Blood flow in hepatic sinusoids in experimental hemorrhagic shock in the rat

Koo, Anthony; Liang, I. Y. S.

doi:10.1016/0026-2862(77)90097-8

Cited by 36 publications

(6 citation statements)

References 21 publications

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“…In agreement with earlier studies (38,39), HS caused hepatic microcirculatory disturbances, i.e., resulted in a reduced V RBC and Q V . However, D S was similar after HS compared with sham shock, and the shock-induced reductions in sinusoidal flow were only moderate, despite the fact that ischemia/ reperfusion of the liver has been shown to result in increased hepatic expression of endothelin-1 (40), a potent vasoconstrictor in the hepatic microcirculation (29,41).…”

Section: Discussionsupporting

confidence: 80%

Protective role of endogenous carbon monoxide in hepatic microcirculatory dysfunction after hemorrhagic shock in rats.

Pannen¹,

Köhler²,

Hole³

et al. 1998

J. Clin. Invest.

158

113

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Maintenance of hepatic microcirculatory flow after ischemia of the liver is essential to prevent hepatic dysfunction. Thus, we determined the differential role of carbon monoxide (CO) and nitric oxide (NO) in the intrinsic control of sinusoidal perfusion, mitochondrial redox state, and bile production in the isolated perfused rat liver after hemorrhagic shock. Administration of tin protoporphyrin-IX (50 M), a specific inhibitor of the CO generating enzyme heme oxygenase, caused a decrease in sinusoidal flow that was more pronounced after shock compared with sham shock, as determined by in situ epifluorescence microscopy. This was associated with a shift in hepatocellular redox potential to a more reduced state (increased fluorescence intensity of reduced pyridine nucleotides in hepatocytes, decreased acetoacetate/ ␤ -hydroxybutyrate ratio in the perfusate) and a profound reduction in bile flow. In sharp contrast, the preferential inhibitor of the inducible isoform of NO synthase S-methylisothiourea sulfate (100 M) did not affect sinusoidal flow, hepatic redox state, or function. This indicates that 1.) endogenously generated CO preserves sinusoidal perfusion after hemorrhagic shock, 2.) protection of the hepatic microcirculation by CO may serve to limit shock-induced liver dysfunction, and 3.) in contrast to CO, inducible NO synthase-derived NO is of only minor importance for the intrinsic control of hepatic perfusion and function under these conditions. ( J. Clin Invest. 1998. 102:1220-1228.)

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Section: Discussionsupporting

confidence: 80%

Protective role of endogenous carbon monoxide in hepatic microcirculatory dysfunction after hemorrhagic shock in rats.

Pannen¹,

Köhler²,

Hole³

et al. 1998

J. Clin. Invest.

158

113

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show abstract

“…However, only few reports are available, analyzing the pathogenic mech anisms within the hepatic microcirculation during hypovolemia [1,2], sepsis [3], trans plantation [4,5] and ischemia-reperfusion [6][7][8][9], This might be due to the lack of ade quate experimental models allowing for in vivo observation of the hepatic microcircula tion. Several techniques have been described for the assessment of the hepatic microvascular perfusion, such as the hydrogen gas clear ance method [10,11], or laser Doppler flowmetry [12] as indirect methods, and intravital microscopy as a direct approach [13].…”

Section: Introductionmentioning

confidence: 99%

In vivo Fluorescence Microscopy for Quantitative Analysis of the Hepatic Microcirculation in Hamsters and Rats

Menger¹,

Marzi

Meßmer³

1991

Eur Surg Res

118

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Using intravital fluorescence microscopy and epi-illumination, the hepatic microcirculatory system of Syrian golden hamsters was analyzed, and the morphology and microhemodynamics were compared to those of rats. After contrast enhancement with 1 µmol/kg acridine orange i.v., the epi-illumination technique allows for visualization of capillary sinusoids and postsinusoidal venules, which are running in parallel with the liver surface, while afferent microvessels could be visualized in only few of the liver lobules investigated. In rat livers, the capillary sinusoids showed morphology similar to that of hamsters, however, postsinusoidal venules could frequently not be observed when applying epi-illumination, since these microvessels are piercing perpendicularly into the depth of the liver tissue. Microhemodynamic analysis, including the sinusoidal perfusion rate, sinusoidal red blood cell velocity and diameters, microvascular white blood cell (WBC) count and the phenomenon of WBC-endothelium interaction, as well as the hepatocellular uptake of the fluorescent compound acridine orange were found to be similar in hamsters as compared to rats. Although transillumination for in vivo microscopy may have the potential to visualize the complete hepatic microcirculatory system due to an increased focus depth, the epi-illumination technique has the advantage for quantitative assessment not only of the morphology of the hepatic microcirculatory system and microvascular blood perfusion, but also allows for evaluation of cellular phenomena within the hepatic microvessels, such as WBC accumulation, WBC-endothelium interaction, phagocytotic activity of Kupffer cells, and hepatocellular transport of fluorescent compounds. Hepatic microcircular disturbances, including accumulation of WBCs and WBC-endothelium interaction are causative in the development of organ failure in conditions such as hemorrhagic and septic shock, and, in particular, postischemic reperfusion injury following liver surgery and liver transplantation. Since accumulation of WBCs and their interaction with the microvascular endothelium are primarily found in postsinusoidal venules, in vivo microscopy of the hamster liver represents a favorable model for studies on cellular phenomena within the hepatic microcirculation.

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“…Although the number of cases with complicated postoperative courses was very small for these very reasons, the serum ALT level was significantly elevated, or the postoperative course was compromised, in two cases with very low mean hepatic SO, values, suggesting that hepatic SO, is possibly useful as a prognostic parameter. Previous reports suggest that the sinusoidal lining cells are the site most vulnerable to ischemia-reperfusion injury and that disturbed microcirculation is one of the main factors leading to subsequent hepatocellular damage [4,13,151. Our previous study showed that prolonged liver ischemia prevents redox recovery after reflow, especially in areas with the greatest concentration of hemoglobin [ll].…”

Section: Discussionmentioning

confidence: 99%

Intraoperative measurement of the graft oxygenation state in living related liver transplantation by near infrared spectroscopy

et al. 1995

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Graft oxygenation plays an important role in successful liver transplantation. Intraoperative changes in the oxygenation state of the liver graft were measured by near infrared spectroscopy in 28 cases of living related liver transplantation. Oxygen saturation of hemoglobin in the liver (hepatic SO2) changed from 81.2% +/- 1.5% (mean +/- SEM) before donation (in the donor) to 49.7% +/- 4.2% after portal reflow, to 58.4% +/- 5.0% after arterial reflow, and then to 71.4% +/- 3.9% before closure. Mean hepatic SO2 was positively correlated with portal flow rate as measured by duplex Doppler sonography. Cases with low portal flow rate showed a high coefficient of variation (SD/mean) of hepatic SO2, indicating heterogeneous tissue oxygenation. Though graft size was expected to affect the graft oxygenation state, hepatic SO2 was fairly independent of the graft-to-recipient weight ratio. In two cases with markedly low hepatic SO2, postoperative graft dysfunction occurred. This study suggest that the method of near infrared spectroscopy is reliable and useful for assessing the graft oxygenation state in liver transplantation.

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Blood flow in hepatic sinusoids in experimental hemorrhagic shock in the rat

Cited by 36 publications

References 21 publications

Protective role of endogenous carbon monoxide in hepatic microcirculatory dysfunction after hemorrhagic shock in rats.

Protective role of endogenous carbon monoxide in hepatic microcirculatory dysfunction after hemorrhagic shock in rats.

In vivo Fluorescence Microscopy for Quantitative Analysis of the Hepatic Microcirculation in Hamsters and Rats

Intraoperative measurement of the graft oxygenation state in living related liver transplantation by near infrared spectroscopy

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