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| Year : 1987 | Volume
: 33
| Issue : 4 | Page : 178-81 |
Platelet adhesiveness, plasma fibrinogen and fibrinolytic activity in cases of essential hypertension.
Mehrotra TN, Mehrotra RR
How to cite this article:
Mehrotra T N, Mehrotra R R. Platelet adhesiveness, plasma fibrinogen and fibrinolytic activity in cases of essential hypertension. J Postgrad Med 1987;33:178 |
How to cite this URL:
Mehrotra T N, Mehrotra R R. Platelet adhesiveness, plasma fibrinogen and fibrinolytic activity in cases of essential hypertension. J Postgrad Med [serial online] 1987 [cited 2023 Mar 27];33:178. Available from: https://www.jpgmonline.com/text.asp?1987/33/4/178/5265 |
Alterations in blood coagulation system have been reported in patients of hypertension. However, there is no unanimity in the results.[2],[14] The level of fibrinolytic activity in cases having high platelet adhesiveness and plasma fibrinogen may play an important role in the pathogenesis or progress of the disease. Despite its large molecular weight, fibrinogen penetrates capillary walls more rapidly than albumin.[9] The fibrinoid material in blood vessel walls is in part composed of fibrin.[10] Persistance of fibrin in vessel wall is said to play an important role in the development of malignant hypertension.[15] Therefore, it appears likely that maintenance of a normal state of balance between factors like platelet adhesive ness and plasma fibrinogen which are likely to increase blood viscosity on one hand and. fibrinolytic system on the ether may play a part in the natural history of the disease. It is for this reason, the present study was carried out in cases of hypertension.
A total of 35 patients with essential hypertension in the age group of 30-60 years were studied. Cases of secondary hypertension including those of renal hypertension were excluded as renal lesions on their own are known to alter fibrinolytic system. A detailed clinical history and a thorough physical examination, including fundus examination were carried out in each patient. Investigations included urine examination including culture, blood urea, electrolytes, X-ray chest, ECG, I.V.P. as well as renal biopsy whenever necessary to exclude secondary hypertension.
A group of 25 normal healthy subjects in the same age group were studied to serve as control.
Platelet adhesiveness was estimated by the method of Easthan[5] using adenosine diphosphate (ADP). Plasma fibrinogen was measured by the method of Ratnoff and Menzie.[11] Fibrinolytic activity was measured by estimating the euglobulin clot lysis time (ELT) using method of Cash.[4]
A total of 60 patients, 35 cases of essential hypertension (25 cases of mild to moderate hypertension and 10 cases of severe and malignant hypertension; Group A) and 25 controls (Group B) were studied. The results are depicted in the following tables [table 1] and [table 2] which clearly state that plasma fibrinogen and platelet adhesiveness were significantly increased in all the cases of hypertension (Group A) as compared to controls (Group B) (p values less than 0.001). Euglobulin clot lysis time on the other hand was significantly decreased (p value less than 0.001) in cases of hypertension (Group A) as compared to normals (Group B), indicating a marked enhancement in fibrinolytic activity.
On further analysis of the results, the significance in platelet adhesiveness, plasma fibrinogen and fibrinolytic activity were more marked in cases of severe and malignant hypertension.
The role of disturbed coagulation fibrinolytic system in the pathogenesis or progression of hypertension is far from clear. It is, however, likely that it may be of importance in the development of severe and malignant hypertension.
Extensive interest has been focussed in recent years on platelet adhesiveness in various disorders. Despite discrepancies in results presented by different authors, there is evidence that increased platelet adhesiveness predisposs to increased coaguablity.[3],[8],[12],[13]
In the present series of hypertensive patients, platelet adhesiveness was increased in all cases, but it was more marked in cases of severe and malignant hypertension indicating hypercoaguable state in these cases. The findings are in agreement with other workers.[2],[11],[15]
The findings of increased fibrinogen in cases of hypertension of our series, however, is contrary to the findings reported by other workers.[2],[14]
Fibrin aggregates are likely to be deposited in the vessel wall in these cases. What initiates the process is not known. It is also known that fibrinogen penetrates capillary walls more rapidly than albumin.[9] Persistence of fibrin deposited in the vessel wall is believed to play an important role in the development of severe and malignant hypertension. It, therefore, appears that increased fibrinogen levels play a significant role in the development of severe and malignant hypertension.
Increase in fibrinolysis may possibly reflect a compensatory effort on the part of the body to dislodge the platelets.
Despite the criticism of substrate variability, euglobulin clot lysis time is perhaps the best available method or assay of circulating plasminogen activator and hence a reliable indicator of fibrinolytic activity.[6],[7] Our data reveal a significant (p value less than 0.001) increase in fibrinolytic activity in our series of hypertensive subjects as compared to healthy controls. A proper functioning fibrinolytic system may also play an important role to keep the glomeruli free of fibrin deposits.
Thus, a dynamic equilibrium as suggested by Astrup[1] between coagulation and fibrinolysis and a significant increase in platelet adhesiveness and fibrinogen with corresponding decrease in euglobin clot lysis (increased fibrinolytic activity) point towards a normal functioning and a balanced state of equilibrium. Alterations noted in the severe and malignant hypertensives were more severe and indicated a poor balance between platelet adhesiveness, fibrinogen and fibrinolytic activity signifying marked disturbances in haemostasis in these cases.
It is, however, not possible to conclude that these alterations are the result or effuse of the severity of hypertension.
| 1. | Astrup, T.: Biological significance of fibriolysis, Lancet, 2: 565-568, 1956.  |
| 2. | Bennet, N. B. and Ogston, D.: Inhibitions of fibrinolytic enzyme system in renal disease. Clin. Sci., 549:30-41, 1970. |
| 3. | Biggs, R., Denson, K. W. E., Reisenberg, D. and McIntyre, C.: The coagulant activity of platelets. Brit. J. Haematol., 15: 283-296, 1968. |
| 4. | Cash, T. D.: Effects of moderate exercise on the fibrinolytic system in normal young men and women. Brit. Med. J., 2: 502-506, 1966. |
| 5. | Easthan, R. D.: Rapid adhesive platelet count in whole blood, J. Clin. Pathol., 17: 45-46, 1964. |
| 6. | Fearnley, G. R.: Fibrinolysis, Arnold, London 1965, p. 35. |
| 7. | Fletcher, A. P., Biederman, O., Moore, D., Alkjaersig, N. and Sherry, S.: Abnormal plasminogen-plasmin system activity (fibrinolysis) in patients with hepatic cirrhosis, its cause and consequences. J. Clin. Invest., 43: 681-695, 1964. |
| 8. | Hirsh, J. and Mcbride, J.: Increased platelet adhesiveness in recurrent venous thrombosis and pulmonary embolism. Brit. Med. J., ii: 797-799, 1965. |
| 9. | Lewis, J. H., Ferguson, E. E. and Schoenfeld, C.: Studies concerning the turnover of fibrinogen I131 in the dog J. Lab. & Clin. Med., 58: 247-258, 1961. |
| 10. | Ooneda, G., Ooyma, Y., Matsuyama, K., Takafama, N., Yoshida, Y., Scleguehi, N. and Acci, I.: Electron microscopic studies in the morphogenesis of fibrinoid degeneration in the mesenteric arteries of hypertensive rats. Angiology, 16:8-17, 1965. |
| 11. | Ratnoff, O. D. and Menzie, C. A.: New method for determination of fibrinogen in small samples of plasma. J. ,Lab. Clin. Med., 37: 316-320, 1951. |
| 12. | Walsh, P. N.: The role of platelets in the contact phase of blood coagulation. Brit. J. Haematol., 22: 237-254, 1972. |
| 13. | Walsh, P. N.: The effects of collagen and kaolin on the intrinsic coagulant activity of platelets. Evidence for an alternative pathway in intrinsic coagulation not requiring factor XII. Brit. J. Haematol., 22: 393-405, 1972. |
| 14. | Wardle, E. N., Menon, I. S. and Rastogi, S. P.: Study of proteins and fibrinolysis in patients with glomerulonephritis. Brit. Med. J., 2: 260-263, 1970. |
| 15. | Weiner, I., Lattes, R. G., Meltzer, B. G. and Spiro, D.: The cellular pathology of experimental hypertension. IV. Evidence for increased vascular permeability, Amer. J. Pathol., 54: 187-194, 1969. |
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