Mechanism of development of pre-eclampsia linking breathing disorders to endothelial dysfunction

Ravinder Jerath, Vernon A Barnes, Hossam E. Fadel

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

High blood pressure is an important component of pre-eclampsia. The underlying mechanism of development of hypertension in pre-eclampsia is complicated and still remains obscure. Several theories have been advanced including endothelial dysfunction, uteroplacental insufficiency leading to generalized vasoconstriction, increased cardiac output, and sympathetic hyperactivity. Increased blood flow and pressure are thought to lead to capillary dilatation, which damages end-organ sites, leading to hypertension, proteinuria and edema. Additional theories have been put forward based on epidemiological research, implicating immunological and genetic factors. None of these theories have been substantiated. Based on a review of literature this paper postulates that the initiating event for the development of pre-eclampsia is intermittent hypoxia associated with irregular breathing during sleep, hypoapnea, apnea, inadequate respiratory excursions during the waking hours and inadequate cardiopulmonary synchronization (abnormal sympatho-vagal balance).

Original languageEnglish (US)
Pages (from-to)163-166
Number of pages4
JournalMedical Hypotheses
Volume73
Issue number2
DOIs
StatePublished - Aug 1 2009

Fingerprint

Pre-Eclampsia
Respiration
Hypertension
Sleep Apnea Syndromes
Immunologic Factors
Vasoconstriction
Proteinuria
Cardiac Output
Dilatation
Edema
Blood Pressure
Research

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Mechanism of development of pre-eclampsia linking breathing disorders to endothelial dysfunction. / Jerath, Ravinder; Barnes, Vernon A; Fadel, Hossam E.

In: Medical Hypotheses, Vol. 73, No. 2, 01.08.2009, p. 163-166.

Research output: Contribution to journalArticle

Jerath, Ravinder ; Barnes, Vernon A ; Fadel, Hossam E. / Mechanism of development of pre-eclampsia linking breathing disorders to endothelial dysfunction. In: Medical Hypotheses. 2009 ; Vol. 73, No. 2. pp. 163-166.
@article{092e27c478b4485bb5fe91543dea1bb1,
title = "Mechanism of development of pre-eclampsia linking breathing disorders to endothelial dysfunction",
abstract = "High blood pressure is an important component of pre-eclampsia. The underlying mechanism of development of hypertension in pre-eclampsia is complicated and still remains obscure. Several theories have been advanced including endothelial dysfunction, uteroplacental insufficiency leading to generalized vasoconstriction, increased cardiac output, and sympathetic hyperactivity. Increased blood flow and pressure are thought to lead to capillary dilatation, which damages end-organ sites, leading to hypertension, proteinuria and edema. Additional theories have been put forward based on epidemiological research, implicating immunological and genetic factors. None of these theories have been substantiated. Based on a review of literature this paper postulates that the initiating event for the development of pre-eclampsia is intermittent hypoxia associated with irregular breathing during sleep, hypoapnea, apnea, inadequate respiratory excursions during the waking hours and inadequate cardiopulmonary synchronization (abnormal sympatho-vagal balance).",
author = "Ravinder Jerath and Barnes, {Vernon A} and Fadel, {Hossam E.}",
year = "2009",
month = "8",
day = "1",
doi = "10.1016/j.mehy.2009.03.007",
language = "English (US)",
volume = "73",
pages = "163--166",
journal = "Medical Hypotheses",
issn = "0306-9877",
publisher = "Churchill Livingstone",
number = "2",

}

TY - JOUR

T1 - Mechanism of development of pre-eclampsia linking breathing disorders to endothelial dysfunction

AU - Jerath, Ravinder

AU - Barnes, Vernon A

AU - Fadel, Hossam E.

PY - 2009/8/1

Y1 - 2009/8/1

N2 - High blood pressure is an important component of pre-eclampsia. The underlying mechanism of development of hypertension in pre-eclampsia is complicated and still remains obscure. Several theories have been advanced including endothelial dysfunction, uteroplacental insufficiency leading to generalized vasoconstriction, increased cardiac output, and sympathetic hyperactivity. Increased blood flow and pressure are thought to lead to capillary dilatation, which damages end-organ sites, leading to hypertension, proteinuria and edema. Additional theories have been put forward based on epidemiological research, implicating immunological and genetic factors. None of these theories have been substantiated. Based on a review of literature this paper postulates that the initiating event for the development of pre-eclampsia is intermittent hypoxia associated with irregular breathing during sleep, hypoapnea, apnea, inadequate respiratory excursions during the waking hours and inadequate cardiopulmonary synchronization (abnormal sympatho-vagal balance).

AB - High blood pressure is an important component of pre-eclampsia. The underlying mechanism of development of hypertension in pre-eclampsia is complicated and still remains obscure. Several theories have been advanced including endothelial dysfunction, uteroplacental insufficiency leading to generalized vasoconstriction, increased cardiac output, and sympathetic hyperactivity. Increased blood flow and pressure are thought to lead to capillary dilatation, which damages end-organ sites, leading to hypertension, proteinuria and edema. Additional theories have been put forward based on epidemiological research, implicating immunological and genetic factors. None of these theories have been substantiated. Based on a review of literature this paper postulates that the initiating event for the development of pre-eclampsia is intermittent hypoxia associated with irregular breathing during sleep, hypoapnea, apnea, inadequate respiratory excursions during the waking hours and inadequate cardiopulmonary synchronization (abnormal sympatho-vagal balance).

UR - http://www.scopus.com/inward/record.url?scp=67349151152&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67349151152&partnerID=8YFLogxK

U2 - 10.1016/j.mehy.2009.03.007

DO - 10.1016/j.mehy.2009.03.007

M3 - Article

C2 - 19364630

AN - SCOPUS:67349151152

VL - 73

SP - 163

EP - 166

JO - Medical Hypotheses

JF - Medical Hypotheses

SN - 0306-9877

IS - 2

ER -