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

In this study, normal nonpregnant, normal full-term pregnant, fasting ketotic and spontaneous pregnancy toxemic guinea pigs were compared to define the mechanism of this disease. In addition to conventional clinical, laboratory and pathologic studies, arterial blood pressure (thoracic and abdominal aortic) measurements and angiography were used. The results showed that in spontaneous cases of pregnancy toxemia, there is an aortic compression just caudal to the renal arteries. This compression reduced the aortic diameter by 22% of prerenal level as compared to 10% for fasting ketotic and normal pregnant guinea pigs. The aortic compression also resulted in a 30% postcompression reduction in blood pressure. No pressure differences were seen in the other groups. The postulated etiology for true toxemia of pregnancy in guinea pigs is, therefore, similar to that of man where aortic compression produces uterine ischemia and the resultant syndrome.
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PMID:True pregnancy toxemia (preeclampsia) in the guinea pig (Cavia porcellus). 51 17

Few studies of the histopathological features of the placenta in cases of fetal death are available. We will describe the placental findings from 24 midtrimester spontaneous abortions and 54 stillborn infants of more than 28 weeks' gestation. In almost 100% of midtrimester abortions and in 48% of the placentas from stillborn infants of more than 28 weeks' gestation, chorioamnionitis, deciduitis, and/or villitis were present. Because of this very high percentage of lesions, which suggests an infectious causation, it is mandatory that studies be performed that might identify pathogens. One third of the stillborn infants of more than 28 weeks' gestation were associated with maternal complications (diabetes, preeclampsia, and urinary tract infection), in addition to placental fetal vasculopathy, ischemia, infarcts, and chorangiosis (villous capillary hyperplasia). We emphasize the use of the placenta for the recognition of maternal diabetes.
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PMID:Pathological features of the placenta in fetal death. 94 56

Pre-eclampsia is characterized by uteroplacental ischemia. Prostaglandins can alter systemic blood pressure as well as regulate blood flow to the fetoplacental unit. In the present study, levels of prostaglandin E were significantly decreased in placental tissue from pre-eclamptic patients. Prostaglandin F, a potent vasoconstrictor, was markedly elevated. These observations indicate that altered placental metabolism of prostaglandins is an important factor in the pathophysiology of pre-eclampsia.
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PMID:Placental prostaglandin levels in pre-eclampsia. 96 40

In order to estimate the human placental lactogen (HPL) level and its value as an indicator of fetoplacental function during labor, we determined HPL levels (N equals 225) before, during, and after labor in normal (N equals 16) and preeclamptic (N equals 14) subjects or in patients with benign intrahepatic cholestasis of pregnancy (N equals 5). During labor, greater decreases in this value were found in preeclamptic than in normal subjects and similarly in mothers with fetoplacental dysfunction than with normal fetoplacental function. The rupture of the membranes had no effect on the level of HPL, which was not related to parity, oxytocin infusion, time interval from rupture of the membranes to delivery, nor to relative placental weight. The half-life of HPL varied in the range of 20-23 minutes immediately after delivery and in the range of 30-39 minutes some time later. During labor, greater decreases in HPL level in cases of preeclampsia or fetoplacental dysfunction may be caused by relative uteroplacental ischemia during uterine contractions, but from this finding it is hard to expect any advantage of HPL as a monitor of fetoplacental function during labor.
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PMID:Human placental lactogen levels during and after labor. 115 51

Several authors have reported the appearance of reversible hypoattenuated cerebral lesions, representing ischemia, in computed tomography scans of patients with severe pre-eclampsia. Hepatic hemorrhage and sometimes rupture have also been reported in this setting, but these problems have apparently never occurred in a patient with reversible ischemia. The authors describe a 34-year-old patient with severe pre-eclampsia in whom reversible cerebral ischemia developed in combination with hepatic and renal hematomas, which subsequently partially resolved.
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PMID:Reversible cerebral, hepatic and renal lesions in severe pre-eclampsia. 173 93

The origin of pre-eclampsia lies in uteroplacental ischemia due to an anomaly of the "vascular insertion" of the placenta. Although the cause of this anomaly remains unknown, it would appear to include both a genetic and an immunological origin possibly favourised by special underlying conditions and certain obstetric circumstances. Prostaglandin imbalance (in particular prostacyclins and Thromboxane A2) appears to be one of the chief factors governing these anomalies. One of the consequences of these mechanisms is the onset of hypertension but other disturbances are essential features. In particular, disseminated intravascular coagulation may occur leading to the release of numerous microthrombi which cause placental (leading to chronic fetal distress), renal, hepatic and cerebral lesions.
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PMID:[Physiopathological elements of pre-eclampsia and the role of the main complementary tests]. 176 67

We report a case with focal neurological deficits suggesting vertebro-basilar system ischemia, in the course of pre-eclampsia. An early CT scan showed a large hypodensity throughout the midbrain. Brainstem auditory evoked potentials initially showed an abolition of III and V pikes suggesting brainstem injury. Two days later both neurological examination and brain stem auditory evoked potentials returned to normal. A CT scan performed three weeks after the onset was normal. These findings suggest a vasospasm which may have been due to sympathomimetic agents given two weeks before the onset of toxemia for preterm labor.
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PMID:[Neurologic manifestations in the vertebro-basilar system revealing pregnancy toxemia]. 178 Jun 12

The HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count) is a severe complication of pre-eclampsia with high risk for mother and fetus. During the last 40 months 27 parturients met the diagnostic criteria for HELLP syndrome in the University Hospital of Kiel (Tables 1-3). In 24 cases cesarean section was performed. Fetal mortality was 17.2%. In 13 women an uneventful clinical course resulted, all other patients developed complications: renal insufficiency (11 cases), disseminated intravascular coagulation (DIC) (4), intracerebral hemorrhage (1), cerebrovascular ischemia (1), eclamptic convulsions (3), reoperation due to intra- or extra-abdominal hemorrhage (4), severe blood loss ex vagina following spontaneous delivery (1), and liver rupture (1). Despite these severe complications no maternal death was observed. DIC, intrauterine death, and a rapid increase in liver enzymes are considered to be serious prognostic factors that could help to identify high-risk patients. The following recommendations for therapy of parturients suffering from HELLP syndrome are given: epidural anesthesia is not an appropriate method in HELLP syndrome because of the risk of epidural hemorrhage due to thrombopenia. At the present time general anesthesia seems to be the method of choice. Inhalation anesthetics such as halothane, enflurane, or isoflurane should probably be omitted in view of the preexisting hepatopathy. The high risk and the unpredictable postpartum course strongly indicate intensive care for parturients with HELLP syndrome. Antihypertensive, antieclamptic therapy and prophylactic measures to avoid renal insufficiency or hemorrhage (e.g. early substitution of erythrocytes, thrombocytes, and coagulation factors) deserve special attention. Co-operation between obstetrician and anesthesiologist is essential to obtain optimal therapy for these high-risk patients.
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PMID:[Anesthesia and intensive therapy of pregnant women with the HELLP syndrome]. 231 3

Plasminogen activator is one of the principal enzymes involved in the fibrinolytic system. The plasminogen activator activity in placental tissue was examined using a chromogenic substrate in 9 patients with pre-eclampsia and in 9 women with uncomplicated pregnancy, who were delivered between 37 and 42 weeks of gestation. In the patients with pre-eclampsia, the plasminogen activator activity was significantly (P less than 0.05) decreased compared with that in the control group of normal pregnant women. The present findings suggest a decreased fibrinolytic activity in the placental tissue of pre-eclamptic patients, which is responsible for fibrin deposition in the placental tissue and may contribute to placental ischemia and insufficiency in pre-eclampsia.
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PMID:Placental plasminogen activator activity in pre-eclampsia. 286 18

The pathophysiology of preeclampsia includes ischemia and microinfarctions of the kidney, which could induce renal tubular cells to release enzymes into urine. We therefore measured the concentrations of two markers of renal tubular damage, N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase, in urine specimens from women with mild or severe preeclampsia and compared the results with those from healthy pregnant and nonpregnant women. The median urinary concentrations of N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase in women without preeclampsia increased progressively through the first, second, and third trimesters and reached maximum values of 1.12 and 0.77 U/mmol creatinine, respectively. Median concentrations of the two enzymes were significantly higher in women with mild preeclampsia (N-acetyl-beta-D-glucosaminidase = 1.40, alanine aminopeptidase = 1.12 U/mmol creatinine) or severe preeclampsia (N-acetyl-beta-D-glucosaminidase = 2.90, alanine aminopeptidase = 1.26 U/mmol creatinine). This increased enzyme excretion indicates subclinical preeclamptic renal tubular damage.
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PMID:Increased tubular enzyme excretion in preeclampsia. 289 Mar 4


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