Effects of ulinastation on rat renal energy metabolism and blood flow in hemorrhagic shock

1995 ◽  
Vol 9 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Masaaki Ueki ◽  
Satoshi Yokono ◽  
Kenji Ogli
Keyword(s):  
Blood Flow ◽  
Energy Metabolism ◽  
Hemorrhagic Shock ◽  
Renal Energy Metabolism

scholarly journals Visualization of three-dimensional microcirculation of rodents’ retina and choroid for studies of critical illness using optical coherence tomography angiography

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jang Ryul Park ◽  
ByungKun Lee ◽  
Min Ji Lee ◽  
Kyuseok Kim ◽  
Wang-Yuhl Oh
Keyword(s):  
Blood Flow ◽  
Optical Coherence Tomography ◽  
Severe Sepsis ◽  
Critical Illness ◽  
Hemorrhagic Shock ◽  
Optical Coherence Tomography Angiography ◽  
Flow Index ◽  
Optical Coherence ◽  
Sepsis Model ◽  
Lactate Levels

AbstractWe developed a method to measure the relative blood flow speed using optical coherence tomography angiography (OCTA) in retina and choroid, and investigated the feasibility of this method for assessing microcirculatory function in rat models of sepsis and hemorrhagic shock. Two sepsis models, 6-h severe sepsis without treatment and 30-h moderate sepsis maintaining mean arterial pressure, and volume controlled hemorrhagic shock and fluid resuscitation model were used to see the change of microcirculation. The blood flow index (BFI), which was calculated from the OCTA images to represent the average relative blood flow, was decreasing during the 6-h severe sepsis model. Its change is in parallel with the mean arterial blood pressure (MAP) and blood lactate levels. In the 30-h moderate sepsis model, the BFI was decreased while maintaining MAP, and lactate was increased. In the hemorrhagic shock model, the change of BFI is in line with MAP and lactate levels. In all models, BFI change is more sensitive in choroid than in retina. This study presents the OCTA-based retinal and choroidal microcirculatory blood flow monitoring method and shows its utility for assessment of critical illness.

Development of Renal Failure in Endotoxemic Rats: Can It Be Explained by Early Changes in Renal Energy Metabolism?

Nephron ◽  
1993 ◽  
Vol 65 (1) ◽  
pp. 88-94 ◽  
Author(s):  
A.A. van Lambalgen ◽  
A.A. van Kraats ◽  
G.C. van den Bos ◽  
T. Teerlink ◽  
H.V. Stel ◽  
...  
Keyword(s):  
Renal Failure ◽  
Energy Metabolism ◽  
Renal Energy Metabolism

Antiadrenergic and Antihistaminic Therapy in Hemorrhagic Shock in Dog and Rat

1956 ◽  
Vol 186 (1) ◽  
pp. 79-84 ◽  
Author(s):  
S. Jacob ◽  
Edward W. Friedman ◽  
Sabin Levenson ◽  
Philip Glotzer ◽  
H. A. Frank ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Blood Loss ◽  
Pressure Gradient ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Venous Pressure ◽  
Survival Period ◽  
Effect Of Treatment ◽  
Antihistaminic Drugs

The influence of pretreatment with dibenamine on the development and course of hemorrhagic shock, and the effect of treatment with dibenamine, rapidly acting antiadrenergic drugs, or antihistaminic drugs after hemorrhagic shock had been allowed to become unresponsive to replacement transfusion, were tested in dogs prepared in advance to permit measurement of portal-caval venous pressure gradient. Preliminary dibenamine administration was also tested in rats submitted to hemorrhagic shock. The conclusions were as follows: 1) The protective effect of dibenamine prior to the induction of hemorrhagic shock in the dog consists mainly of a reduction of the bleeding volume. Intrahepatic vasoconstriction is not reduced. A dog which is not under the influence of dibenamine can tolerate a greater degree of blood loss than a dibenaminized dog. After hemorrhagic shock has been allowed to become refractory to replacement transfusion, antiadrenergic and antihistaminic drugs do not reduce intrahepatic vasoconstriction or increase the survival period or the survival rate. 2) Dibenamine given prior to hemorrhage enables the rat to survive a degree of blood loss which is lethal to the untreated rat. This, in part, appears to be due to better blood flow to the respiratory center.

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