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

We examined the possibility that in preeclampsia complicated by fetal growth retardation, placental energy state is low either because of impaired glycolysis or because of ischemia resulting from reduced maternal placental blood flow. Concentrations of pyruvate and lactate, but not of glycogen and glucose, were significantly low in placentas of mothers with severe preeclampsia, supporting previous indirect evidence of inhibited glycolysis. Nevertheless, direct measurements of adenine nucleotide concentrations did not indicate reduced placental energy level in the preeclamptic placentas. This along with a lack of change of the ratio of lactate/pyruvate concentration (an indication of the redox state of cytoplasmic reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide) is also evidence against the hypothesis of general placental ischemia leading to energy deficiency. However, as glycolysis is an important source of precursors, particularly pyruvate, for synthesis of amino acids and lipids, these results suggest that there is a significant metabolic abnormality in placentas of mothers with severe preeclampsia.
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PMID:Placental glycolysis and energy metabolism in preeclampsia. 360 74

We performed a prospective, controlled, masked study designed to evaluate the ocular manifestations of preeclampsia in 56 patients, including 25 control, 17 mild preeclamptic, and 14 severe preeclamptic patients. There was a statistically significant correlation between the reduction in arteriole to vein ratio and a diagnosis of severe preeclampsia (r = -.32, P = .004). There was also a significant correlation between the number of focal constrictions and a diagnosis of severe preeclampsia (r = .34, P = .005). The arteriole to vein ratio and number of focal constrictions did not differ significantly between normal and mild preeclamptic patients. None of the patients showed background changes of hemorrhages, cotton-wool spots, and exudates, or evidence of choroidal ischemia (including Elschnig's spots and retinal detachment). In contrast to previous reports, the role of the ophthalmologist in the diagnosis and management of preeclampsia appears to be limited.
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PMID:Ocular manifestations of preeclampsia. 382 37

Periarteritis Nodosa (P.A.N.) is a systemic connective tissue disease with a variety of manifestations that includes ocular involvement in 20% of cases. The diagnosis of this condition is difficult due to the absence of any specific clinical signs or laboratory findings. However, histologic studies have demonstrated a segmental vasculitis that is often necrotic. Ocular findings frequently include choroidal involvement that is characteristic. Nevertheless, angiographic studies of this disease are extremely rare. The findings in three patients suspected of having P.A.N. are presented. Fluorescein angiography established the diagnosis of P.A.N. in two cases and ruled-out its presence in the third case. In the first case angiography demonstrated a retinal vasculitis with multiple arteriolar and capillary occlusions. There was also ischemic involvement of the choriocapillaris and a mild anterior optic nerve vasculitis. All findings resolved, leaving numerous Elschnig spots. In the second case the angiogram showed acute multifocal ischemia of the choriocapillaris. The ocular examination and fluorescein angiogram in the third case were entirely normal, thereby ruling-out P.A.N. on the basis of insufficient criteria. Acute multifocal choroidal ischemia is present in a variety of rare conditions: Toxemia of pregnancy, Disseminated Intravascular coagulopathy, Moskowitz Disease (T.T.P.), Leukemia and Malignant Hypertension. However, the presence of multifocal choroidal ischemia in the presence of a systemic connective tissue disorder strongly favors the diagnosis of P.A.N. The relative contributions of co-existent Malignant Hypertension and P.A.N. in producing choroidal ischemia are discussed. The spectrum of clinical manifestations and laboratory findings in P.A.N. as well as hypotheses concerning pathogenesis (immune-complex deposition) are described. Among all systemic vasculitis , only P.A.N., and rarely Scleroderma, feature choroidal involvement. This is possibly due to the fact that the degree of vasculitis in P.A.N. is sufficiently severe to cause clinically significant choroidal involvement.
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PMID:[Fluorescein angiography in the diagnosis of periarteritis nodosa]. 614 75

Pregnancy complicated by hypertension is commonly associated with placental insufficiency, thereby resulting in fetal growth retardation. Furthermore, reduced utero-placental blood flow has been recognized in cases of severe preeclampsia with hypertension. Thus, it must be assumed that histological as well as ultrastructural findings in hypertensive placentas are due to the occlusion or narrowing of the uteroplacental vasculature as well as placental ischemia. Microscopically, these placental changes include infarcts, increased syncytial knots, hypovascularity of the villi, cytotrophoblastic proliferation, thickening of the trophoblastic basement membrane, obliterative enlarged endothelial cells in the fetal capillaries and atherosis of the spiral arteries in the placental bed. In addition, ultrastructural features are characterized by a decreased number of syncytial microvilli, proliferation of cytotrophoblastic cells, focal syncytial necrosis, thickening of trophoblastic basement membrane and narrowing of the fetal capillaries, as a number of studies have demonstrated. These placental abnormalities can be seen not only in human toxemia, but also in animals with experimentally induced toxemia or with spontaneous toxemia.
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PMID:Morphologic changes in the hypertensive placenta. 675 49

PGE1 appears to act as a physiological regulator of uteroplacental blood flow. Its vasodilatory, anti-vasopressor, and platelet stabilizing effects could be expected to counteract the placental ischemia, hypertension and excessive coagulation that are seen in pre-eclampsia. Supplementation with efficient essential fatty acid precursors of PGE1 reduces platelet aggregation, has been used with success in the treatment of hypertension and arterial vasospasm, and might offer a nutritional means of reducing the incidence and severity of pre-eclampsia. Assurance of adequate general nutrition also appears to be of importance in this regard.
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PMID:Nutritional prevention of pre-eclampsia--a special role for 1 series prostaglandin precursors? 689 Jun 22

In two groups of nonpregnant guinea pigs, uterine ischemia was produced by banding the uterine arteries and transecting the ovarian arteries. Since this procedure prevented the increase of uterine blood supply that normally occurs during pregnancy, uteroplacental ischemia resulted when the animals became pregnant. Intraarterial blood pressures were recorded immediately after surgery and again near term. Hypertension, proteinuria and elevated creatinine levels (changes similar to those of human preeclampsia) were consistently found near term in all of the banded animals that became pregnant. These findings support the view that it is possible to develop a toxemia model in the guinea pig.
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PMID:Experimental toxemia in the pregnant guinea pig (Cavia porcellus). 705 72

Pre-eclampsia is a frequent, unpredictable syndrome which is dangerous for both mother and foetus. The concept of placental ischemia has gained wide acceptance among the numerous theories put forward to explain the illness. The setting up of preeclampsia seems to be scheduled in two steps: (1) an absolute or relative placental ischemia due to vascular diseases or hypertrophic placenta, or most often secondary to implantation defect, particularly anomaly with the invasive trophoblast; (2) a diffuse endothelial disease. The connection between these two steps is incompletely disclosed. The authors demonstrate that the maternal immune system which is strongly stressed during all the stages of normal gestation is implicated in pre-eclampsia. Its role is probably not univocal. Foeto-trophoblastic antigens could be poorly recognised. This defect of recognition could lead to the abnormalities of trophoblastic invasion observed in pre-eclampsia. Pre-eclampsia does not seem to be accompanied by an immunological rejection of the foetus. Some genetically predisposed patients do not have a sufficiently competent immune system to neutralise one or more of the toxic products released by the ischemic placenta. Certain types of pre-eclampsia could be auto-immune, with the auto-antibodies directed against certain types of phospholipids or trophoblastic constituents. A disequilibrium between oxidation and anti-oxidation mechanisms involving neutrophils could lead to aggression of the endothelium which is observed in pre-eclampsia. Pre-eclampsia could represent a form of immuno-dystrophy, with the excessive production of adverse cytokines locally, directed against the trophoblast. Without directly implicating the immune system as the trigger of pre-eclampsia, it seems that its role is unclear. In some cases it develops protective mechanisms which, when overwhelmed or inadequate, allows pre-eclampsia to occur. In other cases it can form part of the cascade of aggressions leading to the abnormalities encountered. The integration of these abnormalities in the pathophysiological models, could help improve the classification of pre-eclampsia. This attempt will lead to a more adapted preventive and therapeutic management of pre-eclampsia.
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PMID:Pre-eclampsia: physiology and immunological aspects. 890 80

Retinal detachment is a rare complication of preeclampsia, eclampsia and abruptio placentae. We report a case of bilateral retinal detachment in association with severe preeclampsia complicated with abruptio placentae, intrauterine fetal death and disseminated intravascular coagulation. In obstetric complications, placental thromboplastin may release into maternal circulation and activate the extrinsic coagulation system with resultant disseminated intravascular coagulation. This may be responsible for choroidal ischemia and consequent serous retinal detachment.
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PMID:Retinal detachment in association with preeclampsia and abruptio placentae. 763 40

The powerful vasoconstrictor autacoid thromboxane A2 (TxA2) has pathological roles in many diseases including pre-eclampsia or pregnancy induced hypertension (PIH). Adenosine and other purines are released by tissues during ischemia as occurs in the utero-placental circulation during PIH. These substances, particularly adenosine, may modulate TxA2 constrictor responses. We therefore characterized TxA2 receptors in the umbilical artery in vitro using the competitive antagonist GR32191. Also examined was the Ca2+ channels' involvement in adenosine-induced inhibition of TxA2 vasoconstriction. Results showed that TxA2 receptors on umbilical arteries are identical to those present in platelets, the placenta and umbilical vein. Adenosine was found to inhibit equally constriction involving either voltage or receptor operated Ca2+ channels.
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PMID:Modulation by adenosine of thromboxane A2 receptor-mediated constriction in the human umbilical artery. 795 95

Among 61 patients with severe pregnancy induced hypertension, cerebral lesions were detected on CT scans in 23 cases (37.7%). The positive rates were 5/25 cases in preeclampsia and 18/36 cases in eclampsia. The incidence rate of cerebral lesions in eclampsia was significantly higher than that in preeclampsia (chi 2 test, P < 0.05). Furthermore, it showed that patients with renal impairment and retinal changes were more susceptible to cerebral lesions (P < 0.05), through comparative study of the relationships between either the function of liver and kidney or retinal changes and cerebral lesions. Main manifestations of cerebral lesions were ischemia, edema and infarction. The represented the different pathological stage of cerebral lesions. The cerebral lesions were mainly involved at cortical or subcortical area of bilateral parietal or occipital lobe (60%), secondly at the deep basal ganglia and the superior sagittal sinus. The pathological process of cerebral lesions and the management of pregnancy induced hypertension were analysed.
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PMID:[Cerebral lesions in the severe pregnancy induced hypertension: 61 cases of X-ray computed tomography of the brain]. 824 45


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