I= STUDIES ON THE EFFECT OF VITAMIN E ON HUMAN PLATELET AGGREGATION AND ARACHIDONIC ACID METABOLISM IN PREGNANCY INDUCED HYPERTENSION (PIH)
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Title of Thesis
STUDIES ON THE EFFECT OF VITAMIN E ON HUMAN PLATELET AGGREGATION AND ARACHIDONIC ACID METABOLISM IN PREGNANCY INDUCED HYPERTENSION (PIH)
Author(s)
Dr. Kausar Aamir
Institute/University/Department Details
Department of Pharmacology/ University of Karachi
Session
2004
Subject
Pharmacology
Number of Pages
226
Keywords (Extracted from title, table of contents and abstract of thesis)
vitamin e, pregnancy induced hypertension, human platelet aggregation, arachidonic acid metabolism, pre-eclampsia

Abstract
In Pakistan pregnancy induced hypertension leading to severe pre-eclampsia (PE) is common due to low socioeconomic status and lack of antenatal care. Pregnancy induced hypertension or gestational hypertension caused by pregnancy itself is defined as gestational hypertension developing after twenty weeks of gestation in a previously normotensive women. PIH with protein urea, decreased platelet count and increased cholesterol levels usually corresponds to pre-eclampsia. Management of PIH includes routine antihypertensive drugs, antioxidants for the prevention of pre-eclampsia. Alpha tocopherol is an antioxidant and is the most active in the vitamin E activity. All forms of vitamin E are taken up by the intestinal cells and released into the circulation with chylomicrons. Vitamin E is known to be mobilized from the tissues to the sites of oxidative stress. All antioxidants protect the cells and tissues against toxic lipid peroxides. According to the mechanism of action they may be classified in to I) preventive antioxidants (acting tyo inhibit the initiation of peroxidation process) and ii) chain breaking antioxidants (acting to trap or decompose radicals or peroxide already present in the system. The early provision of antioxidants like vitamin E and vitamin C to women at high risk of developing pre-eclampsia has a marked clinical benefit. Vitamin usage is associated with better endothelial function and less placental dysfunction. Therefore, this study was designed to evaluate the role of antioxidants i.e. vitamin E, C , β-carotenoids and vitamin A but specifically role of vitamin E was evaluated in relation to its effects on platelet aggregation and arachidonic acid metabolism in pregnancy induced hypertensive women. In this study protocol patients were divided into 3 groups i.e. A, B and C, group A (control group) of normotensive pregnant women (n=40), group B (mild PIH women) (n=40) and group C (severe PIH women) (n=30). All 3 groups showed evidence for reduced antioxidant levels and increased free radical generation (oxidative stress in pre-eclampsia). In terms of percentage vitamin C levels were reduced from 42.6% in normotensive (control group) to 31.3% in group B (mild PIH women) (n=40) to 26.1% in group C (severe POH women). Similarly β-carotene reduced from 44.9% in group A (control group) to 41.4% in group B (mild PIH women) (n=40) to 13.7% in group C (severe PIH women). Again serum levels of vitamin A were found reduced from 34.5% in group A (control/normotensive pregnant women) to 32.8% respectively. The same in both group B (mild PIH women) and group C (severe PIH women).

Similarly serum levels of vitamin E (alpha tocopherol) were found reduced from 42.4% in group A (control/normotensive pregnant women) to 40.2% in group B (mild PIH women) to 13.7% in group C (severe PIH women). Where as in blood pressure, systolic blood pressure measured as 121±1.69 or 27.6% in group A (control group) and 144.5±1.10 or 33% in group B (mild PIH women) and 172.6±3.31 or 39.4% in group C (severe PIH women) and diastolic blood pressure measured as 77.7:t1.11 or 26% in group A (control group) and 93±0.80 or 31.2% in group B (mild PIH women) and 127.83±2.07 or 47.7% in group C (severe PIH women). In terms of P value group C showed (P<0.00l) highly significant results as compared to group A and as (P<0.0l) significant as compared to group B respectively. Platelet count result showed the reduction in group A (control group) from 47.7% to 33.8% in group B (mild PIIH women) to 18.5% in group C (severe PIH women) again highly significant (P<0.00l) in group C in comparison to group A but only (P<0.0l) significant in comparison to group B. result were observed as TC (total cholesterol) as 32.3% in group A (control group) slightly raised to 33.7% in group B (mild PIH women) but reduced to 26.1 % in group C (severe PIH women) (P<0.0l). Results observed in TAG (Triacylglycerol) as 27.4% in group A (control group) raised to 36.5% in group B (mild PIH women) to little less 36.1 % in group C (severe PIH women). In HDL-C levels as 38% in group A (control group) reduced to 31 % in group B (mild PIH women) and 31.1 % in group C (severe PIH women) respectively. In LDL-C levels as 31.7% in group A (control group) raised to 34% in group B (mild PIH women) and 34.3% in group C (severe PIH women). In VLDL-C levels as 27.5% in group A (control group) raised to 36.4% in group B (mild PIH women) and 36.1 % in group C (severe PIH women) and with all observed results in the study it is evident that endothelial cell injury reduces the synthesis of vasorelaxing agents, increases the production of vasoconstriction, impairs synthesis of endogenous anticoagulants and increases procoagulant production and oxidative stress has been implicated in the pathophysiology of pre-eclampsia in mild to severe cases of PIH women.
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3714.18 KB
S. No. Chapter Title of the Chapters Page Size (KB)
1 0 Contents
232.16 KB
2 1 Introduction 1
1178.3 KB
  1.1 Effect On Mother 2
  1.2 Effect On The Unborn Baby 3
  1.3 Diagnosis And Treatment 4
  1.4 Definition 4
  1.5 Hypertension In Pregnancy 7
  1.6 Classification 8
  1.7 Pathophysiology 10
  1.8 Pharmacologic Treatment Of Hypertensive Disorders 18
  1.9 Aim To Reduce Blood Pressure ≤140 Mmhg And Diastolic To 90 Mmhg 19
  1.10 Classification 26
  1.11 Trophoblast As The Source Of Factor(S) That Causes Endothelial Cell Injury 28
  1.12 Lipid Peroxide Action 31
  1.13 Terminology And Classification 43
  1.14 Factors Behind Pathophysiology Of Pe 48
  1.15 Predication Of Pe 55
  1.16 Prevention Of Pe 57
  1.17 Management 57
  1.18 Pregnancy Induced Hypertension(PIH) 58
  1.19 Delivery 61
  1.20 Complication Of Severe PE 62
  1.21 Role Of Arachidonic Acid Metabolism In Pih 64
  1.22 Action Of TXA 2 67
  1.23 Prophylactic Measures Of Pe 71
  1.24 Naturally Occurring Antioxidants 71
  1.25 Role Of Antioxidants In Pe 72
  1.26 Antioxidant Defence Sydrem 75
  1.27 Role Of Antioxidants In Pre-Eclamsia 80
  1.28 Vitamin E (Alpha Tocopherol ) 82
  1.29 Vitamin E Lipid Soluble Antioxidant 86
  1.30 Pharmacological Action 90
  1.31 Vitamin C 95
3 2 Materials And Methods 104
377.46 KB
  2.1 Subject Recruitment 104
  2.2 Inclusion Criteria 106
  2.3 Exclusion Criteria 106
  2.4 Parameters 107
  2.5 Sample Collection 108
  2.6 Determination Of Serum Tocopherol 110
  2.7 Ascorbic Acid 112
  2.8 Vitamin A And Î’-Carotene 115
  2.9 Determination Of Serum Totals Cholesterol 117
  2.10 Determination Of Serum Triglycerides 120
  2.11 Determination Of Serum Hdl Cholesterol 122
  2.12 Calculation Of Ldl Cholesterol 125
  2.13 Calculation Of Vldl Cholesterol 125
  2.14 Urinary Excretory Rate Of Albumin 125
4 3 Results 128
431.28 KB
5 4 Discussion 149
296.67 KB
6 5 References 173
364.58 KB
7 6 Appendices 205
1123.85 KB