scholarly journals THE PROBLEM OF POSTOPERATIVE COGNITIVE DYSFUNCTION IN PATIENTS WITH OBESITY IN EMERGENCY SURGERY

Author(s):  
Maisuradze Alla

The occurrence of postoperative cognitive dysfunction is a negative consequence of vascular endothelial dysfunction in patients with grade I-II obesity with appropriate metabolic shifts and comorbid background, which increases the duration of treatment and worsens the prognosis in patients with acute surgical pathology. It is important to add endothelioprotectors to the intensive care unit. L-arginine hydrochloride has been shown to be pathogenetically justified as a prophylaxis for an increase in the level of antigens to von Willebrand factor in the blood of obese patients with acute surgical pathology. Administration of this substance before and during surgery is likely to improve mental performance in the postoperative period in patients with elevated body mass index, who underwent emergency cholecystectomy.

1987 ◽  
Vol 133 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Jan Hendrik Reinders ◽  
Richard C. Vervoorn ◽  
Cornelis L. Verweij ◽  
Jan A. Van Mourik ◽  
Philip G. De Groot

Angiology ◽  
2011 ◽  
Vol 63 (3) ◽  
pp. 194-198 ◽  
Author(s):  
Velore J. Karthikeyan ◽  
Gregory Y. H. Lip ◽  
Sabah Baghdadi ◽  
Deirdre A. Lane ◽  
D. Gareth Beevers ◽  
...  

The pathophysiology of hypertension and preeclampsia involves angiogenesis and endothelial damage/dysfunction, as shown by abnormal growth factors (vascular endothelial growth factor [VEGF], and its receptor sFlt-1) and von Willebrand factor (vWf) in the plasma. Angiogenin and hemoxygenase are abnormal in hypertension and angiogenesis but data on pregnancy are scant. We hypothesized altered angiogenin and hemoxygenase in 38 hypertensive pregnant women (HTPW) compared to 38 normotensive pregnant women (NTPW) and 50 nonpregnant controls (NonPCs). Plasma markers were measured by enzyme-linked immunosorbent assay (ELISA). Hypertensive pregnant women had lower VEGF than NonPCs ( P < .01), vWf was raised in both pregnant groups ( P < .01), but sFlt-1 was no different. Both angiogenin and hemoxygenase were lower in NTPW compared to NonPCs (both p<0.02). In both pregnancy groups, angiogenin correlated with vWf ( r > .33, P < .05), but in NonPCs this was not significant ( r = .13, P = .367). These changes may reflect differences in endothelial cell physiology and pathology in the hypertension in pregnancy.


2021 ◽  
Vol 12 ◽  
Author(s):  
Bin Yu ◽  
Yao Yao ◽  
Xiaofeng Zhang ◽  
Ming Ruan ◽  
Zhennian Zhang ◽  
...  

Background:Ligusticum chuanxiong Hort (LCH) is a famous ethnomedicine in Asia known for its excellent output on stroke treatment, and borneol usually acts as an assistant for its reducing permeability of the blood–brain barrier (BBB) after stroke. Although their synergy against brain ischemia was verified in previous studies, the potential mechanism is still unknown.Methods: The research aimed to explore the exact synergic mechanisms between LCH and borneol on neurogenesis within the areas of the dentate gyrus and subventricular zone. After treating middle cerebral artery occlusion rats with LCH (0.1 g/kg) and/or borneol (0.08 g/kg), the neurological severity score, brain infarct ratio, Nissl staining, Evans blue permeability, BBB ultrastructure, and expressions of von Willebrand factor and tight junction–associated proteins were measured. Co-localizations of Nestin+/BrdU+ and doublecortin+/BrdU+, and expressions of neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP) were observed under a fluorescence microscope. Moreover, astrocyte polarization markers of complement component 3 and pentraxin 3, and relevant neurotrophins were also detected by immunoblotting.Results: Basically, LCH and borneol had different focuses, although both of them decreased infarct areas, and increased quantity of Nissl bodies and expression of brain-derived neurotrophic factor. LCH increased the neurological severity score, NeuN+ cells, and the ratios of Nestin+/BrdU+ and doublecortin+/BrdU+, and decreased GFAP+ cells and ciliary neurotrophic factor expression. Additionally, it regulated the expressions of complement component 3 and pentraxin 3 to transform astrocyte phenotypes. Borneol improved BBB ultrastructure and increased the expressions of von Willebrand factor, tight junction–associated proteins, vascular endothelial growth factor, and vascular endothelial growth factor receptor 2. Unexpectedly, their combined therapy showed more obvious regulations on the Nissl score, Evans blue permeability, doublecortin+/BrdU+, NeuN+ cells, brain-derived neurotrophic factor, and vascular endothelial growth factor than both of their monotherapies.Conclusions: The results indicated that LCH and borneol were complementary to each other in attenuating brain ischemia by and large. LCH mainly promoted neural stem cell proliferation, neurogenesis, and mature neuron preservation, which was probably related to the transformation of reactive astrocytes from A1 subtype to A2, while borneol preferred to maintain the integrity of the BBB, which provided neurogenesis with a homeostatic environment.


1995 ◽  
Vol 74 (06) ◽  
pp. 1573-1577 ◽  
Author(s):  
David B Gubler ◽  
Chad R Ahlstrom ◽  
Lihua Liu ◽  
Jin-Feng Zhou ◽  
Charles J Parker ◽  
...  

SummaryVascular endothelium regulates multiple aspects of platelet function through secretion of a variety of substances, including von Willebrand factor, nitric oxide, and prostacyclin (PGI2). The objective of this study was to determine whether procoagulant albumin (P-AI), a modified form of albumin present in normal human plasma could modulate endothelial cell secretion of these substances. P-AI did not affect constitutive secretion of von Willebrand factor or nitric oxide, but did increase PGI2 secretion in a time- and concentration-dependent manner. Pretreatment of endothelial cells with aspirin, or use of suramin, a broad- specificity inhibitor, prevented the response to P-AI. Prostaglandin H synthase-2 contributed to the P-AI-induced PGI2 secretion. These results indicate that in addition to inducing tissue factor activity and reducing protein C activation and fibrinolysis, P-AI also modulates vascular endothelial cell PGI2 secretion, and potentially, platelet function.


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