Publications by authors named "Steven C Hempleman"

Background: Diabetes damages peripheral tissues; however, its effects on the lung are less known. Lung diffusing capacity (DLCO) is influenced by alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (VC), both of which are reduced in adults with type 1 diabetes (T1D).

Objective: We sought to determine if diabetes duration affects DLCO, DM, VC, and cardiac output (Q).

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Vertebrate carotid bodies and related structures (branchial arch oxygen chemoreceptors in fishes, carotid labyrinth in amphibians, chemoreceptors in the wall of the common carotid and its branches in birds) develop in embryos when neural crest cells, blood vessels, and nerve fibers from sympathetic and cranial nerve ganglia invade mesenchymal primordia in the wall of the 3rd branchial arch. This review focuses on literature published since the 1970s investigating similarities and differences in the embryological development of 3rd arch oxygen chemoreceptors, especially between mammals and birds, but also considering reptiles, amphibians and fishes.

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Respiratory chemoreceptors are neurons that detect PCO(2), PO(2), and/or pH in body fluids and provide sensory feedback for the control of breathing. They play a critical role in coupling pulmonary ventilation to metabolic demand in endothermic vertebrates. During birth in mammals and hatching in birds, the state change from placental or chorioallantoic gas exchange to pulmonary respiration makes acute demands on the neonatal lungs and ventilatory control system, including the respiratory chemoreceptors.

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Birds have rapidly responding respiratory chemoreceptors [intrapulmonary chemoreceptors (IPC)] that provide vagal sensory feedback about breathing pattern. IPC are exquisitely sensitive to CO(2) but are unaffected by hypoxia. IPC continue to respond to CO(2) during hypoxic and even anoxic conditions, suggesting that they may generate ATP needed for signal transduction anaerobically.

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Although avian intrapulmonary chemoreceptors (IPC) have been studied extensively in adults, the maturation of IPC CO(2) sensitivity during development is completely unknown. To begin investigating IPC development we asked two fundamental questions: (1) Are IPC capable of sensing CO(2) during early development, and, if so, how early? And, (2) does IPC CO(2) sensitivity during early development exhibit postnatal maturation compared to IPC discharge characteristics in adult ducks? We addressed these questions by recording from single IPC Anas platyrhynchos ducklings beginning approximately 6 h prior to internal pipping through 4 days of postnatal development. We then compared mean IPC discharge characteristics during early development with mean IPC activity from adult ducks greater than 12 weeks old.

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Intrapulmonary chemoreceptors (IPC) are carbon dioxide sensing neurons that innervate the lungs of birds, control breathing pattern, and are inhibited by halothane and intracellular acidosis. TASK and TREK are subfamilies of tandem-pore domain potassium leak channels, important in setting resting membrane potential, that are affected by volatile anesthetics and acidosis. We hypothesized that such channels might underlie signal transduction in IPC.

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Data indicate that avian intrapulmonary chemoreceptors (IPC) transduce CO2 stimuli by sensing the products of CO2 hydration, [H+] and [HCO3-]. The alphastat regulation hypothesis of physiological pH sensitivity suggests that proteins sense [H+] through changes in the ionization state of imidazole groups (alphaIm). To test whether imidazole is involved with IPC CO2 sensitivity, we administered diethyl pyrocarbonate (DEPC) intravenously while recording from IPC exposed to varying levels of inspired CO2.

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We measured ventilation (VI) and arterial blood gases in Pekin ducks during acclimatization to 3800 m altitude for 1-90 days. Four experimental series were conducted over 4 years using both natural altitude and a hypobaric chamber. PaCO2 decreased to 3.

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Intrapulmonary chemoreceptors (IPC) are neurons that sense tonic and phasic CO2 stimuli in the lungs of birds and diapsid reptiles. IPC are different from most other vertebrate respiratory CO2 receptors because: (1) they are stimulated by low PCO2 and inhibited by high PCO2, (2) they have extremely rapid response characteristics, (3) their CO2 sensitivity is nearly abolished by intracellular inhibitors of carbonic anhydrase, and (4) their CO2 sensitivity is strongly depressed by inhibiting Na+/H+ antiport exchange. Experimental evidence suggests that IPC respond to intracellular pH, not CO2 directly, and that intracellular pH and IPC discharge are determined by a kinetic balance between CO2 hydration/dehydration rates, transmembrane acid/base exchange rates, and intracellular buffering.

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Avian intrapulmonary chemoreceptors (IPC) are vagal respiratory afferents that are inhibited by high lung Pco(2) and excited by low lung Pco(2). Previous work suggests that increased CO(2) inhibits IPC by acidifying intracellular pH (pH(i)) and that pH(i) is determined by a kinetic balance between the rate of intracellular carbonic anhydrase-catalyzed CO(2) hydration/dehydration and transmembrane extrusion of acids and/or bases by various exchangers. Here, the role of amiloride-sensitive Na(+)/H(+) exchange (NHE) in the IPC CO(2) response was tested by recording single-unit action potentials from IPC in anesthetized ducks, Anas platyrhynchos.

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