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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH appears to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Investigators are also attempting to elucidate the placental factors that are responsible for mediating activation/dysfunction of the maternal vascular endothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.
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PMID:Pathophysiology of pregnancy-induced hypertension. 1141 54

Hypertensive disorders of pregnancy are prototypical of maternal conditions associated with reduced uteroplacental blood flow. Hypertensive disorders in pregnancy include chronic hypertension, preeclampsia-eclampsia, superimposed preeclampsia, and gestational hypertension. Pathophysiology of these disorders include deficient uterine vascular modeling in the process of placentation and aberrations of vasomotor regulation. Aberrations of uterine renin-angiotensin system may play a proximate role in the pathogenesis of preeclampsia syndrome. Clinical manifestations are explained in this review based on resultant vasoconstriction and ischemia in systemic and regional circulations. Perinatal implications of hypertensive disorders both in terms of early neonatal outcome and long-term neurodevelopmental effects are described. Methods of antenatal assessment of the fetus and, briefly, principles of clinical management are described.
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PMID:Perinatal implications of maternal hypertension. 1146 57

Oxidative stress is a prominent feature of the placenta in many complications of pregnancy, such as preeclampsia. The cause is primarily unknown, although ischemia-reperfusion injury is one possible mechanism. Our aim was to test this hypothesis by examining the oxidative status of human placental tissues during periods of hypoxia and reoxygenation in vitro. Rapid generation of reactive oxygen species was detected using the fluorogenic probe, 2',7'-dichlorofluorescein diacetate, when hypoxic tissues were reoxygenated. The principal sites were the villous endothelium, and to a lesser extent the syncytiotrophoblast and stromal cells. Increased concentrations of heat shock protein 72, nitrotyrosine residues, and 4-hydroxy-2-nonenal were also observed in the villous endothelial and underlying smooth muscle cells, and in the syncytiotrophoblast. Furthermore, preloading placental tissues with the reactive oxygen species scavengers desferrioxamine and alpha-phenyl-N-tert-butylnitrone reduced levels of oxidative stress after reoxygenation. These changes are consistent with an ischemia-reperfusion injury, and mirror those seen in preeclampsia. Consequently, in vitro hypoxia/reoxygenation may represent a suitable model system for investigating the generation of placental oxidative stress in preeclampsia and other complications of pregnancy.
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PMID:In vitro ischemia-reperfusion injury in term human placenta as a model for oxidative stress in pathological pregnancies. 1154 95

We assessed the effects of melatonin, a powerful scavenger of oxygen free radicals, on ischemia/reperfusion-induced oxidative damage to mitochondria in the rat placenta. In Wistar rats at day 19 of pregnancy, feto-placental ischemia was induced by occluding both utero-ovarian arteries for 20 min. Reperfusion was achieved by releasing the occlusion and restoring circulation for 30 min. Melatonin solution or the vehicle alone was injected intraperitoneally at dose of 10 mg/kg 1 hr before occlusion. Sham-ischemic animals were treated with vehicle. Each group consisted of 10 pregnant rats. We measured placental mitochondrial respiratory control index (RCI; a marker of mitochondrial respiratory activity), the ratio of the added adenosine 5-diphosphate (ADP) concentration to consumption of oxygen during state 3 respiration (ADP/O), and the concentration of thiobarbituric acid reactive substances (TBARS) in each group. RCI and ADP/O were significantly decreased by ischemia/reperfusion, while TBARS were increased. Melatonin prevented these changes. These results indicate that exogenous melatonin protects against ischemia/reperfusion-induced oxidative damage to mitochondria in rat placenta. Melatonin could be useful in treating preeclampsia and possibly other clinical states involving excess free radical production, such as fetal growth restriction and fetal hypoxia.
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PMID:Melatonin protects against oxidative mitochondrial damage induced in rat placenta by ischemia and reperfusion. 1155 74

Studies over the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal-pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during preeclampsia are still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiological mechanisms responsible for the elevation in arterial pressure in women with preeclampsia.
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PMID:Pathophysiology of hypertension during preeclampsia linking placental ischemia with endothelial dysfunction. 1156 64

Hypertension occurs in 10 to 15 p cent of pregnancies. Among them, 10 to 20% also have proteinuria. This situation defines preeclampsia, and involves a serious threat on foetal and even maternal prognosis. Presence of the hepatic (HELLP) syndrome still severely worsens the prognosis. Pathophysiology of preeclampsia is based on a very early abnormality of placentation, leading to insufficient blood supply to the foeto-placental unit. At the maternal level, the main consequence of placental ischemia is diffuse endothelial dysfunction, responsible for systemic vasoconstriction and clotting abnormalities. In such a context, merely lowering blood pressure with drugs is quite inefficient, or even harmful. The prognosis of this disease is mainly related to the pertinence of obstetrical management. An early preventive strategy is the most logical approach of preeclampsia, its modalities remain under discussion. Hypertension has a high recurrence rate on subsequent pregnancies. It is most often linked to a high global vascular risk level, therefore many of those patients will become permanent hypertensives in the near future.
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PMID:[Hypertension in pregnancy]. 1172 13

Abnormal placental implantation presumed to be secondary to maternal genetic susceptibility or immune maladaptation is considered to be fundamental to the pathogenesis of preeclampsia. The reduced placental perfusion resulting in placental ischemia is hypothesized to cause the known endothelial dysfunction, which leads to the clinical manifestations of this disease. Oxidative stress is a postulated linking factor, an aberration that possibly has its genesis via cytokines released from the abnormally implanted and perfused placenta. Clearly the maternal pathophysiologic changes that subsequently produce what is recognized as preeclampsia are present long before the disease makes its clinical appearance.
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PMID:Preeclampsia: pathophysiology and practice considerations for the consulting nephrologist. 1178 69

Cortical blindness in pre-eclampsia due petechial hemorrhages, ischemia, focal edema and infarction of the occipital cortex, is mostly reversible.
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PMID:Acute cortical blindness complicating pre-eclampsia. 1178 56

OBJECTIVE: Life-threatening conditions cause severe changes in the organization and conformation of macromolecules, creating urgent requirements for protein repair to ensure survival. As molecular chaperones, heat shock proteins (HSP) that have specialized functions in protein folding are now well established to restore homeostasis in cells and organisms. Augmentation of HSP synthesis is tightly regulated by stress-inducible heat shock factors (HSF), which are part of a transcriptional signaling cascade with both positive (e.g., HSP) and negative (e.g., proinflammatory cytokines) properties. In this review, we discuss the biological roles and mechanisms of HSP-mediated protection in pathophysiologic conditions (ischemia, sepsis, and preeclampsia) and the regulation for stress-dependent HSP synthesis and speculate about future applications for harnessing HSF and HSP partners as cytoprotective agents. DATA SOURCES: Reactive oxygen species are major pathogenic factors in cell death pathways (e.g., necrosis, apoptosis), in part, because of proteotoxic effects. In intact organisms, forced overexpression of HSP per se affords effective counterbalance against ischemia challenges (e.g., heart and brain) and systemic conditions (e.g., sepsis). Besides stressful conditions, gene-targeting studies have uncovered new functions for heat shock transcription factors (e.g., maintenance of intrauterine pregnancy) in mammals. In parallel, pharmacologic studies using small molecules are paving the way for future prospects to exploit the beneficial properties of HSP, albeit an important but presently elusive goal. CONCLUSIONS: Together, HSF and HSP partners are attractive targets in therapeutic strategies designed to stimulate endogenous protective mechanisms against deleterious consequences of oxidative stress. With further technological advances, it is anticipated that the spotlight on HSP, alone or in combination with other stress response pathways, could, ultimately, reduce injury and accelerate functional recovery of susceptible organs in living organisms including humans.
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PMID:Heat shock factor 1 and heat shock proteins: Critical partners in protection against acute cell injury. 1183 44

Reported causes of pancreatitis in pregnancy include: gallstone disease, hyperlipidemia, alcohol ingestion, viral, and idiopathic. Few reports associate pancreatitis with pregnancy-induced hypertension. A 35-year-old women with pregnancy-induced hypertension and spontaneous rupture of membranes was admitted for induction of labor. Her postpartum course was complicated by acute renal failure that responded well to treatment with Lasix and Albumin. Subsequently, the patient developed acute pancreatitis and recovered following conservative treatment. It is possible that the pancreatic ischemia due to generalized vasoconstriction of preeclampsia and loop diuretics in the setting of oliguria with renal failure, had a synergistic effect on the pancreas. Therefore, we suggest that in postpartum women with pregnancy-induced hypertension and acute renal failure, diuretics should be cautiously used because they may increase the risk of pancreatitis.
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PMID:Pregnancy-induced hypertension complicated by postpartum renal failure and pancreatitis: a case report. 1201 78


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