Varicose veins : symptoms, causes, and treatments /
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Full text (MCPHS users only) |
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| Other Authors: | |
| Format: | Electronic eBook |
| Language: | English |
| Published: |
New York :
Nova Science Publishers,
2011
|
| Series: | Public health in the 21st century series.
Neuroanatomy research at the leading edge. |
| Subjects: | |
| Local Note: | ProQuest Ebook Central |
Table of Contents:
- VARICOSE VEINS: SYMPTOMS, CAUSES AND TREATMENTS ; VARICOSE VEINS: SYMPTOMS, CAUSES AND TREATMENTS ; CONTENTS ; PREFACE ; VARICOSE VEINS ARE CAUSED BY SEGMENTAL FAILURES OF THE VASOREGULATORY ROLE OF THE VENOUS MICROCIRCULATION, MEDIATED BY PLASMA NOREPINEPHRINE ; ABSTRACT ; SECTION 1. ; Introduction ; SECTION 2. ; The Experimental Design ; Turbulence ; The A/V Module ; Cardiac A/V Modules ; Drainage of the A/V Module ; A/V Shunts ; The Structural and Functional Independence of Modules ; The Regulatory Function of the Adrenergic Plexus and the Microcirculation.
- Evidence of the Dilator Effect of Microcirculatory NE In Vivo Factors That Determine and Affect Venous Tone ; The Role of the Vascular Microcirculation ; The Renal Capsular Microcirculation ; The Pharmacology of the Microcirculation ; SECTION 3. ; The Stenotic Constrictor Effect of Isoprenaline; THE VALVE AGGER ; The Role of the Agger in Reflux; The Venodilator Potency of Microcirculatory NE ; In Vivo Plasma NE Concentrations and Varicosities; Varicosities Caused by Orthograde Perfusion ; Arterial Dilitation Caused by Microcirculatory NE ; SECTION 4. ; Validation.
- The Multiplication of Varicosities Therapeutic Options ; SECTION 5. ; The Bipolar Nature of the NE Stimulus; The Roles of Neuronal and Plasma NE in Smooith Muscle Contraction ; The Roles of NE in Smooth Muscle Contraction ; Contraction in the Microcirculation; The Role of the General Microcirculation ; CONCLUSION ; REFERENCES ; THE ROLE OF INFLAMMATION IN THE VARICOSE VEIN PATHOLOGY: NEW INSIGHTS ; ABSTRACT ; 1. INTRODUCTION ; 2. INFLAMMATION AND CHRONIC VENOUS DISEASE ; 2.1. Types and Distribution of Cells ; 2.1.1. Leukocytes ; 2.1.2. Endothelial Cells ; 2.1.3. Other Cells.
- 2.2. Extracelular Matrix 2.3. Inflammatory Mediators ; 2.3.1. Adhesion Molecules ; 2.3.2. MMPs ; 2.3.3. Cytokines ; 2.3.4. Growth Factors ; 2.3.5. Hypoxia-Inducible Factors (HIF) ; 2.3.6. Oxidative Stress ; 2.3.7. Lipid Mediators ; 2.4. Mechanisms for Cell Activation and Inflammation ; 3. THERAPEUTICAL APPROACHES TO CVD ; 3.1. Current Therapies ; 3.1.2. Compressive Therapy ; 3.1.3. Surgical And Interventional Treatment ; 3.2. Pharmacological Therapy ; 3.2.1. Venoactive Drugs ; 3.2.1.1. Flavonoids and its Derivatives ; 3.2.1.2. Other Natural Venoactive Drugs ; 3.2.2. Non-Venoactive Agents.
- 3.2.2.1. Prostaglandin E1 3.2.2.2. Prostacyclin Analogues ; 3.2.2.3. Pentoxifylline ; 3.2.2.4. Acetylsalicylic Acid (ASA) ; 3.2.2.5. Synthetic Peptide ; 3.2.3. Other Potential Pharmacological Agents ; CONCLUSION ; DECLARATION ; REFERENCES ; ASCENDING EVOLUTION OF VARICOSE VEINS: LITERATURE REVIEW AND RATIONALE FOR TREATMENT; ABSTRACT ; INTRODUCTION ; PATHOPHYSIOLOGY OF VARICOSE VEINS AND "RETROGRADE THEORY" ; ASCENDING THEORY ; 1. Ascending Theory: Rationale and Theoretical Assumptions ; 2. Ascending Theory: Clinical Evidence ; A. Clinical Data on Patterns of Venous Varicosities.
