Search PubMed⌕ Search

Biomedical subjects

Neil S Cherniack

Publications and source records attributed to Neil S Cherniack.

11 recordsLinked to original sources
PubMed2004

Oxygen sensing: applications in humans.

Our concepts of oxygen sensing have been transformed over the years. We now appreciate that oxygen sensing is not a unique property limited to "chemoreceptors" but is a common property of tissues and that responses to changes in oxygen levels are not static but can change over time. Respiratory responses initiated at the carotid body are modified by the excitatory and depressant effects of hypoxia at the brain and on the pathways connecting the carotid body to the brain. Equally important is that we are beginning to use our understanding of the cellular and molecular pathways triggered by hypoxia and hyperoxia to identify therapeutic targets to treat diseases such as cancer. We also have a better understanding of the complexities of the human respiratory responses to hypoxia; however, major deficiencies remain in our ability to alter or even measure human ventilatory responses to oxygen deficiency.

Chemoreceptor Cells↗
PubMed2004

Inspiratory muscle weakness in diastolic dysfunction.

OBJECTIVES: To test the hypothesis that patients with well-documented diastolic dysfunction (DD) in the setting of normal systolic function will have inspiratory muscle weakness when compared to normal control subjects, and will experience dyspnea and tachypnea during exercise. BACKGROUND: Respiratory muscle weakness has been described in patients with (systolic) congestive heart failure; however, whether or not patients with DD may present with the findings of congestive heart failure is not known. METHODS: We selected for study 14 patients with DD previously referred for cardiopulmonary evaluation whose diagnosis had been confirmed by data obtained at cardiac catheterization. Seven control subjects matched for age, sex, and weight were recruited from the hospital community. Subjects performed both basic pulmonary function tests and tests of muscle strength: handgrip strength (Hgr), and maximal subatmospheric static inspiratory muscle pressure (Pimax). Subjects then performed a graded exercise test on a bicycle ergometer. Minute ventilation, oxygen consumption, carbon dioxide production, and heart rate were monitored continuously. Echocardiography was performed three times: before exercise, at a selected submaximal exercise level (20% of a predicted maximal workload), and at maximal exercise. Subjects rated their degree of dyspnea using the Borg scale at the same three time intervals. RESULTS: Pimax was - 102 +/- 17 cm H(2)O in control subjects, and - 77 +/- 19 cm H(2)O in patients with DD (p = 0.013) [mean +/- SD]. Hgr was similar between the groups. At the selected submaximal exercise level, patients with DD rated dyspnea to be 2.6 +/- 2.2 Borg scale units (control subjects, 0.5 +/- 0.8 Borg scale units). Hey plots described a rapid, shallow breathing pattern in patients with DD during exercise. Patients with DD and control subjects achieved similar maximal work loads. CONCLUSION: Patients with DD have diminished Pimax, adopt a rapid, shallow breathing pattern during exercise, and experience dyspnea at low work loads when compared to matched control subjects.

Aged↗
PubMed2002

Effects of neural drives on breathing in the awake state in humans.

We have developed a mathematical model of the regulation of ventilation that successfully simulates breathing in the awake as well as in sleeping states. In previous models, which were used to simulate Cheyne-Stokes breathing and respiration during sleep, the controller was only responsive to chemical stimuli, and allowed no ventilation at sub-normal carbon dioxide levels. The current model includes several new features. The chemical controller responds continuously to changes in P(CO(2)) with a lower sensitivity during hypocapnia than in the hypercapnic ranges. Hypoxia interacts multiplicatively with P(CO(2)) over the entire range of activity. The controller in the current model, besides the chemical drive, includes also a neural component. This neural drive increases and decreases as the level of alertness changes, and adds or subtracts from ventilation levels demanded by the chemical controller. The model also includes the effects of post-stimulus potentiation (PSP) and hypoxic ventilatory depression (HVD). While PSP eliminates apneas after a disturbance and also dampens the subsequent dynamics of the respiration, it is not a major factor in the damping of the response. Another finding is that HVD is destabilizing. The model is the first to reproduce results reported in conscious humans after hyperventilation and after acute and longer-term hypoxia. It also reproduces the effects of NREM sleep.

Arousal↗
PubMedDate not supplied

A glandular problem.

Explore the source record for details and available documents.

Diabetic Neuropathies↗