American Federation for Aging Research

Aging underlies all the major causes of death and disability in humans. Over the past two decades, basic researchers have been remarkably successful in identifying the underlying processes of aging, and by modifying those processes have discovered multiple methods of extending life and preserving health in experimental laboratory animals. Although early work relied mostly on dietary or genetic interventions, recently a number of pharmaceutical treatments also appear to slow aging in the laboratory. These successes, combined with the demographic imperative of an aging globe, suggest that it is time to begin to translate these successes into human therapies that in principle could delay many or most diseases and debilitating conditions of later life. Symposium participants will present recent research illuminating the promise for human health. Dr. Austad will present a brief overview of the current state of basic aging research. Dr. Kaeberlein will describe how inhibition of a key biochemical network in mice has already been successfully used to dramatically improve health and how its use in dogs is preparing the stage for human trials. Dr. Kirkland will describe the remarkable health effects brought about by eliminating senescent cells in mice. Finally, Dr. Barzilai will outline the rationale and a specific research plan for the first drug trial in humans aimed at delaying aging.

Aging and disease may make the elderly patient with cardiac disease particularly susceptible to hypotension during spinal anesthesia.We studied 15 men, 59-80 y old, with histories of prior myocardial infarction (n = 9), congestive heart failure (n = 2), and/or stable myocardial ischemia (n = 11) given spinal anesthesia with 50 mg lidocaine in dextrose. Technetium-99m-labeled red blood cell imaging estimated left ventricular ejection fraction (EF) and changes in blood volume in the abdominal organs and legs. Arterial and pulmonary artery catheters provided hemodynamic measurements. Sensory block averaged T4 (range T1-10). Mean arterial pressure decreased 33% +/- 15% (SD) (P < 0.001), secondary to decreases in vascular resistance (SVR), -26% +/- 13% (P < 0.001) and cardiac output, -10% +/- 16% (P = 0.03). EF increased from 53% +/- 11% to 58% +/- 14% (P < 0.001) while left ventricular end-diastolic volume (LVEDV) decreased (-19% +/- 9%, P < 0.001). Blood volume increased in the legs (6% +/- 6%, P = 0.006), kidneys (10% +/- 9%, P < 0.001), and mesentery (7% +/- 5%, P 0.001) but not in the liver or spleen. Cardiac function was well maintained. We concluded that the primary mechanism of hypotension was a decrease in SVR, not cardiac output, despite the decrease in LVEDV. (Anesth Analg 1997;85:99-105)