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B Hoop

Publications and source records attributed to B Hoop.

At least 19 recordsLinked to original sources
PubMed2000

Fluctuations and fractal noise in biological membranes.

Our understanding of cell structure and function derives from applications of a variety of physical and life science disciplines, methods and models to an important physiological process, namely, the exchange and transport of ions and molecules across biological membranes. We know that ion transport through membranes arises from a diversity of interrelated and interactive physical and chemical phenomena over a wide range of spatial and temporal scales. Among these phenomena common to all cellular structure and function include metabolism, kinetics of molecules, chemically mediated alteration of cell membrane electrical potential, membrane ion conductance, electrical signal propagation, and modulation by chemo- and mechanoreceptive mechanisms. This review focuses on the unique information contained in fluctuations in electrical properties associated with cell membrane ion transport.

Animals↗
PubMed1999

Brainstem amino acid neurotransmitters and hypoxic ventilatory response.

The ventilatory response to acute hypoxia in mammalian species is biphasic, an initial hyperventilatory response is followed by a reduction in ventilation within 2-3 min below the peak level (roll-off). Brain amino acid neurotransmitters also change during hypoxia. This study explores the role of neurotransmitters in anesthetized adult Sprague Dawley rats mechanically ventilated during 20 min of 10% O2 breathing. Phrenic nerve activity was recorded, and microdialysate concentrations of selected amino acids were determined at 3- to 5-min intervals in respiratory chemosensitive areas of the ventrolateral medulla (VMS) 1.25-2.00 mm below the surface. Phrenic nerve output was biphasic during hypoxia, concurrent with a rapid glutamate and gradual GABA increase. Taurine first decreased, then increased. In both intact and chemodenervated animals, time-dependent change in phrenic nerve activity during hypoxia was associated with corresponding changes in glutamate, GABA, and taurine concentrations, suggesting that cumulative effects of changes in the concentration of these three amino acids could account for response of the phrenic nerve to hypoxia.

Animals↗
PubMed1996

Quantitative high-resolution measurement of cerebrovascular physiology with slip-ring CT.

PURPOSE: To implement and validate spiral slip-ring CT for use in cerebrovascular studies. METHODS: Continuous data were acquired from an experimental, first-pass, iodine contrast, bolus study by unidirectional X-ray tube rotation, and images were reconstructed at 100-millisecond intervals. Functional maps of cerebral blood volume (CBV) and cerebral blood flow (CBF) were constructed with voxel-by-voxel gamma variate fitting. Reproducibility studies, different injection volumes and sites, and CO2 challenge were applied to verify the technique. RESULTS: Average absolute cortical gray and white matter and basal ganglia results were reproducible within +/- 0.8 ml/100 g for CBV and +/- 20 ml/100 g per minute for CBF, CBV response to changing arterial CO2 tension was significant only in cortical gray matter and basal ganglia; CBF response was significant in gray and white matter, as well as in the basal ganglia. CONCLUSION: Functional CT and constructed functional maps provide an optimal, high-resolution tool with which to visualize cerebrovascular parameters and their changes.

Animals↗
PubMed1992

Role of glutamate as the central neurotransmitter in the hypoxic ventilatory response.

Recent data suggest that the increase in ventilation during hypoxia may be related to the release of the excitatory amino acid neurotransmitter glutamate centrally. To further investigate this, we studied the effects of MK-801, a selective noncompetitive N-methyl-D-aspartate receptor antagonist, on the hypoxic ventilatory response in lightly anesthetized spontaneously breathing intact dogs. The cardiopulmonary effects of sequential ventriculocisternal perfusion (VCP) at the rate of 1 ml/min with mock cerebrospinal fluid (CSF, control) and MK-801 (2 mM) were compared during normoxia and 8 min of hypoxic challenge with 12% O2. Minute ventilation (VE), tidal volume (VT), and respiratory frequency (f) were recorded continuously, and hemodynamic parameters [heart rate (HR), blood pressure (MAP), cardiac output (CO), pulmonary arterial pressure, and pulmonary capillary wedge pressure] were measured periodically. Each dog served as its own baseline control before and after each period of sequential VCP under the two different O2 conditions. During 15 min of normoxia, there were no significant changes in the cardiopulmonary parameters with mock CSF VCP, whereas with MK-801 VCP for 15 min, VE decreased by approximately 27%, both by reductions in VT and f (17 and 9.5%, respectively). HR, MAP, and CO were unchanged. During 8 min of hypoxia with mock CSF VCP, VE increased by 171% associated with increased VT and f (25 and 125%, respectively). HR, MAP, and CO were likewise augmented. In contrast, the hypoxic response during MK-801 VCP was characterized by an increased VE of 84%, mainly by a rise in f by 83%, whereas the VT response was abolished. The cardiovascular excitation was also inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Brain glutamate metabolism during metabolic alkalosis and acidosis.

Glutamate modifies ventilation by altering neural excitability centrally. Metabolic acid-base perturbations may also alter cerebral glutamate metabolism locally and thus affect ventilation. Therefore, the effect of metabolic acid-base perturbations on central nervous system glutamate metabolism was studied in pentobarbital-anesthetized dogs under normal acid-base conditions and during isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid transfer rates of radiotracer [13N]ammonia and of [13N]glutamine synthesized de novo via the reaction glutamate+NH3-->glutamine in brain glia were measured during normal acid-base conditions and after 90 min of acute isocapnic metabolic alkalosis and acidosis. Cerebrospinal fluid [13N]ammonia and [13N]glutamine transfer rates decreased in metabolic acidosis. Maximal glial glutamine efflux rate jm equals 85.6 +/- 9.5 (SE) mumol.l-1 x min-1 in all animals. No difference in jm was observed in metabolic alkalosis or acidosis. Mean cerebral cortical glutamate concentration was significantly lower in acidosis [7.01 +/- 0.45 (SE) mumol/g brain tissue] and tended to be larger in alkalosis, compared with 7.97 +/- 0.89 mumol/g in normal acid-base conditions. There was a similar change in cerebral cortical gamma-aminobutyric acid concentration. Within the limits of the present method and measurements, the results suggest that acute metabolic acidosis but not alkalosis reduces glial glutamine efflux, corresponding to changes in cerebral cortical glutamate metabolism. These results suggest that glutamatergic mechanisms may contribute to central respiratory control in metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1991

Glutamic acid and gamma-aminobutyric acid neurotransmitters in central control of breathing.

We review recent cross-disciplinary experimental and theoretical investigations on metabolism of the amino acid neurotransmitters glutamic acid and gamma-aminobutyric acid (GABA) in the brain during hypoxia and hypercapnia and their possible role in central control of breathing. The roles of classical modifiers of central chemical drive to breathing (H+ and cholinergic mechanisms) are summarized. A brief perspective on the current widespread interest in GABA and glutamate in central control is given. The basic biochemistry of these amino acids and their roles in ammonia and bicarbonate metabolism are discussed. This review further addresses recent work on central respiratory effects of inhibitory GABA and excitatory glutamate. Current understanding of the sites and mechanisms of action of these amino acids on or near the ventral surface of the medulla is reviewed. We focus particularly on tracer kinetic investigations of glutamatergic and GABAergic mechanisms in hypoxia and hypercapnia and their possible role in the ventilatory response to hypoxia. We conclude with some speculative remarks on the critical importance of these investigations and suggest specific directions of research in central mechanisms of respiratory control.

Animals↗
PubMed1990

Brain glutamate metabolism during hypoxia and peripheral chemodenervation.

Glutamate stimulates resting ventilation by altering neural excitability centrally. Hypoxia increases central ventilatory drive through peripheral chemoreceptor stimulation and may also alter cerebral perfusion and glutamate metabolism locally. Therefore the effect of hypoxia and peripheral chemodenervation on cerebrospinal fluid (CSF) transfer rate of in vivo tracer amidated central nervous system glutamate was studied in intact and chemodenervated pentobarbital-anesthetized dogs during normoxia and after 1 h of hypoxia induced with 10 or 12% O2 in N2 breathing at constant expired ventilation and arterial CO2 tension. Chemodenervation was performed by bilateral sectioning of the carotid body nerves and cervical vagi. CSF transfer rates of radiotracer 13NH4+ and [13N]glutamine synthesized via the reaction, glutamate + NH4(+)----glutamine, in brain glia were measured during normoxia and after 1 h of hypoxia. At normoxia, maximal glial glutamine efflux rate jm = 103.3 +/- 11.2 (SE) mumol.l-1.min-1 in all animals. After 1 h of hypoxia in intact animals, jm = 78.4 +/- 10.0 mumol.l-1.min-1. In denervated animals, jm was decreased to 46.3 +/- 4.3 mumol.l-1.min-1. During hypoxia, mean cerebral cortical glutamate concentration was higher in denervated animals (9.98 +/- 1.43 mumol/g brain tissue) than in intact animals (7.63 +/- 1.82 mumol/g brain tissue) and corresponding medullary glutamate concentration tended to be higher in denervated animals. There were no differences between mean glutamine and gamma-aminobutyric acid concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Central respiratory effects of glutamine synthesis inhibition in dogs.

Glutamic acid is an excitatory neurotransmitter that may have a significant role in the central chemical drive of ventilation. Therefore cardiorespiratory function was measured in pentobarbital sodium-anesthetized dogs before and after central inhibition of glutamate metabolism by means of methionine sulfoximine (MSO), a specific inhibitor of glutamine synthase (GS) catalyzing amidation of glutamate to glutamine. GS was inhibited centrally by perfusing the ventriculocisternal space with artificial cerebrospinal fluid (CSF) containing 92.5 mmol MSO per liter at a fixed pH, perfusion rate, and pressure. After GS inhibition, CSF transfer rate of [13N]glutamine synthesized from 13NH4+ amidation of glutamate was reduced five-fold, and minute ventilation increased from 2.90 +/- 0.41 (SE) l/min (0.164 +/- 0.020 l.min-1.kg body wt-1) to 4.46 +/- 0.52 l/min (0.254 +/- 0.029 l.min-1.kg body wt-1). This increase in ventilation with endogenous glutamate and the increase in ventilation previously observed during ventriculocisternal perfusion of exogenous glutamate are compared quantitatively via a model of central neurotransmitter glutamate chemoreception. The results support the hypothesis that the endogenous brain glutamate is important in the central chemical drive of ventilation.

Animals↗
PubMed1987

Chloride flux from blood to CSF: inhibition by furosemide and bumetanide.

Movement of chloride from blood to cerebrospinal fluid (CSF) is one of the factors that may be involved in regulation of CSF [Cl-], which is important to CSF acid-base balance. We made quantitative measurements of the unidirectional flux of radiolabeled chloride between blood and CSF in anesthetized dogs, using 38Cl, a short-lived isotope (half-life 37.3 min). This allowed multiple studies to be performed in a given animal. A three-compartment model for the blood, CSF, brain extracellular fluid, and ventriculocisternal perfusion system was used to determine the flux rate. With normocapnia, the flux was 0.01.1 min-1. The influx could be reproducibly measured for three separate determinations in the same animal over a period of 6 h, being 98 +/- 6% of the control first run on the second run and 113 +/- 6% on the third. Furosemide and bumetanide, inhibitors of sodium-coupled chloride movement, lowered the flux to 43 +/- 3% and 55 +/- 6% of control, respectively. The combination of hypercapnia and furosemide lowered the influx to 63 +/- 9% of control. These results indicate that a major mechanism of chloride entry into CSF is sodium-coupled chloride transport.

Animals↗
PubMed1986

[A model of the central control of respiration].

Central respiratory drive is very much dependent upon the CO2-tension, the H+-content and the ionic composition of the blood and the extracellular fluid of the brain. Ventilation is linearly related in the steady state to the H+-content in the cerebrospinal fluid (CSF). Semiaquatic turtles are an excellent model to study central chemical control of ventilation, and in particular their tolerance to asphyxia. Their ability to maintain prolonged dives is seemingly incongruous with highly-developed mechanisms of central chemical control of ventilation. Experiments were performed on four groups of turtles subjected to two hours of either apneic dives, hypercapnia, anoxia or anoxia plus hypercapnia. One additional group was breathing room air and served as control. At the end of the two-hour period the animals were immediately decapitated and the heads instantly frozen in liquid nitrogen. Brain tissue was removed from the skull and free aminoacids were measured chromatographically. Gamma-aminobutyric acid (GABA) increased significantly in those animals subjected to anoxia (p less than 0.01). These results suggest that the central ventilatory drive during diving and related experimental conditions may be related to alterations in brain concentrations of aminoacid neurotransmitters. GABA is a potent inhibitor of respiratory responses which may function under physiologic and pathophysiologic circumstances to modify ventilatory drive. The role of taurine is not yet clear and has to be further investigated.

Acid-Base Equilibrium↗
PubMed1986

Central cardiorespiratory effects of glutamate in dogs.

Metabolism of certain amino acid neurotransmitters such as glutamate and gamma-aminobutyric acid (GABA) are closely linked in the brain to CO2 fixation and H+ metabolism. Additionally they may also affect central modulation of cardiorespiratory function. Therefore central cardiorespiratory effects of L-glutamate were determined in lightly anesthetized dogs using ventriculocisternal perfusion with artificial cerebrospinal fluid (CSF) (pH 7.25-7.28) containing 30 or 60 mM glutamate at a flow rate of 1.0 ml/min for 20 min followed by perfusion with artificial CSF alone. Tidal volume and minute ventilation increased with 60 mM glutamate, as did respiratory drive. These changes returned to normal with mock CSF perfusion. Glutamate (30 mM) had no significant effect on ventilation. At both concentrations, glutamate significantly increased mean femoral arterial pressure and mean pulmonary arterial pressure, which was accompanied by bradycardia. All these increases rapidly returned to normal with mock CSF perfusion. Cardiac output and pulmonary capillary wedge pressure did not change with glutamate perfusion. The results suggest that glutamate may have a significant central excitatory role in modulation of ventilatory drive as well as of hemodynamic functions.

Animals↗
PubMed1986

Effect of centrally administered gamma-aminobutyric acid on metabolic function.

gamma-Aminobutyric acid (GABA) content of the brain increases during hypoxia and hypercapnia and GABA by itself is a central ventilatory depressant and may depress metabolism as well. Therefore the effect of centrally administered GABA by ventriculocisternal perfusion on O2 consumption (VO2) and CO2 production (VCO2) was studied in pentobarbital-anesthetized dogs. GABA (30 mM) in mock cerebrospinal fluid (CSF) was perfused for 15 min at the rate of 1.0 ml/min followed by perfusion with mock CSF alone. Body temperature, perfusion pressure, and CSF pH were kept constant. Minute ventilation (VE) was kept constant mechanically. Under these conditions, VO2, VCO2, alveolar ventilation (VA), and relative pulmonary dead space volume (VD/VT) were measured. During perfusion with 30 mM GABA, mean VO2 (+/- SE) decreased from 96.5 +/- 3.3 to 81.9 +/- 5.1 ml/min, VCO2 from 72.1 +/- 3.8 to 60.7 +/- 3.0 ml/min, and VA from 1.7 +/- 0.1 to 1.3 +/- 0.1 l/min. VD/VT increased from 0.55 +/- 0.02 to 0.65 +/- 0.01. Perfusion with mock CSF alone restored these parameters to initial levels within 15 min. We conclude that centrally administered GABA depresses VO2 and VCO2. This reduction in metabolic function is independent of the central modulatory effects of GABA on respiration.

Acid-Base Equilibrium↗
PubMed1986

Reversible depression of ventilation and cardiovascular function by ventriculocisternal perfusion with gamma-aminobutyric acid in dogs.

Gamma-aminobutyric acid (GABA) is a putative central neurotransmitter that depresses respiratory neurons and has a metabolism in the brain that is tied to CO2 fixation and H+ metabolism. Therefore, the effect of 3 concentrations of GABA (10, 30, and 50 mM) in different groups of pentobarbital-anesthetized dogs was investigated by ventriculocisternal perfusion for 15 to 45 min. During multiple perfusion sequences, tidal volume (VT) and respiratory frequency were recorded continuously, whereas heart rate (HR), mean systemic arterial pressure (Psa), cardiac output, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure were monitored periodically. Minute ventilation decreased by a reduction in VT. The mean VT (+/- SEM) decreased after 15 min of GABA perfusion from 365.9 +/- 19.5 to 151.0 +/- 15.0 ml with 50 mM GABA in mock CSF, from 272.8 +/- 25.1 to 110.6 +/- 7.4 with 30 mM GABA, and from 223.6 +/- 22.3 to 155.3 +/- 21.8 with 10 mM GABA. A decrease in mean inspiratory flow was associated with the reduction in VT. The decrease in ventilation was associated with respiratory acidosis. At each GABA concentration, mean Psa decreased, whereas HR fell only with 50 mM. Other cardiovascular parameters did not change. Perfusion with mock CSF alone restored cardiorespiratory depression caused by GABA. Mean Psa fell with GABA whether ventilation was kept constant mechanically or not. These results support the hypothesis of a GABA-sensitive mechanism via a population of receptors that affect respiratory and cardiovascular function and are accessible by ventriculocisternal perfusion.

Animals↗