A Model for the Genesis of Arterial Pressure Mayer Waves from Heart Rate and Sympathetic Activity

Both theoretic models and cross-spectral analyses suggest that an oscillating sympathetic nervous outflow generates the low frequency arterial pressure fluctuations termed Mayer waves. Fluctuations in heart rate also have been suggested to relate closely to Mayer waves, but empiric models have not assessed the joint causative influences of hemt rate and sympathetic activity. Therefore, we constructed a model based simply upon the hemodynamic equation deriving from Ohm's Law. With this model, we determined time relations and relative contributions of heart rate and sympathetic activity to the genesis of arterial pressure Mayer waves. We assessed data from eight healthy young volunteers in the basal state and in a high sympathetic state known to produce concurrent increases in sympathetic nervous outflow and Mayer wave amplitude. We fit the Mayer waves (0.05-0.20 Hz) in mean arterial pressure by the weighted sum ofleading oscillations in heart rate and sympathetic nerve activity. This model of our data showed heart rate oscillations leading by 2-3.75 seconds were responsible for almost half of the variance in arterial pressure (basal R^2=0.435±0.140, high sympathetic R^2=0.438±0.180). Surprisingly, sympathetic activity (lead 0-5 seconds) contributed only modestly to the explained variance in Mayer waves during either sympathetic state (basal: ∆R^2=0.046±0.026; heightened: ∆R^2=0.085±0.036). Thus, it appears that heart rate oscillations contribute to Mayer waves in a simple linear fashion, whereas sympathetic fluctuations contribute little to Mayer waves in this way. Although these results do not exclude an important vascular sympathetic role, they do suggest that additional Ji1ctors, such as sympathetic transduction into vascular resistance, modulate its influence.Binda and Fred Shuman Foundation; National Institute on Aging (AG14376)

A Model for the Genesis of Arterial Pressure Mayer Waves from Heart Rate and Sympathetic Activity

Both theoretic models and cross-spectral analyses suggest that an oscillating sympathetic nervous outflow generates the low frequency arterial pressure fluctuations termed Mayer waves. Fluctuations in heart rate also have been suggested to relate closely to Mayer waves, but empiric models have not assessed the joint causative influences of hemt rate and sympathetic activity. Therefore, we constructed a model based simply upon the hemodynamic equation deriving from Ohm's Law. With this model, we determined time relations and relative contributions of heart rate and sympathetic activity to the genesis of arterial pressure Mayer waves. We assessed data from eight healthy young volunteers in the basal state and in a high sympathetic state known to produce concurrent increases in sympathetic nervous outflow and Mayer wave amplitude. We fit the Mayer waves (0.05-0.20 Hz) in mean arterial pressure by the weighted sum ofleading oscillations in heart rate and sympathetic nerve activity. This model of our data showed heart rate oscillations leading by 2-3.75 seconds were responsible for almost half of the variance in arterial pressure (basal R^2=0.435±0.140, high sympathetic R^2=0.438±0.180). Surprisingly, sympathetic activity (lead 0-5 seconds) contributed only modestly to the explained variance in Mayer waves during either sympathetic state (basal: ∆R^2=0.046±0.026; heightened: ∆R^2=0.085±0.036). Thus, it appears that heart rate oscillations contribute to Mayer waves in a simple linear fashion, whereas sympathetic fluctuations contribute little to Mayer waves in this way. Although these results do not exclude an important vascular sympathetic role, they do suggest that additional Ji1ctors, such as sympathetic transduction into vascular resistance, modulate its influence.Binda and Fred Shuman Foundation; National Institute on Aging (AG14376)

Urethral Defect in Setting of Recurrent Urethral Foreign Body Insertion.

We present a case of recurrent episodes of foreign body insertion into the urethra, ultimately resulting in urethral defect at the penoscrotal junction. We have decided against treating the urethral defect as it facilitates nonoperative retrieval of the urethral foreign bodies. We present our experience and rationale for the clinical management of this complex patient

Reversibility of the catalytic ketonization of carboxylic acids and of beta-keto acids decarboxylation

Decarboxylation of beta-keto acids in enzymatic and heterogeneous catalysis has been considered in the literature as an irreversible reaction due to a large positive entropy change. We report here experimental evidence for its reversibility in heterogeneous catalysis by solid metal oxide(s) surfaces. Ketones and carboxylic acids having 13C-labeled carbonyl group undergo 13C/12C exchange when heated in an autoclave in the presence of 12CO2 and ZrO2 catalyst. In the case of ketones, the carbonyl group exchange with CO2 serves as evidence for the reversibility of all steps of the catalytic mechanism of carboxylic acids ketonic decarboxylation, i.e. enolization, condensation, dehydration and decarboxylation