Normal red blood cell cardiac output in hyperkinetic syndrome of alcoholic cirrhosis

2001 ◽  
Vol 34 (0) ◽  
pp. 68
Author(s):  
S Moeller
2016 ◽  
Vol 120 (10) ◽  
pp. 1132-1140 ◽  
Author(s):  
Gonzalo Ferrara ◽  
Vanina Siham Kanoore Edul ◽  
Enrique Martins ◽  
Héctor Saúl Canales ◽  
Carlos Canullán ◽  
...  

The alterations in O2 extraction in hemodilution have been linked to fast red blood cell (RBC) velocity, which might affect the complete release of O2 from Hb. Fast RBC velocity might also explain the normal mucosal-arterial Pco2 (ΔPco2). Yet sublingual and intestinal microcirculation have not been completely characterized in extreme hemodilution. Our hypothesis was that the unchanged ΔPco2 in hemodilution depends on the preservation of villi microcirculation. For this purpose, pentobarbital-anesthetized and mechanically ventilated sheep were submitted to stepwise hemodilution ( n = 8), hemorrhage ( n = 8), or no intervention (sham, n = 8). In both hypoxic groups, equivalent reductions in O2 consumption (V̇o2) were targeted. Microcirculation was assessed by videomicroscopy, intestinal ΔPco2 by air tonometry, and V̇o2 by expired gases analysis. Although cardiac output and superior mesenteric flow increased in hemodilution, from the very first step (Hb = 5.0 g/dl), villi functional vascular density and RBC velocity decreased (21.7 ± 0.9 vs. 15.9 ± 1.0 mm/mm2 and 1,033 ± 75 vs. 850 ± 79 μm/s, P < 0.01). In the last stage (Hb = 1.2 g/dl), these variables were lower in hemodiution than in hemorrhage (11.1 ± 0.5 vs. 15.4 ± 0.9 mm/mm2 and 544 ± 26 vs. 686 ± 70 μm/s, P < 0.01), and were associated with lower intestinal fractional O2 extraction (0.61 ± 0.04 vs. 0.79 ± 0.02, P < 0.01) but preserved ΔPco2 (5 ± 2 vs. 25 ± 4 mmHg, P < 0.01). Therefore, alterations in O2 extraction in hemodilution seemed related to microvascular shunting, not to fast RBC velocity. The severe microvascular abnormalities suggest that normal ΔPco2 was not dependent on CO2 washout by the villi microcirculation. Increased perfusion in deeper intestinal layers might be an alternative explanation.


1977 ◽  
Vol 42 (3) ◽  
pp. 420-425 ◽  
Author(s):  
G. E. Tempel ◽  
X. J. Musacchia ◽  
S. B. Jones

Mechanisms underlying the elimination or marked depression of renal function in hibernation and hypothermia were investigated through measurements of blood pressure, heart rate, red blood cell and plasma volumes, and relative distribution of cardiac output. Hamsters (Mesocricetus auratus) were made hypothermic (rectal temperature (Tre), 7 degrees C) by exposure to helox and cold, or permitted to hibernate with several weeks of cold exposure (Ta approximately 5 degrees C). Mean arterial pressure, 120 Torr in normothermic control animals, demonstrated a 55% and 60% decrease during hibernation and hypothermia, respectively. As the animals rewarmed from hypothermia or aroused from hibernation, blood pressure increased rapidly at 8–12 degrees C, more gradually at 12–17 degrees C, and plateaued thereafter. Blood pressure rapidly returned to near control levels whereas heart rate remained at less than one-half control value at the highest temperature examined. Red blood cell volume, 26.2 +/- 0.6 ml/kg body wt in the control animals appeared unaffected by hypothermia. Plasma volume, by contrast, decreased from control values of 33.0 +/- 0.8 to 21.3 +/- 0.6 ml/kg body wt in hypothermia, a decrease of approximately 35%. Distribution of cardiac output to various organs in hibernation and hypothermia followed a similar pattern. Relative flow to the heart, lung, diaphragm, and brown fat increased while the fraction distributed to the visceral organs appeared to decrease. The normothermic control kidney received approximately 16% of the cardiac output while the hibernating and hypothermic kidneys received approximately 10% and 6%, respectively. The data are discussed in terms of the determinants of glomarular filtration rate and explain, in part, the elimination or marked reduction in renal function observed in depressed metabolic states.


2001 ◽  
Vol 34 (5) ◽  
pp. 782-783 ◽  
Author(s):  
Jens H Henriksen ◽  
Flemming Bendtsen ◽  
Søren Møller

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