Intravenous AICAR During Hyperinsulinemia Induces Systemic Hemodynamic Changes but Has No Local Metabolic Effect

2011 ◽  
Vol 51 (10) ◽  
pp. 1449-1458 ◽  
Author(s):  
Marlies Bosselaar ◽  
Paul Smits ◽  
Luc J. C. van Loon ◽  
Cees J. Tack
1999 ◽  
Vol 94 (6) ◽  
pp. 1632-1637 ◽  
Author(s):  
Roberto Cleva ◽  
Vincenzo Pugliese ◽  
Bruno Zilberstein ◽  
William Abrao Saad ◽  
Henrique Walter Pinotti ◽  
...  

2009 ◽  
Vol 11 (5) ◽  
pp. 271-276 ◽  
Author(s):  
Sebastião R. Ferreira-Filho ◽  
Anna Carolina C. R. Ferreira ◽  
Paulo C. Oliveira ◽  
Jorge F. M. Moreira ◽  
Eduardo C. Ribeiro ◽  
...  

PEDIATRICS ◽  
1982 ◽  
Vol 69 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Alan Hill ◽  
Jeffrey M. Perlman ◽  
Joseph J. Volpe

The relationship of pneumothorax to the occurrence of intraventricular hemorrhage (IVH) has been studied in the premature newborn. The major objective of the study was to determine whether the systemic hemodynamic changes that occur with pneumothorax are reflected in the cerebral circulation and whether these changes play a role in pathogenesis of IVH. Blood flow velocity was measured in the anterior cerebral arteries by a transcutaneous Doppler technique in nine infants who developed pneumothorax in the first 3 days of life. At the time of pneumothorax there was a marked increase in flow velocity, especially during diastole, and, with resolution of pneumothorax, flow velocity returned to normal levels over the ensuing hours. The changes in flow velocity correlated closely with systemic hemodynamic changes that occurred with pneumothorax, ie, an increase in mean systemic blood pressure, especially diastolic pressure. IVH, documented by serial ultrasound scans, was observed shortly after pneumothorax in the nine infants. The data thus demonstrate a marked increase in flow velocity in the cerebral circulation at the time of pneumothorax. This increase is of importance in the genesis of IVH as is suggested further by the occurrence of IVH soon after the cerebral hemodynamic changes.


Hepatology ◽  
1989 ◽  
Vol 9 (2) ◽  
pp. 269-273 ◽  
Author(s):  
Abraham Koshy ◽  
Catherine Girod ◽  
Samuel S. Lee ◽  
Antoine Hadengue ◽  
Raimondo Cerini ◽  
...  

2012 ◽  
Vol 17 (3) ◽  
pp. 110-115 ◽  
Author(s):  
Sebastião Rodrigues Ferreira-Filho ◽  
Anna Carolina de Castro Rodrigues Ferreira ◽  
Paulo César de Oliveira

Maturitas ◽  
1996 ◽  
Vol 27 ◽  
pp. 110
Author(s):  
L Lugones ◽  
J Alflet ◽  
A Belardo ◽  
M Tutzer ◽  
CR Galarza ◽  
...  

2002 ◽  
Vol 940 (1-2) ◽  
pp. 55-60 ◽  
Author(s):  
Pier Luigi Parmeggiani ◽  
Adele Azzaroni ◽  
Marcella Calasso

2018 ◽  
Vol 132 (12) ◽  
pp. 1341-1343
Author(s):  
Audrey Payancé ◽  
Pierre-Emmanuel Rautou

Data on the consequences of cirrhosis regression on portal hypertension and on splanchnic and systemic hemodynamic are scarce. Previous studies have reported a decrease in hepatic venous pressure gradient following antiviral treatment in patients with hepatitis B or C related cirrhosis. However, these studies did not investigate splanchnic and systemic hemodynamic changes associated with virus control. To fill this gap in knowledge, in a recent issue of Clinical Science, Hsu et al. (vol. 132, issue 6, 669-683) used rat models of cirrhosis induced by thioacetamide and by bile duct ligation and provided a comprehensive analysis of the effects of cirrhosis regression on splanchnic and systemic hemodynamics. They observed a significant reduction in portal pressure accompanied by a normalization of systemic hemodynamic (normal cardiac index and systemic vascular resistance) and a decrease in intrahepatic vascular resistance. No change in extrahepatic vascular structures were observed despite normalization of collateral shunting, meaning that portosystemic collaterals persist but are not perfused. One intriguing part of their results is the only marginal effect of cirrhosis regression on liver hyperarterialisation. This result suggests that changes in splanchnic hemodynamic features induced by cirrhosis remain when hepatic vascular resistance decreases, raising the hypothesis of an autonomous mechanism persisting despite regression of intrahepatic vascular resistance. Microbiota changes and bacterial translocation might account for this effect. In conclusion cirrhosis regression normalizes systemic hemodynamics, but some splanchnic hemodynamic changes persist including extrahepatic angiogenesis and liver hyperarterialization.


2022 ◽  
Vol 8 (1) ◽  
pp. 154-159
Author(s):  
A. Subanova

A study was carried out of women with arterial hypotension against the background of the development of the pathological state of the fetus and newborns born to women living in two different climatic regions of Osh city and in the highlands of Chon-Alay district of Osh region. In the pathogenesis of pregnancy complications caused by arterial hypotension, the leading importance is attached to vascular disorders and microcirculation disorders, leading to systemic hemodynamic changes in the body of a pregnant woman. It was found that in mountainous terrain, arterial hypotension and exogenous hypoxia affect the “mother–placenta–fetus–newborn” system, increasing the load on the respiratory, circulatory and hematopoietic organs of the mother, and also leads to impaired placental function.


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