Comparison of low-volume versus standard-volume left ventriculography.

Left ventriculography provides useful information about cardiac function, wall motion, and mitral regurgitation (MR). However, standard volumes of contrast agent frequently are associated with ventricular ectopy. This study compares the use of low-volume (Low-vol) ventriculography to standard volume (Std-vol) ventriculography. Left ventricular (LV) ejection fraction (EF), changes in LV end-diastolic pressure (LVEDP), the incidence of ectopy, and > 2+ MR were prospectively determined from the random order use of standard (15 mL/ second for 3 sec) and low-volume (15 mL/sec for 1 sec) contrast agents in 102 patients. Each patient served as his or her own control. Twenty-seven percent of the 204 ventriculograms were not interpretable due to ectopy. Ectopy > or = 3 beats was more common with Std-vol angiograms (41% vs. 14%, P < 0.001). Post-injection LVEDP increased from baseline after both Std-vol and Low-vol injections (P < 0.001). In patients for whom both angiograms could be interpreted (n = 58), no differences were noted between planimetered EFs (Low-vol = 61 +/- 20% vs. Std-vol = 62 +/- 20%, with r = 0.87; P < 0.001). A Bland-Altman test of agreement indicated a mean difference +/- 95% CI = -2 +/- 19%. Low-volume ventriculography reduces contrast load and ectopy while providing similar estimates of EF compared with standard volumes.

Hepatic apoptotic activity following transient normothermic inflow occlusion and reperfusion in the swine model.

Accelerated hepatic apoptosis was first described in portal vein-ligated livers but has since been reported in a variety of liver injuries. Because porto-prival states can induce apoptosis we sought to determine whether transient ischemic periods followed by reperfusion would trigger such cell death. The cytokines TNF-alpha and TGF-beta are known to facilitate apoptosis and are released in response to a number of stimuli including ischemia. We also investigated alterations in plasma and tissue levels of these cytokines which might lend support to their role in increased apoptotic activity following ischemia/reperfusion. Female pigs were used as the experimental model. Inflow occlusion of portal and hepatic arterial blood was performed to a portion of the swine liver directing the entire splanchnic flow to the remaining hepatic lobes for a period of 2 h. The livers were then reperfused and plasma and tissue samples taken for determination of apoptotic activity utilizing cell death immunoperoxidase staining of 3'-OH DNA ends generated by fragmentation and ELISA assay of histone-associated DNA fragments. Plasma and tissue levels of TNF-alpha and plasma levels of TGF-beta were determined by ELISA assay. An increase in apoptotic activity following reperfusion was seen at Day 2 and Day 4 compared to preischemic values by the cell death stain. The ELISA cell death assay showed an increase in apoptotic activity at 60 min, Day 2, and Day 4. Moreover, the ELISA cell death assay showed enhanced apoptotic activity in "hyperperfused" hepatic lobes compared to preischemic, or resting, liver. This was also observed when compared to sham-operated animals. Surprisingly, there was no detectable increase in plasma TNF-alpha or TGF-beta levels following ischemia/reperfusion, although homogenized liver TNF-alpha levels were increased at 60 min and Day 2 following reperfusion. We conclude that transient hepatic inflow occlusion followed by reperfusion can induce increased apoptotic activity in the swine model. Furthermore, increased apoptotic activity also occurs in the hyperperfused liver raising the possibility of a locally active factor or global hepatic expression of receptor activity in response to ischemia/reperfusion. This period of ischemia/reperfusion did not produce a detectable increase in circulating cytokine levels, and accelerated apoptosis could not be linked to heightened TNF-alpha or TGF-beta plasma activity. Higher tissue levels of TNF-alpha could reflect enhanced binding to TNF cell surface receptors or amplified receptor expression.