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N S Cherniack

Publications and source records attributed to N S Cherniack.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Perceptual contributions to optimization of breathing.

Besides regulating the energetic cost of breathing, optimization of breathing may involve the alleviation of an uncomfortable breathing sensation. In this article, we consider perceptual contributions to the optimization of breathing. Just as the cost function proposed by Poon depends on ventilation and arterial PCO2 so does the sense of dyspnea. Consequently, we examined the relationship between breathing discomfort and Poon's cost function. Based on our model and psychophysical studies, it appears that breathing discomfort, which can integrate chemical and mechanical inputs to the respiratory controller, may not operate simply as an estimate of a cost function. We explain how our reflex control model can dynamically minimize a cost function such as Poon's. Also, we consider the influence of willful adjustments of ventilation on breathing discomfort. From this we infer that ventilatory optimization may emerge from automatic reflexes and behavioral responses that involve excitatory chemical and inhibitory neuromechanical feedbacks.

Dyspnea↗
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Effect of adenosine on chemosensory activity of the cat aortic body.

Adenosine, which is released during hypoxia, increases carotid chemoreceptor discharge. It is not known if adenosine also may stimulate the aortic chemoreceptors. The purpose of this study was to investigate if adenosine also can stimulate aortic chemoreceptors. The effect of adenosine (0.01, 0.1 and 1.0 mumol/kg) on aortic chemoreceptor discharge was studied in seven anesthetized, paralyzed and artificially ventilated adult cats. Intra-aortic injections of adenosine produced an increase in chemoreceptor discharge, which reached its peak between 10 and 20 s. The chemoreceptor augmentation increased with higher doses of adenosine. Adenosine also caused a fall in blood pressure. The increase of chemoreceptor discharge was not related to fall in arterial blood pressure. Since adenosine is released during hypoxia, it is suggested that part of the cardiovascular changes induced by hypoxia is due to stimulation of aortic chemoreceptors by adenosine.

Adenosine↗
PubMedDate not supplied

Substance P and mitochondrial oxygen consumption: evidence for a direct intracellular role for the peptide.

Substance P (SP), a member of the tachykinin group of peptides, has been shown to augment the sensory discharge of the carotid body, an oxygen sensing chemoreceptor. In this study we present evidence that the excitatory effect of SP, in part, could arise from a direct effect of the peptide on mitochondrial oxidative phosphorylation. Measurement of the partition coefficient of SP showed that the peptide has a relatively high apolar partition, which could be consistent with its distribution across lipid bilayers and in intracellular organelles. In addition, the effects of three concentrations of SP were tested on oxygen consumption of mitochondria isolated from rat hearts. The results showed that while the lower concentration of the peptide (0.5 microM) did not affect O2 consumption, higher concentrations, i.e., 1 and 2 microM, enhanced the rate of state 4 respiration by 52 and 64%, respectively. The rate of state 3 respiration, on the other hand, was unaltered with 0.5 and 1 microM, and was only slightly decreased with 2 microM of the peptide. The ADP:O ratio was unaffected by any concentrations of SP tested. The peptide-induced effect on state 4 respiration was even more pronounced with glutamate as a respiratory substrate and in presence of K+ in the medium. These results indicate that SP, in addition to its more accepted role as a neurotransmitter or modulator in the carotid body, may elicit intracellular response by interfering directly with oxidative phosphorylation.

Adenosine Diphosphate↗