Blood volume, hemodynamic, and metabolic changes in hemorrhagic shock in normal and splenectomized dogs

Chien, Shu; Dellenback, RJ; Usami, Shunsuke; Burton, DA; Gustavson, PF; Magazinovic, V

doi:10.1152/ajplegacy.1973.225.4.866

Cited by 40 publications

(17 citation statements)

References 10 publications

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“…In dogs, in response to hemorrhage, the spleen serves as the blood reservoir and could compensate the hypotension by contracting and expelling the intrasplenic blood to the circulation (5). In the present study, however, splenectomy did not aggravate the antigen-induced hypotension.…”

Section: Discussioncontrasting

confidence: 58%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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August 22, 2007; doi:10.1152/ajpregu.00904.2006.-Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (Psa) from 92 Ϯ 2 to 39 Ϯ 3 (SE) mmHg but only slightly increased portal venous pressure (Ppv) from 6.4 Ϯ 0.1 cmH2O to the peak of 9.9 Ϯ 0.5 cmH2O at 3.5 min after antigen. Elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy, attenuated anaphylactic hypotension. Ligation of these arteries alone, but not partial hepatectomy (70%), similarly attenuated anaphylactic hypotension. In contrast, isolated sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction but, rather, substantial constriction in response to the anaphylaxisassociated platelet-activating factor, indicating that venoconstriction in mice in vivo may be induced by mediators released from extrahepatic tissues. These results suggest that splanchnic vascular beds are involved in BALB/c mouse anaphylactic hypotension. They presumably act as sources of chemical mediators to cause the anaphylaxisinduced portal hypertension, which induced splanchnic congestion, resulting in a decrease in circulating blood volume and, thus, systemic arterial hypotension. Mouse hepatic anaphylactic venoconstriction may be induced by factors outside the liver, but not by anaphylactic reaction within the liver. anaphylactic shock; hepatic circulation; portal hypertension; splanchnic congestion ANAPHYLACTIC HYPOTENSION appears to be caused primarily by a decrease in blood flow to the heart, because left ventricular function is relatively well preserved during anaphylactic shock (1, 2). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a decrease in effective circulating blood volume. The latter could be due to vasodilation with the peripheral pooling and increased vascular permeability with a shift of intravascular fluid to the extravascular space (1, 2).In canine experimental models of anaphylactic shock, an increase in resistance to venous return is important in the pathogenesis of circulatory collapse (27): increased venous resistance decreases venous return, with a resultant decrease in stroke volume and systemic arterial pressure. Indeed, eviscerated dogs did not develop anaphylactic shock (19). In addition, Enjeti et al. (9) reported that the severity of the anaphylactic shock could be decreased by occlusion of the descending aorta. In dogs, the anaphylaxis-induced increase in venous resistance is partly caused by constriction of the hepatic veins (27, 30), which induces pooling of blood in the liver, as well as in upstream splanchnic organs. In addition, we recently demonstrated that the liver and splanchnic vascular beds are involved in rat anaphylactic hypotension by showing that elimination of splanchnic ci...

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Section: Discussioncontrasting

confidence: 58%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The pulmonary and systemic vascular hindrances, parameters reflecting the contribution of geometric factors to PVR and SVR, were calculated by dividing mean PVR and mean SVR, respectively, with blood viscosity [20]. A change in vascular hindrance may be interpreted as an effect of acetazolamide and/or hypoxia on pulmonary remodelling or vasoconstriction/vasodilation.…”

Section: Measurements Of Blood Volumementioning

confidence: 99%

Acetazolamide and chronic hypoxia: effects on haemorheology and pulmonary haemodynamics

et al. 2012

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We tested the effect of acetazolamide on blood mechanical properties and pulmonary vascular resistance (PVR) during chronic hypoxia.Six groups of rats were either treated or not treated with acetazolamide (curative: treated after 10 days of hypoxic exposure; preventive: treated before hypoxic exposure with 40 mg?kg) and either exposed or not exposed to 3 weeks of hypoxia (at altitude .5,500 m). They were then used to assess the role of acetazolamide on pulmonary artery pressure, cardiac output, blood volume, haematological and haemorheological parameters.Chronic hypoxia increased haematocrit, blood viscosity and PVR, and decreased cardiac output. Acetazolamide treatment in hypoxic rats decreased haematocrit (curative by -10% and preventive by -11%), PVR (curative by -36% and preventive by -49%) and right ventricular hypertrophy (preventive -20%), and increased cardiac output (curative by +60% and preventive by +115%). Blood viscosity was significantly decreased after curative acetazolamide treatment (-16%) and was correlated with PVR (r50.87, p,0.05), suggesting that blood viscosity could influence pulmonary haemodynamics. The fall in pulmonary vascular hindrance (curative by -27% and preventive by -45%) after treatment suggests that acetazolamide could decrease pulmonary vessels remodelling under chronic hypoxia.The effect of acetazolamide is multifactorial by acting on erythropoiesis, pulmonary circulation, haemorheological properties and cardiac output, and could represent a pertinent treatment of chronic mountain sickness.

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“…However, like Chien et al [6], the present authors believe,that hypovolaemic stress models would be more usefully related to actual states Of quantified hypovolaemia, the rate and degree obtained being recorded. As catecholamine release dominates the response observed in hypovolaemic stress and has been shown to be correlated to rates of bleeding or developing hypovolaemia [5], the logic of approaching the process of interpreting results obtained from hypovolaemic stress with residual BV data is overwhelming and practical.…”

Section: Discussionmentioning

confidence: 62%

“…The purpose of these investigations was to compare the double isotope dilution technique (]25IHSA and 51Cr RBC) with the simple haematocrit determination [1,6,14] for the estimation of BV haemorrhage.…”

Section: Introductionmentioning

confidence: 99%

Comparison of isotope dilution technique and haematocrit determination for blood volume estimation in rats subjected to haemorrhage

1984

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The method of posthaemorrhagic blood volume (BV) determination by simple haematocrit measurement has been compared with the conventional isotope dilution technique. 51Cr tagged erythrocytes and 125IHSA were used to estimate RBC volume and plasma volume in non-starved male Sprague-Dawley rats. Two series of experiments were carried out by two different investigatory groups. Haemorrhage was inflicted by 60 or 90 min of haemorrhagic hypotension at 70 mm Hg, causing 41% and 56% loss of the initial estimated BVs, respectively. There was agreement in both series for the initial blood volume indices; RBC volume, 2.82 ml x 100 g-1 b.wt.; plasma volume 3.33 ml x 100 g-1 b.wt. and F cells, 0.91. Using the RBC volume data, the calculated residual BVs after haemorrhage corresponded accurately to the isotope measurements in both series. It is concluded that non-splenectomized rats may be used for accurate BV analysis after haemorrhage if the basal data for the strain used are known.

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Blood volume, hemodynamic, and metabolic changes in hemorrhagic shock in normal and splenectomized dogs

Abstract: Blood volume, hemodynamic, and metabolic changes in hemorrhagic shock in normal and splenectomized dogs. Am. J. Physiol. 225(4): 866-879. 1973.-Normal and splenectomized beagles were subjected to 3 hr of oligemic hypotension.

Cited by 40 publications

References 10 publications

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Acetazolamide and chronic hypoxia: effects on haemorheology and pulmonary haemodynamics

Comparison of isotope dilution technique and haematocrit determination for blood volume estimation in rats subjected to haemorrhage

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