Biomedical subjects

W F Nolan

Publications and source records attributed to W F Nolan.

11 recordsLinked to original sources

PubMed1990

A problem-solving approach to teaching electrochemical driving force to undergraduates.

The diversity of students in the typical undergraduate general physiology course demands consideration of several important education objectives: the instructor seeks to provide students with a sound understanding of basic physiological concepts, sharpen their analytical skills, and demonstrate how universal physicochemical laws determine function within living systems. These objectives converge in a problem-solving approach to electrochemical driving force and ion flux across biological membranes.

Electrochemistry↗

PubMed1987

Effect of dopamine antagonism on carotid chemoreceptor interspike intervals.

As a means of examining the role of dopamine in chemotransduction, we examined the spike interval pattern from single carotid body chemoreceptors before and following dopamine antagonism. Before dopamine antagonism, chemoreceptor joint interval variability was less than the variability of the same spike interval series placed in shuffled order. This lower variability was abolished by dopamine antagonism with haloperidol. These data suggest that dopamine release reduces chemoreceptor interspike variability in vivo and that endogenous, local dopamine release is related to the activity level of a single chemoreceptor afferent.

Action Potentials↗

PubMed1986

Effect of hypocapnia on ventral medullary blood flow and pH during hypoxia in cats.

Ventral medullary blood flow was measured in 33 chloralose-urethan anesthetized cats during 60 min of isocapnia-hypoxia, mild hypocapnia-hypoxia, or severe hypocapnia-hypoxia. In an additional group of six animals we measured ventral medullary extracellular fluid (ECF) pH during mild hypocapnia-hypoxia. The increase in blood flow during hypoxia was reduced by mild hypocapnia and eliminated by severe hypocapnia. With the exception of an initial decrease in ECF [H+], which occurred during the first 10 min of mild hypocapnia-hypoxia, ECF [H+] increased progressively throughout the exposure and recovery periods and was significantly elevated from the control value by the first 10 min of the recovery period. The results suggest that hypocapnia affects the hypoxic cerebrovascular response of the ventral medulla and that this phenomenon could affect the regulation of ventral medullary ECF [H+].

Animals↗

PubMed1985

Haloperidol-induced suppression of carotid chemoreception in vitro.

Effects of antagonism of endogenous dopamine with haloperidol on single-unit frequency, interspike interval distribution, and interval serial dependency of the cat sinus nerve were tested using an in vitro carotid body-sinus nerve superfusion technique. A dose dependency of inhibition by haloperidol (0.05-2.0 microgram/ml) was observed. Superfusion with 1-2 microgram/ml haloperidol significantly reduced frequency within 5 min (P less than 0.05) and caused a complete cessation of firing within 25 min in 5 of 10 chemoreceptor units. Frequency recovered to control during drug washout. Acetylcholine (10-micrograms/ml superfusion or 500-micrograms bolus) increased sinus nerve activity under control conditions but not during superfusion with haloperidol. No effect of haloperidol on impulse serial dependency was detected. However, interval distribution was significantly altered by haloperidol in five of six chemoreceptor units. Our results suggest an excitatory role for dopamine in carotid chemoreception.

Action Potentials↗

PubMed1985

Interspike interval dependency from arterial chemoreceptors.

The carotid body impulse generator has been previously characterized as a Poisson-type random process. We examined the validity of this characterization by analyzing sinus nerve spike trains for interspike interval dependency. Fifteen single chemoreceptive afferents were recorded in vivo under hypoxic-hypercapnic conditions, and approximately 1,000 consecutive interspike intervals for each fiber were timed and analyzed for serial dependence. The same set of intervals placed in shuffled order served as a control series without serial dependence. The original spike interval trains showed significantly negative first-order serial correlation coefficients and less variability in joint interval distributions than did the shuffled interval trains. These results suggest that the chemoreceptor afferent train is not random and may reflect a negative feedback system operating within the carotid body that limits variation about a mean frequency.

Action Potentials↗

PubMed1984

beta-Adrenoceptor blockade spares chemoreceptor responsiveness to hypoxia.

The effect of beta-adrenoceptor blockade on the carotid body chemoreceptor response to hypoxia was assessed in anesthetized and paralyzed cats. Propranolol, atenolol and ICI 118,551 each abolished the enhancement of chemoreceptor activity produced by i.v. infusion of exogenous isoproterenol; however, the blocking drugs did not significantly diminish the increase in chemoreceptor neural discharge induced by hypoxia. These results do not support the hypothesis that beta-adrenergic receptors play an essential role in the chemoreceptor response to oxygen deprivation.

Animals↗

PubMed1984

Non-random chemoreceptor activity during superfusion in vitro.

As a means of probing the chemotransducer, impulse sequences from in vitro, superfused sinus nerve-carotid body preparations were analyzed for departures from randomness. Twelve of 17 spike trains showed interval histograms that did not differ significantly from exponential. Thus these sequences resembled a Poisson (random) process with respect to time-independence of probability of occurrence of an event. However, 5 spike trains departed significantly from the exponential distribution forcing rejection of the Poisson model in these cases. Furthermore, mean interval vs standard deviation analysis revealed a significant positive correlation among intervals. These data suggest that the carotid body impulse generator possesses an intrinsic regularity and that the Poisson model does not accurately describe the in vitro sinus nerve interspike interval sequence.

Action Potentials↗

PubMed1982

Effect of craniotomy on regional brain blood flow and ECF pH changes during isocapnic hypoxia.

Regional cerebrovascular responses to 30 min of isocapnic hypoxia were examined in anesthetized rabbits. In some of the animals, a left-side craniotomy was performed and cortical ECF pH was measured either 1 mm or 2-3 mm below the surface. In the animals with open cranium, the increase in blood flow during hypoxia was greater in the right cortex than in the left cortex. In animals with closed cranium, the increases in blood flow were equal in both right and left crania. ECF pH measured 1 mm below the cortical surface decreased throughout the entire 30 min of exposure, while pH measured 2-3 mm below the surface was increased for the first 6 min, after which it began to decrease. Our results indicate that craniotomy reduces the local vasodilation in response to hypoxia which in turn favors a decrease in local ECF pH.

Animals↗

PubMed1982

Ventral medullary extracellular fluid pH and blood flow during hypoxia.

Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

Animals↗

PubMed1982

Cerebral interstitial fluid acid-base status follows arterial acid-base perturbations.

Cerebral interstitial fluid (ISF) pH of ventral medulla or thalamus, cisternal cerebrospinal fluid (CSF) pH, and arterial blood pH, PCO2, and [HCO-3] were measured in chloralose-urethan-anesthetized, gallamine-paralyzed New Zealand White rabbits during 30-min episodes of either HCl or NaHCO3 intravenous infusions. ISF pH was measured continuously with glass microelectrodes (1- to 2-microns tip diameter). Cisternal CSF pH was measured continuously with an indwelling pH probe (1-mm tip diameter). Both ventral medullary and thalamic ISF [H+] changed significantly, whereas arterial PCO2 remained constant. CSF [H+] did not change. We conclude from these data that 1) changes in blood acid-base conditions are rapidly reflected in cerebral ISF and 2) transient differences in [H+] and [HCO-3] can exist between cerebral ISF and CSF.

Acidosis↗

PubMed1978

Thermally induced peripheral blood flow changes in chickens.

Changes in wattle blood flow (Q) and vascular resistance (R) were examined during both local heating of the wattle and/or general body heating of unanesthetized, male White Leghorn chickens. Q increased and R decreased during both local and general heating. Termination of heating reversed the response. Beta stimulation with isoproterenol markedly reduced R and increased Q in normothermic birds, suggesting the presence of beta receptors in the wattle vasculature. Alpha blockade with phenoxybenzamine also resulted in pronounced vasodilatation, suggesting tonic alpha-sympathetic tone in the wattle vasculature under normothermic conditions. Neither cholinergic blockade with atropine sulfate nor beta-adrenergic blockade with propranolol altered the vascular response to general heating when administered near its peak. Release of alpha-sympathetic tone is believed to subserve the response to general heating.

Acetylcholine↗