Biomedical subjects

Ming Shu

Publications and source records attributed to Ming Shu.

6 recordsLinked to original sources

PubMed2005

[Establishment of a porcine model of acute hepatic failure by intraportal injection of D-galactosamine and lipopolysaccharide].

OBJECTIVE: To develop a clinically relevant porcine model of acute hepatic failure (AHF). METHODS: Twenty-two healthy pigs were randomly divided into 5 groups: group I (n = 3, intraportally administered with normal saline), group II [n = 5, intraportally administered with 1 microg/kg of lipopolysaccharide (LPS)], group III [n = 5, intraportally administered with 0.5 g/kg of D-galactosamine (D-Gal)], group IV (n = 6, intraportally administered with 0.5 g/kg of D-Gal plus 1 microg/kg LPS), and group V [n = 3, intraportally administered with 0.5 g/kg of D-Gal plus 1 microg/kg LPS and then receiving auxiliary partial orthotopic liver transplantation (APOLT)], Blood samples were collected to examine the arpartate transaminase (AST), total bilirubin, lactic acid, blood ammonia, prothrombin time (PT), blood sugar, and creatine at different time points. Autopsy was performed on the dead animals. Eight days after the APOLT laparotomy was performed again on the surviving pigs to take specimens of the original and transplanted liver to undergo pathological examination. RESULTS: All the pigs in the groups I and II survived with minimal changes in liver function tests. Two of the 5 pigs in the group III died (40%), 5 pigs in the group IV (5/6, 83%) died within 120 h, with a significant increase in aspartate transaminase 48 h after (4912 U/L +/- 759 U/L). In comparison with those of the group 1 and 2, the TBIL, blood ammonia, lactic acid, and PT 48 h after of the group 4 were all significantly higher and the blood sugar was significantly lower (all P < 0.05). Reversal of AHF in the pigs in the group V following APOLT was observed and the liver function returned near to normal level on the 7th postoperative day and regeneration of the native liver was confirmed histologically. CONCLUSION: The porcine model of AHF induced by a combination of D-gal (0.5 g/kg) and LPS (1 microg/kg) will be of much use in the development of APOLT for AHF.

Animals↗

PubMed2003

RV instantaneous intraventricular diastolic pressure and velocity distributions in normal and volume overload awake dog disease models.

Intraventricular diastolic right ventricular (RV) flow field dynamics were studied by functional imaging using three-dimensional (3D) real-time echocardiography with sonomicrometry and computational fluid dynamics in seven awake dogs at control with normal wall motion (NWM) and RV volume overload with diastolic paradoxical septal motion. Burgeoning flow cross section between inflow anulus and chamber walls induces a convective pressure rise, which represents a "convective deceleration load" (CDL). High spatiotemporal resolution dynamic pressure and velocity distributions of the intraventricular RV flow field revealed time-dependent, subtle interactions between intraventricular local acceleration and convective pressure gradients. During the E-wave upstroke, the total pressure gradient along intraventricular flow is the algebraic sum of a pressure decrease contributed by local acceleration and a pressure rise contributed by a convective deceleration that partially counterbalances the local acceleration gradient. This underlies the smallness of early diastolic intraventricular gradients. At peak volumetric inflow, local acceleration vanishes and the total adverse intraventricular gradient is convective. During the E-wave downstroke, the strongly adverse gradient embodies the streamwise pressure augmentations from both local and convective decelerations. It induces flow separation and large-scale vortical motions, stronger in NWM. Their dynamic corollaries on intraventricular pressure and velocity distributions were ascertained. In the NWM pattern, the strong ring-like vortex surrounding the central core encroaches on the area available for flow toward the apex. This results in higher linear velocities later in the downstroke of the E wave than at peak inflow rate. The augmentation of CDL by ventriculoannular disproportion may contribute to E wave and E-to-A ratio depression with chamber dilatation.

Animals↗

PubMed2003

Diastolic right ventricular filling vortex in normal and volume overload states.

Functional imaging computational fluid dynamics simulations of right ventricular (RV) inflow fields were obtained by comprehensive software using individual animal-specific dynamic imaging data input from three-dimensional (3-D) real-time echocardiography (RT3D) on a CRAY T-90 supercomputer. Chronically instrumented, lightly sedated awake dogs (n = 7) with normal wall motion (NWM) at control and normal or diastolic paradoxical septal motion (PSM) during RV volume overload were investigated. Up to the E-wave peak, instantaneous inflow streamlines extended from the tricuspid orifice to the RV endocardial surface in an expanding fanlike pattern. During the descending limb of the E-wave, large-scale (macroscopic or global) vortical motions ensued within the filling RV chamber. Both at control and during RV volume overload (with or without PSM), blood streams rolled up from regions near the walls toward the base. The extent and strength of the ring vortex surrounding the main stream were reduced with chamber dilatation. A hypothesis is proposed for a facilitatory role of the diastolic vortex for ventricular filling. The filling vortex supports filling by shunting inflow kinetic energy, which would otherwise contribute to an inflow-impeding convective pressure rise between inflow orifice and the large endocardial surface of the expanding chamber, into the rotational kinetic energy of the vortical motion that is destined to be dissipated as heat. The basic information presented should improve application and interpretation of noninvasive (Doppler color flow mapping, velocity-encoded cine magnetic resonance imaging, etc.) diastolic diagnostic studies and lead to improved understanding and recognition of subtle, flow-associated abnormalities in ventricular dilatation and remodeling.

Animals↗

PubMed2002

RV functional imaging: 3-D echo-derived dynamic geometry and flow field simulations.

We describe a novel functional imaging approach for quantitative analysis of right ventricular (RV) blood flow patterns in specific experimental animals (or humans) using real-time, three-dimensional (3-D) echocardiography (RT3D). The method is independent of the digital imaging modality used. It comprises three parts. First, a semiautomated segmentation aided by intraluminal contrast medium locates the RV endocardial surface. Second, a geometric scheme for dynamic RV chamber reconstruction applies a time interpolation procedure to the RT3D data to quantify wall geometry and motion at 400 Hz. A volumetric prism method validated the dynamic geometric reconstruction against simultaneous sonomicrometric canine measurements. Finally, the RV endocardial border motion information is used for mesh generation on a computational fluid dynamics solver to simulate development of the early RV diastolic inflow field. Boundary conditions (tessellated endocardial surface nodal velocities) for the solver are directly derived from the endocardial geometry and motion information. The new functional imaging approach may yield important kinematic information on the distribution of instantaneous velocities in the RV diastolic flow field of specific normal or diseased hearts.

Animals↗

PubMed2002

Right ventricular diastolic relaxation in conscious dog models of pressure overload, volume overload, and ischemia.

OBJECTIVE: Limitations in clinical understanding of right ventricular relaxation can be attributed to the paucity of information from basic studies in animal models of right ventricular disease. This study examined, in the conscious state, right ventricular relaxation dynamics under normal conditions (n = 15) and in subacute (2-5 weeks) canine models of right ventricular pressure overload (n = 6), volume overload (n = 7), and free wall ischemia (n = 7). METHODS: Right-heart micromanometric measurements were obtained by using multisensor catheters. A new algorithm was developed to obtain representative ensemble averages of hemodynamic waveform data sets. Right ventricular relaxation was analyzed by using an exponential model with 3 parameters: P(0), tau, and P(b). Significant changes versus control values were determined by means of analysis of variance and the Student unpaired t test with Bonferroni's adjustment. RESULTS: In the state of pressure overload, right ventricular pressure decay exhibits an increased P(0) (56.2 +/- 19.1 vs 13.1 +/- 5.1 mm Hg [mean +/- SD]) and prolonged tau (57.1 +/- 2.8 vs 27.8 +/- 3.9 ms); there is also a decreased P(b) (-7.9 +/- 1.5 vs 0.28 +/- 1.8 mm Hg). The only significant change in volume overload is an increased asymptote, P(b) (5.3 +/- 2.9 mm Hg). In right ventricular ischemia, prolongation of tau (41.4 +/- 13.0 ms) and decreased P(b) (-1.95 +/- 1.1 mm Hg) attain high significance. CONCLUSIONS: Distinctive abnormalities in right ventricular relaxation dynamics accompany pressure overload, volume overload, and ischemia and may contribute to clinical right ventricular dysfunction.

Animals↗

PubMed2002

Right ventricular diastolic function in canine models of pressure overload, volume overload, and ischemia.

By limiting filling, abnormalities of right ventricular (RV) diastolic function may impair systolic function and affect adaptation to disease. To quantify diastolic RV pressure-volume relations and myocardial compliance (MC), a new sigmoidal model was developed. RV micromanometric and sonomicrometric data in alert dogs at control (n = 16) and under surgically induced subacute (2-5 wk) RV pressure overload (n = 6), volume overload (n = 7), and ischemia (n = 6) were analyzed. The conventional exponential model detected no changes from control in the passive filling pressure-volume (P(pf)-V) relations. The new sigmoidal model revealed significant quantifiable changes in P(pf)-V relations. Maximum RV MC (MC(max)), attained during early filling, is reduced from control in pressure overload (P = 0.0016), whereas filling pressure at maximum MC (P(MCmax)) is increased (P = 0.0001). End-diastolic RV MC increases significantly in volume overload (P = 0.0131), whereas end-diastolic pressure is unchanged. In ischemia, MC(max) is decreased (P = 0.0102), with no change in P(MCmax). We conclude that the sigmoidal model quantifies important changes in RV diastolic function in alert dog models of pressure overload, volume overload, and ischemia.

Animals↗