Postoperative Pain and Length of Stay Lowered by Use of Exparel in Immediate, Implant-Based Breast Reconstruction.

Background: Patients undergoing mastectomy and prosthetic breast reconstruction have significant acute postsurgical pain, routinely mandating inpatient hospitalization. Liposomal bupivacaine (LB) (Exparel; Pacira Pharmaceuticals, Inc., Parsippany, N.

The quality-of-life benefits of breast reconstruction do not diminish with age.

Background And Objectives: Older women rarely receive post-mastectomy breast reconstruction (PMBR). While there is a perception that PMBR is less beneficial in this age group, quality-of-life (QOL) data related to PMBR in older women remain scarce.

Methods: Women with AJCC stage 0-III breast cancer who underwent a mastectomy were surveyed.

Development of contractile dysfunction in rat heart failure: hierarchy of cellular events.

The cellular mechanisms underlying the development of congestive heart failure (HF) are not well understood. Accordingly, we studied myocardial function in isolated right ventricular trabeculae from rats in which HF was induced by left ventricular myocardial infarction (MI). Both early-stage (12 wk post-MI; E-pMI) and late, end-stage HF (28 wk post-Mi; L-pMI) were studied.

Left ventricular myofilament dysfunction in rat experimental hypertrophy and congestive heart failure.

It is currently unclear whether left ventricular (LV) myofilament function is depressed in experimental LV hypertrophy (LVH) or congestive heart failure (CHF). To address this issue, we studied pressure overload-induced LV hypertrophy (POLVH) and myocardial infarction-elicited congestive heart failure (MICHF) in rats. LV myocytes were isolated from control, POLVH, and MICHF hearts by mechanical homogenization, skinned with Triton, and attached to micropipettes that projected from a sensitive force transducer and high-speed motor.

Protein kinase C epsilon induces systolic cardiac failure marked by exhausted inotropic reserve and intact Frank-Starling mechanism.

Myofilament dysfunction is a common point of convergence for many forms of heart failure. Recently, we showed that cardiac overexpression of PKC epsilon initially depresses myofilament activity and then leads to a progression of changes characteristic of human heart failure. Here, we examined the effects of PKC epsilon on contractile reserve, Starling mechanism, and myofilament activation in this model of end-stage dilated cardiomyopathy.

Impact of beta-myosin heavy chain isoform expression on cross-bridge cycling kinetics.

Myosin heavy chain (MHC) isoforms alpha and beta have intrinsically different ATP hydrolysis activities (ATPase) and therefore cross-bridge cycling rates in solution. There is considerable evidence of altered MHC expression in rodent cardiac disease models; however, the effect of incremental beta-MHC expression over a wide range on the rate of high-strain, isometric cross-bridge cycling is yet to be ascertained. We treated male rats with 6-propyl-2-thiouracil (PTU; 0.

Depressed cardiac tension cost in experimental diabetes is due to altered myosin heavy chain isoform expression.

Cardiac disease in diabetes presents as impaired left ventricular contraction and relaxation; however, the mechanisms underlying contractile protein dysfunction during the progression of disease are unknown. Accordingly, we assessed Ca(2+)-dependent tension development and tension-dependent ATP consumption (tension cost) in a rat model early (6 wk) and late (12 wk) after the onset of diabetes (50 mg/kg iv streptozotocin) using mechanical force- and enzyme-coupled UV absorbance measurements. Myofilament Ca(2+) sensitivity and maximal tension were unchanged between groups at either time point.