Hemodynamic effects of dobutamine in an intact animal model

1992 ◽  
Vol 20 (9) ◽  
pp. 1322-1329 ◽  
Author(s):  
DONALD D. VERNON ◽  
JEREMY S. GARRETT ◽  
WILLIAM BANNER ◽  
J. MICHAEL DEAN
Keyword(s):  
Animal Model ◽  
Intact Animal ◽  
Hemodynamic Effects

Hemodynamic Effects of Infusions of Epinephrine and Arterenol in Normal and Shocked Dogs

1957 ◽  
Vol 189 (2) ◽  
pp. 224-228 ◽  
Author(s):  
H. Duane Collier ◽  
Frederick H. Meyers ◽  
G. H. Schmitt
Keyword(s):  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Positive Inotropic Effect ◽  
Intact Animal ◽  
Species Difference ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Hemodynamic Effects ◽  
Dilution Technique ◽  
Isolated Hearts

Levarterenol and l-epinephrine were infused into dogs and the effect on cardiac output and other measurements derived by the dye dilution technique were observed. In contrast to epinephrine, arterenol decreased or left unchanged the cardiac output, suggesting that there is not a species difference between dog and man and that arterenol and epinephrine are qualitatively different in their cardiovascular effects. In previous studies which disagree with this conclusion arterenol was administered by a rapid intravenous injection. The changes in cardiac output correlated well with the changes in total peripheral resistance, and the rise in peripheral resistance induced by arterenol is suggested as the factor which in the intact animal modifies the positive inotropic effect of arterenol apparent in isolated hearts. Circulating plasma volume, intrathoracic blood volume and cardiac output also rose and fell together. No difference in response to the two agents was apparent between normal dogs and those in which cardiogenic shock had been induced.

Hemodynamic Effects of Connection to Continuous Renal Replacement Therapy in a Pediatric Animal Model

2018 ◽  
Vol 42 (6) ◽  
pp. 640-646 ◽  
Author(s):  
Sarah Nicole Fernández Lafever ◽  
Maria Jose Santiago ◽  
Jorge López ◽  
Rafael González ◽  
María José Solana ◽  
...  
Keyword(s):  
Animal Model ◽  
Renal Replacement Therapy ◽  
Continuous Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Hemodynamic Effects

scholarly journals Demonstration of endothelial adhesion of sickle cells in vivo: a distinct role for deformable sickle cell discocytes

Blood ◽  
1992 ◽  
Vol 79 (6) ◽  
pp. 1602-1611 ◽  
Author(s):  
ME Fabry ◽  
E Fine ◽  
V Rajanayagam ◽  
SM Factor ◽  
J Gore ◽  
...  
Keyword(s):  
Animal Model ◽  
Intact Animal ◽  
Ex Vivo ◽  
Sickle Cells ◽  
Endothelial Monolayers ◽  
Quantitative Studies ◽  
Tissue Edema ◽  
In Vivo Animal Model ◽  
Von Willebrand

Abstract Different morphologic and density classes of sickle cells (SS) may play distinct roles in the generation of vasoocclusion, explaining the complexity of this phenomena. The densest SS red blood cells (RBCs) (SS4) can induce vasoocculsion in ex vivo microcirculatory preparations as well as in an intact animal model. Previous studies of the interaction of SS deformable discocytes with endothelial monolayers or the rat ex vivo mesocecum preparation have shown adhesion that is desmopressin (dDAVP)-stimulated, von Willebrand factor (vWF)-mediated, and limited to the small venules. However, in vivo adhesion of SS RBCs to the endothelium has neither been demonstrated nor characterized; and, in particular, the relation of adhesion to vasoocclusion is unknown. Using an intact animal model that involves injecting saline- washed, density-defined SS RBCs into the femoral artery of a rat, we find that: (1) Quantitative studies of RBCs retained in the rat thigh using 99mTc-labeled RBCs and gamma camera imaging showed that dDAVP induces a threefold increase in retention of normal (AA) cells and deformable SS discocytes (SS2). (2) electron microscopy and Microfil injection show that the retention of SS2 cells is due to adhesion to the vascular endothelium with no evidence of obstruction. (3) H-1 magnetic resonance imaging showed that retention of SS4 cells induced a dose-dependent increase in tissue edema (presumable secondary to tissue hypoxia), while retention of AA or SS2 cells produced no change. We conclude that endothelial adhesion of deformable SS discocytes can be demonstrated in an in vivo animal model, that this adhesion is enhanced by dDAVP (presumably related to, but not necessarily limited to the release of vWF), and that this phenomenon per se does not lead to vasoocclusion. Nevertheless, adhesion of deformable SS discocytes may have consequences. We hypothesize that adhesion of SS discocytes could narrow the lumen of postcapillary venules and facilitate secondary trapping of SS4 cells and lead to subsequent vasoocclusion.

scholarly journals OP09.10: Hemodynamic effects of sildenafil administration in an animal model of preeclampsia

2011 ◽  
Vol 38 (S1) ◽  
pp. 83-83
Author(s):  
S. Herraiz ◽  
B. Pellicer ◽  
A. Pellicer ◽  
V. Serra
Keyword(s):  
Animal Model ◽  
Hemodynamic Effects

scholarly journals Airway Strain during Mechanical Ventilation in an Intact Animal Model

2007 ◽  
Vol 176 (8) ◽  
pp. 786-794 ◽  
Author(s):  
Scott E. Sinclair ◽  
Robert C. Molthen ◽  
Steve T. Haworth ◽  
Christopher A. Dawson ◽  
Christopher M. Waters
Keyword(s):  
Mechanical Ventilation ◽  
Animal Model ◽  
Intact Animal

Halothane and the Reperfusion Injury in the Intact Animal Model

1993 ◽  
Vol 76 (4) ◽  
pp. 734???744 ◽  
Author(s):  
Andr?? Coetzee ◽  
Johan Moolman
Keyword(s):  
Animal Model ◽  
Reperfusion Injury ◽  
Intact Animal

scholarly journals A Blood-Brain Barrier Disruption Model Eliminating the Hemodynamic Effect of Ketamine

2004 ◽  
Vol 31 (2) ◽  
pp. 248-253 ◽  
Author(s):  
David Fortin ◽  
Robert Adams ◽  
Ariane Gallez
Keyword(s):  
Animal Model ◽  
Carotid Artery ◽  
Blood Brain Barrier ◽  
Common Carotid Artery ◽  
Evans Blue ◽  
Infusion Rate ◽  
Hemodynamic Effects ◽  
Blood Brain Barrier Disruption ◽  
The Common ◽  
Brain Barrier Disruption

AbstractObjective:We propose a simple modification to an established blood-brain barrier disruption (BBBD) animal model that allows us to use ketamine/xylazine as the anaesthetic agent, therefore decreasing the complexity and the cost of the model, while maintaining similar efficiency.Methods:Sixty-two Long Evans rats were anaesthetized by intraperitoneal injection of ketamine/ xylazine. Osmotic BBBD was performed by administering 25% mannitol into the internal carotid artery in a retrograde fashion from the external carotid. The infusion rate of mannitol, as well as the duration was adjusted in a stepwise fashion to identify optimal parameters for BBBD and minimize complications. As a supplementary step to previously reported models, a vascular clip was applied to the common carotid artery prior to the infusion of mannitol, therefore isolating our model system from the depressant hemodynamic effects of ketamine/xylazine. Evans blue dye was used to control for BBBD intensity.Results:Using this model at an initial infusion rate of 0.15 ml/sec, a significant incidence of brain hemorrhage (75%) and a death rate of 62.5% were observed. Decreasing the infusion rate in a stepwise fashion, 0.08 ml/sec was found to produce optimal BBBD, as demonstrated by Evans blue staining. At this rate, 6/7 animals depicted grade II staining, whereas one animal depicted grade IV.Conclusion:The application of a clip to the common carotid artery prior to mannitol infusion allowed us to isolate the cerebral circulation from the depressant hemodynamic effects of ketamine/xylazine. This supplementary step produced consistent and efficient BBBD in our animal model.

scholarly journals Demonstration of endothelial adhesion of sickle cells in vivo: a distinct role for deformable sickle cell discocytes

Blood ◽  
1992 ◽  
Vol 79 (6) ◽  
pp. 1602-1611 ◽  
Author(s):  
ME Fabry ◽  
E Fine ◽  
V Rajanayagam ◽  
SM Factor ◽  
J Gore ◽  
...  
Keyword(s):  
Animal Model ◽  
Intact Animal ◽  
Ex Vivo ◽  
Sickle Cells ◽  
Endothelial Monolayers ◽  
Quantitative Studies ◽  
Tissue Edema ◽  
In Vivo Animal Model ◽  
Von Willebrand

Different morphologic and density classes of sickle cells (SS) may play distinct roles in the generation of vasoocclusion, explaining the complexity of this phenomena. The densest SS red blood cells (RBCs) (SS4) can induce vasoocculsion in ex vivo microcirculatory preparations as well as in an intact animal model. Previous studies of the interaction of SS deformable discocytes with endothelial monolayers or the rat ex vivo mesocecum preparation have shown adhesion that is desmopressin (dDAVP)-stimulated, von Willebrand factor (vWF)-mediated, and limited to the small venules. However, in vivo adhesion of SS RBCs to the endothelium has neither been demonstrated nor characterized; and, in particular, the relation of adhesion to vasoocclusion is unknown. Using an intact animal model that involves injecting saline- washed, density-defined SS RBCs into the femoral artery of a rat, we find that: (1) Quantitative studies of RBCs retained in the rat thigh using 99mTc-labeled RBCs and gamma camera imaging showed that dDAVP induces a threefold increase in retention of normal (AA) cells and deformable SS discocytes (SS2). (2) electron microscopy and Microfil injection show that the retention of SS2 cells is due to adhesion to the vascular endothelium with no evidence of obstruction. (3) H-1 magnetic resonance imaging showed that retention of SS4 cells induced a dose-dependent increase in tissue edema (presumable secondary to tissue hypoxia), while retention of AA or SS2 cells produced no change. We conclude that endothelial adhesion of deformable SS discocytes can be demonstrated in an in vivo animal model, that this adhesion is enhanced by dDAVP (presumably related to, but not necessarily limited to the release of vWF), and that this phenomenon per se does not lead to vasoocclusion. Nevertheless, adhesion of deformable SS discocytes may have consequences. We hypothesize that adhesion of SS discocytes could narrow the lumen of postcapillary venules and facilitate secondary trapping of SS4 cells and lead to subsequent vasoocclusion.

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