu Toktosunovna Kurmanbekova, Salkyn Tursunalievna Beishenalieva, Igor Ananievich Rachkov, Kadyr Beckbalaevich Chekirov, Nurzhamal Taichievna Omurzakova

Kyrgyzstan-Turkey Manas University, Mira Avenue, 56, 720042, Bishkek, Kyrgyz Republic

Corresponding Author: Gulbubu Toktosunovna Kurmanbekova, Kyrgyzstan-Turkey Manas University, Mira Avenue, 56, 720042, Bishkek, Kyrgyz Republic
Table 1: Hemostasis of blood taken from the heart of rabbits after
a 15-day intramuscular injection of a peptide derived from the
gallbladder wall of patients OFH after LCE (fraction -[OFXG.sub.3]).

                                              Healthy animals
Indications                                      (control)

Platelet quantity (x[10.sup.9]/l)           367,8 [+ or -] 10,4
Platelet adhesion (%)                        33,8 [+ or -] 1,7
Platelet aggregation (s)                     22,0 [+ or -] 0,7
Clotting time Lee-White (min) in              5,1 [+ or -] 0,53
  non-siliconized tube
in siliconized tube                           7,1 [+ or -] 0,7
Starting clotting (s)                       483,8 [+ or -] 21,7
Duration of blood clotting (s)              253,0 [+ or -] 2,8
Closing clotting (s)                        720,1 [+ or -] 21,9
Blood viscosity (unit of activity)            2,6 [+ or -] 0,5
The density of blood (units of activity)     0,02 [+ or -] 0,5
Plasma recalcification time (s)             120,0 [+ or -] 2,3
Plasma kaolin time (s)                       89,3 [+ or -] 1,0
Kaolin cephalin time (s)                     39,3 [+ or -] 1,2
ACT (s) for 6 min.                           20,0 [+ or -] 1,2
for 8 min.                                   11,0 [+ or -] 1,0
for 10 min.                                   7,1 [+ or -] 0,5
PTH (min.)                                   14,6 [+ or -] 1,1
Prothrombin time (s)                         25,3 [+ or -] 1,2
Thrombin time (s)                            48,0 [+ or -] 1,1
Free heparin (s)                              9,3 [+ or -] 0,3
Antithrombin III (s)                         45,3 [+ or -] 3,5
Fibrinogen (g/liter)                          1,9 [+ or -] 0,2
Total euglobulin fibrinolysis (min)          20,0 [+ or -] 0,0
Hageman-dependent fibrinolysis (min)        320,0 [+ or -] 0,0
Ethanol sample                                     10 (-)
Protamine sulfate sample                           10(-)

                                             After infiltration
                                             of layer (fraction)
Indications                                     [OFXG.sub.3]

Platelet quantity (x[10.sup.9]/l)           166,0 [+ or -] 8,0 *
Platelet adhesion (%)                        41,0 [+ or -] 2,5 *
Platelet aggregation (s)                     31,0 [+ or -] 3,3 *
Clotting time Lee-White (min) in              1,4 [+ or -] 0,08 *
  non-siliconized tube
in siliconized tube                           1,5 [+ or -] 0,08 *
Starting clotting (s)                       153,3 [+ or -] 8,8 *
Duration of blood clotting (s)              296,6 [+ or -] 3,5 *
Closing clotting (s)                        433,0 [+ or -] 17,3 *
Blood viscosity (unit of activity)            1,6 [+ or -] 0,08 *
The density of blood (units of activity)     0,02 [+ or -] 0,0
Plasma recalcification time (s)              60,3 [+ or -] 3,8 *
Plasma kaolin time (s)                       39,0 [+ or -] 0,8 *
Kaolin cephalin time (s)                     25,0 [+ or -] 0,8 *
ACT (s) for 6 min.                            8,0 [+ or -] 0,3 *
for 8 min.                                    7,0 [+ or -] 0,3 *
for 10 min.                                   6,0 [+ or -] 0,3 *
PTH (min.)                                    4,6 [+ or -] 0,08 *
Prothrombin time (s)                         25,2 [+ or -] 1,6
Thrombin time (s)                            24,0 [+ or -] 1,6 *
Free heparin (s)                             10,0 [+ or -] 1,6
Antithrombin III (s)                          0,3 [+ or -] 2,1
Fibrinogen (g/liter)                          2,0 [+ or -] 0,1
Total euglobulin fibrinolysis (min)         420,0 [+ or -] 2,1
Hageman-dependent fibrinolysis (min)        319,6 [+ or -] 3,8
Ethanol sample                                   4(+); 6 (-)
Protamine sulfate sample                         4(+); 6 (-)

Note. * P < 0.05 when compared to healthy animals.

Table 2: Hemostasis of blood taken from the heart of rabbits on
the 10th day after the 15-day intramuscular injection of a peptide
derived from the patients' gallbladder wall after OFH LCE
(fraction - [OFXG.sub.3]).

                                        Healthy animals
Indications                                (control)

Platelet quantity (x[10.sup.9]/l)     367,8 [+ or -] 10,4
Platelet adhesion (%)                  33,8 [+ or -] 1,7
Platelet aggregation (s)               22,0 [+ or -] 0,7
Clotting time Lee-White (min)           5,1 [+ or -] 0,5
  in non-siliconized tube
in siliconized tube                     7,1 [+ or -] 0,7
Starting clotting (s)                 483,8 [+ or -] 21,7
Duration of blood clotting (s)        253,0 [+ or -] 2,8
Closing clotting (s)                  720,1 [+ or -] 21,9
Blood viscosity (unit of activity)      2,6 [+ or -] 0,5
The density of blood                   0,02 [+ or -] 0,5
  (units of activity)
Plasma recalcification time (s)       120,0 [+ or -] 2,3
Plasma kaolin time (s)                 89,3 [+ or -] 1,0
Kaolin cephalin time (s)               39,3 [+ or -] 1,2
ACT (s) for 6 min.                     20,0 [+ or -] 1,2
for 8 min.                             11,0 [+ or -] 1,0
for 10 min.                             7,1 [+ or -] 0,5
PTH (min)                              14,6 [+ or -] 1,1
Prothrombin time (s)                   25,3 [+ or -] 1,2
Thrombin time (s)                      48,0 [+ or -] 1,1
Free heparin (s)                        9,3 [+ or -] 0,3
Fibrinogen (g/liter)                    1,9 [+ or -] 0,2
Ethanol sample                              10 (-)
Protamine sulfate sample                    10 (-)

                                       After infiltration
                                      of layer (fraction)
Indications                               [OFXG.sub.3]

Platelet quantity (x[10.sup.9]/l)     151,6 [+ or -] 3,5 *
Platelet adhesion (%)                  35,0 [+ or -] 1,4 *
Platelet aggregation (s)               40,0 [+ or -] 0,7 *
Clotting time Lee-White (min)           2,8 [+ or -] 0,1 *
  in non-siliconized tube
in siliconized tube                     3,1 [+ or -] 0,03 *
Starting clotting (s)                 483,8 [+ or -] 21,7
Duration of blood clotting (s)        253,0 [+ or -] 2,8
Closing clotting (s)                  720,1 [+ or -] 21,9
Blood viscosity (unit of activity)      2,6 [+ or -] 0,5
The density of blood                   0,02 [+ or -] 0,0
  (units of activity)
Plasma recalcification time (s)        98,5 [+ or -] 1,1 *
Plasma kaolin time (s)                 54,5 [+ or -] 1,1 *
Kaolin cephalin time (s)               51,8 [+ or -] 0,3 *
ACT (s) for 6 min.                      9,0 [+ or -] 0,3 *
for 8 min.                              7,0 [+ or -] 0,3
for 10 min.                             6,0 [+ or -] 0,3 *
PTH (min)                              1,05 [+ or -] 0,01 *
Prothrombin time (s)                   35,5 [+ or -] 0,3 *
Thrombin time (s)                      29,8 [+ or -] 1,6 *
Free heparin (s)                        5,3 [+ or -] 0,3 *
Fibrinogen (g/liter)                   1,15 [+ or -] 0,01 *
Ethanol sample                               10 (-)
Protamine sulfate sample                     10 (-)

Note. * P < 0.05 when compared to healthy animals.

Table 3: Hemostasis of blood taken from the heart of rabbits
on the 20th day after the 15-day intramuscular injection of a
peptide derived from the gallbladder wall of patients after
OFH LCE (fraction - [OFXG.sub.3])

                                               Healthy animals
Indications                                       (control)

Platelet quantity (x[10.sup.9]/l)            367,8 [+ or -] 10,4
Platelet adhesion (%)                         33,8 [+ or -] 1,7
Platelet aggregation (s)                      22,0 [+ or -] 0,7
Clotting time Lee-White (min)                  5,1 [+ or -] 0,5
  in non-siliconized tube
in siliconized tube                            7,1 [+ or -] 0,7
Starting clotting (s)                        483,8 [+ or -] 21,7
Duration of blood clotting (s)               253,0 [+ or -] 2,8
Closure blood clotting (s)                   720,1 [+ or -] 21,9
Blood viscosity (unit of activity)             2,6 [+ or -] 0,5
The density of blood (units of activity)      0,02 [+ or -] 0,0
Plasma recalcification time (s)              120,0 [+ or -] 2,3
Plasma kaolin time (s)                        89,3 [+ or -] 1,0
Kaolin cephalin time (s)                      39,3 [+ or -] 1,2
ACT (s) for 6 min.                            20,0 [+ or -] 1,2
for 8 min.                                    11,0 [+ or -] 1,0
for 10 min.                                    7,1 [+ or -] 0,5
PTH (min.)                                    14,6 [+ or -] 1,1
Prothrombin time (s)                          25,3 [+ or -] 1,2
Thrombin time (s)                             48,0 [+ or -] 1,1
Free heparin (s)                               9,3 [+ or -] 0,3
Fibrinogen (g/liter)                           1,9 [+ or -] 0,2
Total euglobulin fibrinolysis (min)        > 420,0 [+ or -] 0,0
Hageman-dependent fibrinolysis (min)         320,0 [+ or -] 0,0
Ethanol sample                                      10 (-)
Protamine sulfate sample                            10 (-)

                                             After infiltration
                                             of layer (fraction)
Indications                                     [OFXG.sub.3]

Platelet quantity (x[10.sup.9]/l)           159,1 [+ or -] 2,8 *
Platelet adhesion (%)                        40,3 [+ or -] 0,7 *
Platelet aggregation (s)                     35,3 [+ or -] 0,7 *
Clotting time Lee-White (min)                 2,0 [+ or -] 0,01 *
  in non-siliconized tube
in siliconized tube                           3,1 [+ or -] 0,03 *
Starting clotting (s)                       131,3 [+ or -] 7,1 *
Duration of blood clotting (s)               97,8 [+ or -] 0,8 *
Closure blood clotting (s)                  212,5 [+ or -] 12,0 *
Blood viscosity (unit of activity)            2,6 [+ or -] 0,0
The density of blood (units of activity)     0,02 [+ or -] 0,0
Plasma recalcification time (s)              67,5 [+ or -] 1,1 *
Plasma kaolin time (s)                       23,3 [+ or -] 0,7 *
Kaolin cephalin time (s)                     24,1 [+ or -] 0,7 *
ACT (s) for 6 min.                            9,0 [+ or -] 0,3 *
for 8 min.                                    8,0 [+ or -] 0,3 *
for 10 min.                                   6,0 [+ or -] 0,3 *
PTH (min.)                                    2,0 [+ or -] 0,01 *
Prothrombin time (s)                         28,3 [+ or -] 0,7 *
Thrombin time (s)                            27,0 [+ or -] 0,3 *
Free heparin (s)                              2,8 [+ or -] 0,3 *
Fibrinogen (g/liter)                          1,6 [+ or -] 0,03
Total euglobulin fibrinolysis (min)         181,6 [+ or -] 3,5 *
Hageman-dependent fibrinolysis (min)        178,8 [+ or -] 2,5 *
Ethanol sample                                     10 (-)
Protamine sulfate sample                           10 (-)

Note. * P < 0.05 when compared to healthy animals.
COPYRIGHT 2014 American-Eurasian Network for Scientific Information
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2014 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Kurmanbekova, Gulbubu Toktosunovna; Beishenalieva, Salkyn Tursunalievna; Rachkov, Igor Ananievich; C
Publication:Advances in Environmental Biology
Article Type:Report
Date:Jun 1, 2014
Words:4753
Previous Article:Analysis of sodium alginate physicochemical parameters for obtaining vegetative analogue of pharmaceutical gelatin.
Next Article:The character of diploid variation chromosome set of animal species Bos Taurus, Bos Grinniens, Ovis Aries and Equus Caballus.
Topics:

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters