Biomedical subjects

J F Green

Publications and source records attributed to J F Green.

At least 19 recordsLinked to original sources

PubMed1995

Influence of background vagal C-fiber activity on eupneic breathing pattern in anesthetized dogs.

In 19 dogs anesthetized with xylazine and alpha-chloralose, we examined the influence of background vagal C-fiber activity on the breathing pattern using a modified perineural capsaicin treatment. In seven dogs, we tested the efficacy of this treatment by recording compound action potentials before and after capsaicin application. In the remaining 12 dogs, we examined the effect of vagal perineural capsaicin on the Hering-Breuer expiratory facilitatory inflation reflex, pulmonary chemoreflex, and breathing pattern (tidal volume and expiratory and inspiratory times). Neither the peak height nor integral of the A wave of the compound action potential was significantly affected. However, the peak height and integral of the C wave of the compound action potential were significantly affected. However, the peak height and integral of the C wave of the compound action potential were significantly reduced. The myelinated fiber-initiated Hering-Breuer reflex remained intact after perineural capsaicin, but the C-fiber-initiated pulmonary chemoreflex was abolished. Perineural capsaicin increased tidal volume (0.399 +/- 0.031 to 0.498 +/- 0.058 liter; P < 0.05), expiratory time (3.62 +/- 0.31 to 4.82 +/- 0.68 s; P < 0.05), inspiratory time (1.49 +/- 0.12 to 1.72 +/- 0.17 s; P < 0.10) and total time per breath (5.11 +/- 1.08 to 6.54 +/- 0.82 s; P < 0.05). We conclude that background vagal C-fiber activity exerts an inhibitory effect on tidal volume and an excitatory effect on breathing frequency.

Action Potentials↗

PubMed1994

Pulmonary mechanics of dogs during transtracheal jet ventilation.

STUDY OBJECTIVE: To quantify the delivered tidal volume and other selected measurements of pulmonary mechanics in an animal model during transtracheal jet ventilation (TTJV), with comparison to positive-pressure mechanical ventilation (PPMV) and spontaneous breathing. DESIGN: Prospective, nonblinded laboratory animal study. INTERVENTIONS: Seven mongrel dogs weighing 24.5 +/- 3.7 kg were anesthetized, paralyzed, and placed within a specially designed volume plethysmograph with the head and neck externalized. Ventilation was performed using TTJV under variable inspiratory time:expiratory time ratios (TI:TE) (1:1, 1:2, 1:3, 1:4, 1.5:2.5, 2:1, 2:2, 3:1, and 4:1) and variable driving air pressures (40, 45, and 50 psi). The dogs then were ventilated with PPMV. Tidal volume, tracheal pressure, transpulmonary pressure, air flow, arterial pressure, central venous pressure, and arterial blood gases were measured during spontaneous ventilation, TTJV, and PPMV. Quasistatic compliance of the lungs was measured after all methods of ventilation. Statistical significance was accepted at P < .05. RESULTS: There was no significant difference between delivered tidal volume during TTJV (446 +/- 69 mL at a TI:TE of 1:3 and 45 psi) and spontaneous breathing (506 +/- 72 mL). TTJV delivered a tidal volume significantly higher than the standard 15 mL/kg volume used for mechanical ventilation in dogs. Tracheal pressure and transpulmonary pressure were not significantly different between TTJV and PPMV. Variations in TI:TE had no significant effect on most of the measured variables, specifically tidal volume or transpulmonary pressure. Minute ventilation increased significantly and PCO2 decreased significantly as frequency increased during TI:TE settings of 1:1, 1:2, and 2:1. Increases in the driving air pressure during TTJV significantly increased the tidal volume as it was raised from 40 psi to 50 psi. There was no change in quasistatic lung compliance during any method of ventilation. CONCLUSION: TTJV delivers an effective tidal volume comparable to both spontaneous breathing and PPMV in a dog model. In the absence of upper-airway obstruction, there was no significant difference in the pulmonary pressures, resistance, and compliance during TTJV, as compared to mechanical ventilation. Variation in TI:TE during TTJV had no major effect on pulmonary mechanics, except to increase minute ventilation and decrease PCO2 as the frequency was increased significantly. Increasing the driving air pressure to the TTJV apparatus significantly augmented delivered tidal volume due to increased air flow.

Animals↗

PubMed1994

Effects of graded upper-airway obstruction on pulmonary mechanics during transtracheal jet ventilation in dogs.

STUDY OBJECTIVE: To quantify the effects of graded upper-airway obstruction on the delivered tidal volume and selected parameters of pulmonary mechanics during transtracheal jet ventilation (TTJV) in a dog model. DESIGN: Laboratory study in which seven dogs were anesthetized, paralyzed, and placed within a volume plethysmograph with the head and neck externalized. INTERVENTIONS: Ventilation was performed using TTJV at 45 psi and a frequency of 15 beats per minute. The upper trachea was occluded progressively using a Foley catheter balloon to induce tracheal pressure levels of approximately 150%, 200%, 250%, and 300% of the tracheal pressure obtained during TTJV-c. Tidal volume, tracheal pressure, transpulmonary pressure, airflow, arterial blood pressure, central venous pressure, and arterial blood gases were measured during all conditions of ventilation. Quasistatic compliance curves of the lungs were measured at the conclusion of spontaneous breathing, TTJV-c, and TTJV (at all levels of obstruction). Minute ventilation and pulmonary flow resistance were calculated for each condition of ventilation. RESULTS: Application of graded upper-airway obstruction during TTJV yielded mean tracheal pressures of 130% (level 1), 190% (level 2), 220% (level 3), and 230% (level 4) of that obtained during TTJV-c (10.9 +/- 2.0 cm H2O). Tidal volume significantly increased with each level of obstruction except between levels 3 and 4 (spontaneous breathing, 506 +/- 72 mL; TTJV-c, 446 +/- 69 mL; level 1, 663 +/- 139 mL; level 2, 780 +/- 140 mL; level 3, 931 +/- 181 mL; and level 4, 944 +/- 135 mL). During TTJV at obstruction level 1, transpulmonary pressure was not significantly higher than either spontaneous breathing or TTJV-c, but did significantly increase during higher levels of obstruction. The mean arterial PCO2 significantly decreased at all levels of obstruction due to significantly increased minute ventilation, with a concomitant increase in arterial pH. There was no significant difference seen in the quasistatic compliance of the lungs among spontaneous breathing, TTJV-c, or TTJV at any level of upper airway obstruction. CONCLUSION: Partial upper-airway obstruction increases the delivered tidal volume, minute ventilation, and transpulmonary pressure of the lungs during TTJV, with consequent decreases in the arterial PCO2 as the amount of obstruction increases. No significant changes were seen in the quasistatic compliance of the lungs, pulmonary flow resistance, or alveolar:arterial gradient, lending support to the position that TTJV is a safe technique under conditions of partial upper-airway obstruction. However, due to significant increases in tidal volume and functional residual capacity and decreases in mean arterial blood pressure, concerns still exist during near-total or total upper-airway obstruction.

Airway Obstruction↗

PubMed1992

Plate and screw fixation of selected condylar fractures of the mandible.

The majority of condylar fractures can be treated with closed reduction and intermaxillary fixation. In this study, we examine the use of open reduction with plate and screw fixation for the treatment of condylar fractures. Fourteen patients with 18 subcondylar fractures underwent open reduction and fixation using miniplates (12 patients) and lag screws (two patients). Thirteen patients and 16 condylar fractures had adequate follow-up for analysis of results. The follow-up period ranged from 7 to 46 months with a mean of 24 months. Bony union was obtained in all fractures with no permanent facial nerve injuries and good mandibular opening (average of 45 mm). We conclude that condylar fractures can be opened and fixed with plates and screws with good results without the use of intermaxillary fixation. This technique can be an effective approach for the treatment of selected condylar fractures.

Adolescent↗

PubMed1992

Pulmonary C-fiber stimulation by capsaicin evokes reflex cholinergic bronchial vasodilation in sheep.

We investigated changes in bronchial blood flow (Qbr) associated with capsaicin-induced stimulation of pulmonary C-fibers in seven anesthetized and two unanesthetized sheep. A Doppler flow probe chronically implanted around the common bronchial artery provided a signal (delta F, kHz) linearly related to bronchial arterial blood velocity (Vbr, cm/s), which was proportional to Qbr. An index of bronchial vascular conductance (Cbr, in arbitrary units) was calculated as the ratio of Vbr to systemic arterial pressure (Pa). Right atrial injection of capsaicin evoked a prompt pulmonary chemoreflex (apnea, bradycardia, and hypotension), with immediate increases in Vbr (average +34%) and Cbr (+63%) that reached a maximum approximately 7 s after the injection. A second increase in Vbr, but not in Cbr, occurred approximately 12 s later, coinciding with an increase in Pa. Vagal cooling (0 degrees C) prevented the pulmonary chemoreflex; it also abolished the immediate increases in Vbr and Cbr in four of six sheep and substantially reduced them in two sheep; it did not affect the late increases in Vbr and Pa. Results after atropine indicated that the immediate increases in Vbr and Cbr were mainly cholinergic. In two sheep a small residual vasodilation survived combined cholinergic and adrenergic blockade and may have been due to peripheral release of neurokinins.

Animals↗

PubMed1991

Multireceptor activation of the pulmonary chemoreflex.

Schertel et al. (J. Appl. Physiol. 61: 1237-1240, 1984) reported that pulmonary C fibers initiate the prompt apnea followed by rapid shallow breathing evoked by pulmonary arterial injections of capsaicin. However, doubt has remained as to whether these changes in breathing pattern are induced exclusively by direct stimulation of pulmonary C fibers or whether secondary stimulation of slowly adapting pulmonary stretch receptors by capsaicin-induced reflex bronchoconstriction also contributes to the response. To determine the contribution of this secondary mechanism to changes in breathing pattern, we evoked the pulmonary chemoreflex in spontaneously breathing dogs before and after blockade of muscarinic receptors with atropine. Right atrial injections of capsaicin before the administration of atropine induced a classical pulmonary chemoreflex, i.e., apnea, hypotension, and bradycardia followed by rapid shallow breathing and bronchoconstriction. After atropine, all components of the pulmonary chemoreflex induced by right atrial injections of capsaicin remained intact except bronchoconstriction. However, the absolute magnitude of the change in each component of the reflex except apnea was significantly attenuated. We conclude that the classic pulmonary chemoreflex is a complex phenomenon initiated primarily by stimulation of pulmonary C fibers but significantly influenced by secondary stimulation of slowly adapting pulmonary stretch receptors.

Animals↗

PubMed1991

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog.

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Abdomen↗

PubMed1990

A theoretical description of arterial pressure-flow relationships with verification in the isolated hindlimb of the dog.

We developed and tested a new two-compartment serial model of the arterial vasculature which unifies the capacitance (downstream arterial compliance) and waterfall (constant downstream pressure load) theories of blood flow through the arteries. In this model, blood drains from an upstream compliance through a resistance into a downstream compliance which empties into the veins through a downstream resistance which terminates in a constant pressure load. Using transient arterial pressure data obtained from an isolated canine hindlimb preparation, we tested this model, using a stop-flow technique. Numerical parameter estimation techniques were used to estimate the physiologic parameters of the model. The downstream compliance was found to be more than ten times larger than the upstream compliance and the constant pressure load was significantly above venous pressures but decreased in response to vasodilation. Our results support the applicability of both the capacitance and waterfall theories.

Animals↗

PubMed1990

Pulmonary afferent control of breathing as end-expiratory lung volume decreases.

We studied reflex changes in breathing elicited by graded reductions in end-expiratory lung volume (EEVL) and the vagal nerves responsible. The chests of nine dogs anesthetized with alpha-chloralose were opened, and the lungs were ventilated by a phrenic nerve-driven servo-respirator. The immediate effects of a 50% reduction in end-expiratory transpulmonary pressure (EEPtp) from control (EEVL equivalent to functional residual capacity) were to significantly increase both tidal volume (VT) and breathing frequency (f) from 0.402 +/- 0.101 to 0.453 +/- 0.091 liter (mean +/- SD) and 11.8 +/- 5.4 to 15.7 +/- 6.4 breaths/min, respectively (P less than 0.05). Further reductions in EEPtp to 0 cmH2O did not change VT but augmented f to 19.6 +/- 6.6 breaths/min (P less than 0.05). The increase in f as EEVL decreased was due entirely to a reduction in expiratory time. Vagotomy abolished these reflexes. By 90 s after reduction in EEVL, arterial PCO2 fell significantly and VT returned to or below control values. We therefore repeated these experiments in five dogs whose blood gases were controlled by cardiopulmonary bypass. There were no secondary changes in VT and by 90 s breathing pattern could be characterized as rapid and deep. In another eight dogs submitted to the same collapse protocol, we recorded action potentials from all known categories of pulmonary vagal afferents. These studies demonstrated that the changes in breathing pattern induced by a 50% reduction in EEPtp were due to a withdrawal of slowly adapting stretch receptor activity; however, continued increases in f as EEVL was reduced further were due to increases in rapidly adapting stretch receptor activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1988

Effect of pulmonary arterial PCO2 on breathing pattern.

We studied breathing patterns and tidal volume (VT)-inspiratory time (TI) relationships at three steady-state levels of pulmonary arterial PCO2 (PpCO2) in 10 anesthetized dogs. To accomplish this we isolated and then separately pump perfused the pulmonary and systemic circulations, which allowed us to control blood gases in each circuit independently. To ventilate the lungs at a rate and depth determined by central drive, we used an electronically controlled positive-pressure ventilator driven by inspiratory phrenic neural activity. Expiratory time (TE) varied inversely with PpCO2 over the range of PpCO2 from approximately 20 to 80 Torr. VT and TI increased with rising PpCO2 over the range from approximately 20 to 45 Torr but did not change further as PpCO2 was raised above the middle level of approximately 45 Torr. Thus minute ventilation increased as a function of TE and VT as PpCO2 was increased over the lower range and increased solely as a function of TE as PpCO2 was increased over the upper range. The VT-TI relationship shifted leftward on the time axis as PpCO2 was lowered below the middle level but did not shift in the opposite direction as PpCO2 was raised above the middle level. In addition to its effect on breathing pattern, we found that pulmonary hypocapnia depressed inspiratory drive.

Animals↗

PubMed1987

Respiratory reflexes in the anesthetized miniature swine.

To assess the suitability of the miniature swine for studies of the control of breathing we evaluated the response of these animals to commonly used respiratory stimuli. Hanford miniature pigs were anesthetized with alpha chloralose and allowed to breathe spontaneously. Rapid lung inflations induced a prolonged expiratory pause proportional to load. Mechanical stimulation of the upper airways induced coughing. Central venous injections of C-fiber stimulants produced bradycardia, hypotension with apnea and/or rapid shallow breathing. CO2 rebreathing increased ventilation primarily through an increase in tidal volume; inspiratory time was not changed. Bilateral vagotomy caused a slower, deeper pattern of breathing, and significantly attenuated the ventilatory response to CO2; all other reflexes were abolished by vagotomy. Cooling the vagus nerves caused reversible blockade of the cough, inflation and C-fiber mediated reflexes in that order. We conclude that the pig can serve as a useful animal in which to study the control of breathing.

Anesthesia↗

PubMed1987

Effects of end-expired pressure on phrenic output in servo-ventilated dogs.

The pattern of breathing induced by increases in end-expired lung volume (EEVL) was determined in 9 anesthetized dogs. The pulmonary and systemic circulations were separately pump-perfused and the lungs were ventilated with a servo-ventilator actuated from the phrenic neurogram. EEVL was increased as a continuous ramp by slowly raising end-expired transpulmonary pressure from 1.5 to 12 cm H2O. Tidal volume (VT), inspiratory time (TI), and expiratory time (TE) were measured at vagal temperatures of 39 degrees C and 7 degrees C and following vagotomy. At a vagal temperature of 39 degrees C, increasing EEVL produced significant reductions in VT and TI while greatly prolonging TE. Vagal cooling to 7 degrees C, substantially altered the reflex response to increased EEVL. At 7 degrees C, VT decreased as EEVL increased, but the reduction was not so pronounced as at 39 degrees C. In addition, both TI and TE shortened. Increasing EEVL following vagotomy had no consistent effects on breathing pattern. We conclude that increasing EEVL stimulates tachypneic promoting pulmonary afferent nerves, most likely pulmonary C-fibers, but at normal vagal temperature their effect is masked by the stronger reflex inhibition of slowly adapting pulmonary stretch receptors.

Animals↗

PubMed1987

A phrenic nerve-actuated electronically controlled positive-pressure ventilator.

We have constructed an electronically controlled positive-pressure ventilator actuated by phrenic neural activity for use in open-chested or paralyzed experimental animals for the study of breathing pattern. A Bird Mark 14 positive-pressure ventilator was modified such that flow is a linear function of a command signal. Flow is delivered by advancing an air valve with a servo-motor that is controlled by one of three different operational modes. In two of the modes, the difference between the electronic average of inspiratory phrenic activity (moving average) and a feedback signal determines the inspiratory flow. The feedback signal is derived from either tracheal pressure or an electronic measure of inspired volume. In the third mode, the moving average is differentiated to provide control of inspiratory flow and volume. Physiological flow profiles were created using all three operational modes. Integration of an air-valve position signal provides an electronic measure of tidal volume. An additional feature of this ventilator allows inspiratory flow and duration to be predetermined for a given breath.

Animals↗

PubMed1986

Effect of pulmonary arterial PCO2 on slowly adapting pulmonary stretch receptors.

We recorded pulmonary stretch receptor (PSR) activity in anesthetized dogs and examined the effect of varying pulmonary arterial PCO2 (PpCO2) in both the naturally perfused and vascularly isolated pulmonary circulations while ventilating the lungs with room air. Steady-state increases in PpCO2 from approximately 25 to 50 Torr and from 50 to 70 Torr decreased PSR activity (impulses/ventilatory cycle) by 15 and 9%, respectively (P less than 0.001). Rapid increases in PpCO2 from approximately 50 to 80 Torr in a right-heart bypass preparation (with pulmonary blood flow constant) decreased PSR activity by 27%. Depression of firing, which was proportionately greater in deflation, was not dependent on changes in lung mechanics. Results show that loading CO2 intravascularly depresses PSR activity, the effects extending above as well as below resting PpCO2. Rapidly increasing PpCO2 above the resting level markedly depresses PSR activity during the transient. We conclude that PSRs may contribute to altered breathing resulting from changes in mixed venous PCO2 over the physiological range.

Adaptation, Physiological↗

PubMed1986

Rapid shallow breathing evoked by capsaicin from isolated pulmonary circulation.

Recently Green et al. (J. Appl. Physiol. 57:562-567, 1984) reported that pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin; however, their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is still in dispute. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulations in dogs anesthetized with either halothane or alpha-chloralose as the lungs were ventilated with a servo-controlled ventilator driven by phrenic nerve activity. Injection of capsaicin (10 micrograms/kg) into the pulmonary artery of the isolated pulmonary circulation evoked an immediate apnea followed by rapid shallow breathing. Injection of the same dose of capsaicin into the left atrium of the isolated pulmonary circulation had no effect. By contrast, when capsaicin was administered at a slower rate into the pulmonary artery (10-20 micrograms X kg-1 X min-1) rapid shallow breathing occurred but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers can evoke rapid shallow breathing.

Anesthesia↗

PubMed1986

Quantification of the transition from oocyte-coded to embryo-coded glucose phosphate isomerase in mouse embryos.

A quantitative electrophoretic analysis of glucose phosphate isomerase (GPI-1) allozymes produced by heterozygous Gpi-1sa/Gpi-1sb mouse embryos has enabled us to estimate separately the contributions of GPI-1 enzyme that were oocyte coded, encoded by the embryonic, maternally derived Gpi-1sa allele and encoded by the embryonic, paternally derived Gpi-1sb allele. The oocyte-coded GPI-1 activity is stable until 2 1/2 days and then declines and is exhausted by 5 1/2 to 6 1/2 days post coitum (p.c.). The maternally and paternally derived Gpi-1s alleles are probably usually activated synchronously but several possible exceptions were observed. This activation was first detected in 2 1/2-day embryos. Total GPI-1 activity falls to a minimum around 3 1/2 to 4 1/2 days, even though embryonic gene expression has already begun. The profile of oocyte-coded GPI-1 activity is consistent with the suggestion (Harper & Monk, 1983) that there is a mechanism for the removal of oocyte-coded gene products at around 2 1/2 days p.c. The method of analysis described is applicable to other dimeric enzymes with electrophoretic variants.

Animals↗

PubMed1985

Measurement of bronchial blood flow in the sheep by video dilution technique.

Bronchial blood flow was determined in five adult anaesthetised sheep by the video dilution technique. This is a new fluoroscopic technique for measuring blood flow that requires only arterial catheterisation. Catheters were placed into the broncho-oesophageal artery and ascending aorta from the femoral arteries for contrast injections and subsequent videotape recording. The technique yields bronchial blood flow as a percentage of cardiac output. The average bronchial artery blood flow was 0.6% (SD 0.20%) of cardiac output. In one sheep histamine (90 micrograms) injected directly into the bronchial artery increased bronchial blood flow by a factor of 6 and histamine (90 micrograms) plus methacholine (4.5 micrograms) augmented flow by a factor of 7.5 while leaving cardiac output unchanged. This study confirms the high degree of reactivity of the bronchial circulation and demonstrates the feasibility of using the video dilution technique to investigate the determinants of total bronchial artery blood flow in a stable animal model avoiding thoracotomy.

Animals↗

PubMed1985

Reflex tracheal contraction evoked in dogs by bronchodilator prostaglandins E2 and I2.

Bronchodilator prostaglandins E2 and I2 may cause airway irritation and bronchoconstriction in human subjects. These experiments were designed to test the hypothesis that this paradoxical bronchoconstriction is a vagal reflex triggered by stimulation of airway afferents. We recorded smooth muscle tension in an innervated upper tracheal segment in anesthetized dogs and injected prostaglandins into the general circulation or into a bronchial artery or administered them as aerosol to the lungs. Prostaglandins usually caused tracheal contraction, which survived vagal cooling to 5-7 degrees C but was abolished at 0 degrees C. Vagally mediated tracheal contraction was also evoked when prostacyclin was injected into the pulmonary circulation of dogs whose pulmonary and systemic circulations were independently pump perfused. Recordings of afferent vagal impulses indicated that bronchial arterial injection of prostaglandins stimulated bronchial C-fibers; aerosols of prostaglandin stimulated pulmonary and bronchial C-fibers and C-fibers in extrapulmonary airways. We postulate that in susceptible human subjects concentrations of these prostaglandins too low to have direct bronchodilator effects may cause reflex bronchoconstriction by stimulating afferent vagal C-fibers in the lower airways.

Action Potentials↗