Physiological stress increases renal injury in eNOS-knockout mice.

African Americans have a fourfold greater likelihood of developing end-stage renal disease (ESRD) compared with Caucasians. It has been proposed that the increased prevalence may be explained by non-traditional factors such as environmental stress and psychosocial factors. In this study, we used infrequent running to exhaustion as a physiological stressor to mimic real life experiences, such walking up stairs when an elevator is malfunctioning or running to catch a bus, to study its effect on renal injury in a hypertensive mouse model (endothelial nitric oxide synthase-deficient mice; eNOS(-/-)).

Anesthesia for the patient with tracheal stenosis.

Tracheal stenosis may occur secondary to trauma, tumors, infection, inflammatory diseases, or iatrogenic causes. Understanding these lesions requires a basic understanding of the physics of airflow. All of these patients must be carefully evaluated and require a series of tests, including pulmonary function tests and radiographic studies.

The effect of salt on renal damage in eNOS-deficient mice.

African Americans have an increased incidence of end-stage renal disease and are characterized as having reduced bioavailability of nitric oxide and salt-sensitivity. We propose that endothelial nitric oxide synthase (eNOS) knockout mice (eNOS(-/-)) are a suitable model of hypertension-associated renal injury as seen in African Americans. Therefore, the purpose of this study was to determine whether older eNOS(-/-) mice have hypertension-associated renal injury and if dietary salt modulates this injury.

Perioperative beta-blocker and statin therapy.

Purpose Of Review: Perioperative beta-blockade and statin therapy have been advocated to reduce cardiac risk of noncardiac surgery. This review evaluates recent articles published on the cardioprotective effects of perioperative therapy with these medications.

Recent Findings: Initial studies evaluating beta-blocker therapy during the perioperative period suggested that beta-blockers may be beneficial in reducing cardiac deaths and myocardial infarctions.

Acute modulation of endothelial Akt/PKB activity alters nitric oxide-dependent vasomotor activity in vivo.

The serine/threonine protein kinase Akt (protein kinase B) phosphorylates endothelial cell nitric oxide synthase (eNOS) and enhances its ability to generate nitric oxide (NO). Because NO is an important regulator of vasomotor tone, we investigated whether Akt can regulate endothelium-dependent vasomotion in vivo using a rabbit femoral artery model of gene transfer. The endothelium of isolated femoral arteries was infected with replication-defective adenoviral constructs expressing beta-galactosidase, constitutively-active Akt (myr-Akt), or dominant-negative Akt (dn-Akt).