James A. Caccitolo

Impaired renal vascular endothelial function in vitro in experimental hypercholesterolemia

Hypercholesterolemia (HC) induces alterations in systemic vascular reactivity, which can manifest as an attenuated endothelium-dependent relaxation, partly consequent to an impairment in nitric oxide (NO) activity. To determine whether experimental HC has a similar effect on renal vascular function, renal artery segments obtained from pigs fed a HC (n=5) or normal (n=5) diet were studied in vitro. Endothelium-dependent relaxation was examined using increasing concentrations of acetylcholine (Ach), calcium ionophore A23187, and Ach following pre-incubation with N(G)-monomethyl-L-arginine or L-arginine (L-ARG). The NO-donor diethylamine (DEA) was used to examine smooth muscle relaxation response and cyclic GMP generation in endothelium-denuded vessels. The expression of endothelial NO synthase (eNOS) in the renal arteries was examined using Western blotting. Endothelium-dependent relaxation to Ach was significantly attenuated in the HC group compared to normal (53.3+/-9.1 vs. 98.8+/-3.7%, P<0.005), but normalized after pre-incubation with L-ARG (82.3+/-13.8%, P=0.21). Receptor-independent endothelium-dependent relaxation to A23187 was also significantly blunted in HC (75.2+/-10.5 vs. 115.5+/-4.2%, P<0. 017). Smooth muscle relaxation and cyclic GMP generation in response to DEA were greater in denuded HC vessels, while relaxation of intact vessels to nitroprusside was unaltered. In the HC vessels eNOS was almost undetectable. In conclusion, experimental HC attenuates in vitro endothelium-dependent relaxation of the porcine renal artery, possibly due to low bioavailability of NO. These vascular alterations in HC could play a role in the pathogenesis of renal disease or hypertension, supporting a role for HC as a risk factor for renovascular disease.

The current role of parathyroid cryopreservation and autotransplantation in parathyroid surgery: An institutional experience☆

BACKGROUND Hypoparathyroidism after cervical exploration is a rare but problematic complication. Cryopreservation and subsequent autotransplantation of parathyroid tissue are infrequently used to combat this problem; effective usage of this surgical adjunct remains variable. METHODS From 1981 through 1995 we performed 3080 cervical explorations for hyperparathyroidism. Cryopreservation was performed in 112 (3.6%) patients. This review evaluates our indications and usage of cryopreservation and autotransplantation and the eventual outcome after autotransplantation. RESULTS Of 81 women and 31 men, 106 (95%) had undergone previous exploration for hyperparathyroidism or thyroid disease. The primary indication for cryopreservation was uncertainty about the viability and number of remaining parathyroid glands. After operation 23 patients (20%) were permanently hypocalcemic and became autotransplantation candidates. Thirteen patients underwent a total of 15 autotransplantations (median postoperative interval, 7 months). Although 6 of 15 grafts (40%) were shown to secrete parathyroid hormone, only three patients (23%) were normocalcemic without supplemental therapy. CONCLUSIONS Cryopreservation with autotransplantation is in theory a sound but difficult practice to correct postexploration hypocalcemia. The principal indication for cryopreservation is the uncertainty regarding the status of remaining normal parathyroid tissue. Because we cannot predict postexploration hypocalcemia, cryopreservation plays a small but sometimes integral role in parathyroid surgery. Indications for cryopreservation in our practice are rare, and the rate of cryopreservation tissue usage is low.

Transmyocardial and Percutaneous Myocardial Revascularization: Current and Future Role in the Treatment of Coronary Artery Disease

Transmyocardial revascularization (TMR) is a new treatment modality under evaluation in patients with severely symptomatic, diffuse coronary artery disease, in whom the potential for medical or interventional management has been exhausted. Preliminary clinical trials show improved ischemic symptoms within the first 3 months in about 70% of TMR-treated patients. The original proposed mechanism of surgical or catheter-based TMR (percutaneous myocardial revascularization [PMR]) was that channels mediate direct blood flow between the left ventricular cavity and ischemic myocardium. However, several alternative explanations for the clinical success of TMR have recently been suggested, including improved perfusion by angiogenesis, an anesthetic effect by nerve destruction, and a potential placebo effect. This article reviews the clinical role of TMR/PMR, its possible pathophysiologic mechanisms, and its controversies. It provides an overview of the actual scientific and clinical status of TMR and details future directions.

WITHDRAWN: Erratum to “Impaired renal vascular endothelial function in vitro in experimental hypercholesterolemia” [ATH 154 (2001) 195–201]

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