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Biomedical subjects

J F Green

Publications and source records attributed to J F Green.

At least 19 recordsLinked to original sources
PubMed2000

Interaction of vagal lung afferents with inhalation of histamine aerosol in anesthetized dogs.

In seven alpha-chloralose anesthetized dogs we examined the contribution of lung afferents to the rapid, shallow breathing induced by inhalation of 10 breaths of histamine aerosol. In four spontaneously breathing dogs, the inhalation of histamine caused an increased respiratory frequency, decreased tidal volume, and decreased dynamic lung compliance. Selective blockade of pulmonary C-fibers abolished a reflex-induced increase in respiratory frequency but did not significantly affect the reductions in tidal volume or lung compliance. Terbutaline treatment in combination with C-fiber blockade abolished the reductions in tidal volume and lung compliance induced by histamine. In three separate alpha-chloralose anesthetized, open-chest, mechanically ventilated dogs, we recorded an increase in the inspiratory activity of rapidly adapting pulmonary stretch receptors (RARs) induced by the inhalation of histamine aerosol. Selective C-fiber blockade abolished histamine-induced increases in RAR activity while only partially attenuating reductions in lung compliance. We conclude that the increase in RAR activity induced by histamine depends on intact C-fibers and not on a direct effect of histamine on RARs or an indirect effect of histamine reducing lung compliance. In addition, our data illustrate the multiple interactions that occur between the various vagal afferents and their roles in the reflexes induced by histamine inhalation.

Administration, Inhalation↗
PubMed2000

Antisaccade and smooth pursuit eye movements in healthy subjects receiving sertraline and lorazepam.

Patients suffering from some psychiatric and neurological disorders demonstrate abnormally high levels of saccadic distractibility when carrying out the antisaccade task. This has been particularly thoroughly demonstrated in patients with schizophrenia. A large body of evidence has been accumulated from studies of patients which suggests that such eye movement abnormalities may arise from frontal lobe dysfunction. The psychopharmacology of saccadic distractibility is less well understood, but is relevant both to interpreting patient studies and to establishing the neurological basis of their findings. Twenty healthy subjects received lorazepam 0.5 mg, 1 mg and 2 mg, sertraline 50 mg and placebo in a balanced, repeated measures study design. Antisaccade, no-saccade, visually guided saccade and smooth pursuit tasks were carried out and the effects of practice and drugs measured. Lorazepam increased direction errors in the antisaccade and no-saccade tasks in a dose-dependent manner. Sertraline had no effect on these measures. Correlation showed a statistically significant, but rather weak, association between direction errors and smooth pursuit measures. Practice was shown to have a powerful effect on antisaccade direction errors. This study supports our previous work by confirming that lorazepam reliably worsens saccadic distractibility, in contrast to other psychotropic drugs such as sertraline and chlorpromazine. Our results also suggest that other studies in this field, particularly those using parallel groups design, should take account of practice effects.

Adolescent↗
PubMed1999

Capsaicin-sensitive C-fiber-mediated protective responses in ozone inhalation in rats.

To assess the role of lung sensory C fibers during and after inhalation of 1 part/million ozone for 8 h, we compared breathing pattern responses and epithelial injury-inflammation-repair in rats depleted of C fibers by systemic administration of capsaicin as neonates and in vehicle-treated control animals. Capsaicin-treated rats did not develop ozone-induced rapid, shallow breathing. Capsaicin-treated rats showed more severe necrosis in the nasal cavity and greater inflammation throughout the respiratory tract than did control rats exposed to ozone. Incorporation of 5-bromo-2'-deoxyuridine (a marker of DNA synthesis associated with proliferation) into terminal bronchiolar epithelial cells was not significantly affected by capsaicin treatment in rats exposed to ozone. However, when normalized to the degree of epithelial necrosis present in each rat studied, there was less 5-bromo-2'-deoxyuridine labeling in the terminal bronchioles of capsaicin-treated rats. These observations suggest that the ozone-induced release of neuropeptides does not measurably contribute to airway inflammation but may play a role in modulating basal and reparative airway epithelial cell proliferation.

Administration, Inhalation↗
PubMed1999

Breathing pattern response and epithelial labeling in ozone-induced airway injury in neutrophil-depleted rats.

To test the hypothesis that neutrophils enhance the repair of ozone (O3)-injured airway epithelium, we investigated breathing pattern responses and airway epithelial injury and repair in rats depleted of neutrophils using rabbit antirat neutrophil serum (ANS) and control rats treated with normal rabbit serum (NRS). Thirty-seven Wistar rats were exposed to O3 (1 ppm) or filtered air (FA) for 8 h followed by 8 h in FA. O3-exposed NRS- and ANS-treated rats showed similar progressive decreases in tidal volume and increase in breathing frequency, with maximal changes occurring at 8 h of exposure, whereas FA-exposed rats showed no significant changes. O3-exposed ANS-treated rats showed more epithelial necrosis in the nasal cavity, bronchi, and distal airways than did O3-exposed NRS-treated rats. Incorporation of 5-bromo-2-deoxyuridine (BrdU), a measure of cellular proliferation, was assessed using an optical disector to count BrdU- labeled terminal bronchiolar epithelial cells. O3-exposed ANS-treated rats had significantly less BrdU- labeled epithelial cells than did O3-exposed NRS-treated rats. We conclude that neutrophils contribute to the repair process by enhancing the proliferation of O3-injured airway epithelial cells.

Animals↗
PubMed1998

The effects of chlorpromazine and lorazepam on abnormal antisaccade and no-saccade distractibility.

BACKGROUND: Abnormally high levels of saccadic distractibility have been demonstrated to occur in patients with schizophrenia. Converging evidence implicates frontal cortical dysfunction as a mechanism; however, much of the neuropharmacology of saccadic distractibility has not yet been established. METHODS: We measured antisaccade, no-saccade, and visually guided saccade components in healthy subjects following single doses of lorazepam 2 mg, chlorpromazine 50-100 mg, and placebo. Visual analogue rating scales (VARS) provided a subjective measure of sedation. RESULTS: Lorazepam, but not chlorpromazine, was shown to cause an increase in saccadic distractibility in both the antisaccade and no-saccade tasks. Peak visually guided saccade velocity was decreased by lorazepam and chlorpromazine in a dose-dependent manner, with corresponding changes seen in VARS. Lorazepam, unexpectedly, did not affect peak antisaccade velocity. The background level of antisaccade directional errors was 6.43%, which is relatively low compared to control groups in patient studies. CONCLUSIONS: These results support the view that abnormal saccadic distractibility in patients with schizophrenia is not due to an acute effect of antipsychotic medication. The use of benzodiazepines and the level of task practice are highlighted as possible confounding variables in patient studies. The implications of these results for the current neuropathological theories of abnormal saccadic distractibility are discussed.

Adult↗
PubMed1998

Control of ventilation during lung volume changes and permissive hypercapnia in dogs.

We investigated the effect changes in end-expiratory lung volume (EEVL) had on the response to progressive hypercapnia (CO2-response curve) in eight open-chest, anesthetized dogs, in order to clarify the role that vagal lung mechanoreceptors have in altered respiratory drive during permissive hypercapnia. The dogs were ventilated using a positive-pressure ventilator driven by phrenic neural activity. Systemic arterial CO2 tension (PaCO2) was elevated by increasing the fraction of CO2 delivered to the ventilator. EEVL was altered from approximated functional residual capacity ("FRC") to 1.5 and 0.5 "FRC" by changing positive end-expiratory pressure. Although the tidal volume (VT)-PaCO2 and inspiratory time (TI)-PaCO2 relationships were not affected, decreasing EEVL from 1.5 "FRC" to "FRC" and then to 0.5 "FRC" caused a significant (p < 0.01) upward shift in the CO2-response curves for minute ventilation (V I) and frequency (f ), and a significant (p < 0.01) downward shift in the CO2- response curve for expiratory time (TE). We conclude that these shifts were explained by a decrease in the inhibitory activity of slowly adapting pulmonary stretch receptors (PSRs) as EEVL was lowered. In addition, increases in EEVL from 0.5 "FRC" to 1.5 "FRC" caused a significant (p < 0.05) increase in the apneic threshold, which we attribute to an inhibitory effect on central drive caused by increased PSR activity.

Adaptation, Physiological↗
PubMed1997

The effects of haloperidol on visual search, eye movements and psychomotor performance.

The effects of single doses of haloperidol (2, 4 and 6 mg) were compared with lorazepam 2.5 mg and placebo in 15 healthy subjects. Visual search strategy was measured, along with a range of psychomotor and eye movement tests. Patients with Parkinson's disease have been shown to exhibit a shift from parallel to serial processing in visual search, but we demonstrated that this does not occur following administration of either haloperidol or lorazepam. Haloperidol was detected by visual analogue rating scales and peak saccadic velocity, the latter being the more sensitive measure. Haloperidol had no statistically significant effect on smooth pursuit position error, velocity error or saccadic intrusions. Digit symbol substitution performance was clearly diminished by haloperidol, but there was no effect on the continuous attention test. Lorazepam decreased performance in all tests apart from saccadic latency.

Adolescent↗
PubMed1996

A comparison of the sedative and amnestic effects of chlorpromazine and lorazepam.

The effects of single doses of chlorpromazine (100 mg) and lorazepam (0.5, 1 and 2 mg) were compared with placebo in a battery of tests of information processing, working and semantic memory. Peak saccadic velocity was used to provide a precise and reliable measure of sedation and its results were found to be consistent with those using visual analogue rating scales. Chlorpromazine 100 mg was equally sedative to lorazepam 2 mg. Lorazepam caused dose-dependent deterioration in performance in many of the memory tests, whereas an equally sedative dose of chlorpromazine did not. These data therefore support the view that benzodiazepine-induced amnesia is not secondary to sedation. Peak saccadic velocity has considerable advantages over visual analogue scales as a measure of sedation, since it is objective and has a demonstrated low coefficient of variation. It is suggested that saccadic eye movement measurement will permit considerably more reliable and precise separation of the sedative and amnestic effects of drugs and will allow investigation of amnesia caused by clinically relevant doses of psychotropic drugs.

Adult↗
PubMed1996

Neonatal capsaicin treatment increases the severity of ozone-induced lung injury.

To test the hypothesis that lung sensory C fibers protect the small distal airways and alveoli from oxidant injury, we compared the effects of inhalation of ozone (1 ppm) or filtered air for 8 h on lung injury and lung inflammation in four groups of rats: (1) normal rats exposed to filtered air; (2) normal rats exposed to ozone; (3) rats treated as neonates with capsaicin (50 mg/kg, intraperitoneally) and subsequently exposed to filtered air; and (4) rats treated as neonates with capsaicin and subsequently exposed to ozone. All rats were allowed to recover in filtered air for 0, 4, 16, and 40 h before necropsy. Rats exposed to filtered air (Groups 1 and 3) showed normal airway and parenchyma structure. Normal untreated rats exposed to ozone showed a random distribution of mild, interstitial inflammatory changes and epithelial necrosis of bronchi and bronchiolar epithelium. However, rats treated with capsaicin and subsequently exposed to ozone demonstrated severe acute interstitial inflammation and epithelial coagulate necrosis in all airways, especially in small, peripheral airways and parenchyma; all of these changes were statistically significant. These findings support our hypothesis that lung sensory C fibers protect the distal airways from oxidant injury during acute ozone inhalation.

Air↗
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↗
PubMed1993

Contribution of vagal afferents to respiratory reflexes evoked by acute inhalation of ozone in dogs.

Acute inhalation of ozone induces vagally mediated rapid shallow breathing and bronchoconstriction. In spontaneously breathing anesthetized dogs, we attempted to determine whether afferent vagal C-fibers in the lower airways contributed to these responses. Dogs inhaled 3 ppm ozone for 40-70 min into the lower trachea while cervical vagal temperature was maintained successively at 37, 7, and 0 degrees C. At 37 degrees C, addition of ozone to the inspired air decreased tidal volume and dynamic lung compliance and increased breathing frequency, total lung resistance, and tracheal smooth muscle tension. Ozone still evoked significant effects when conduction in myelinated vagal axons was blocked selectively by cooling the nerves to 7 degrees C. Ozone-induced effects were largely abolished when nonmyelinated vagal axons were blocked by cooling to 0 degree C, breathing during ozone inhalation at 0 degree C being generally similar to that during air breathing at 0 degree C, except that minute volume and inspiratory flow were higher. We conclude that afferent vagal C-fibers in the lower airways make a major contribution to the acute respiratory effects of ozone and that nonvagal afferents contribute to the effects that survive vagal blockade.

Administration, Inhalation↗
PubMed1993

Acute inhalation of ozone stimulates bronchial C-fibers and rapidly adapting receptors in dogs.

To identify the afferents responsible for initiating the vagally mediated respiratory changes evoked by acute exposure to ozone, we recorded vagal impulses in anesthetized, open-chest, artificially ventilated dogs and examined the pulmonary afferent response to ozone (2-3 ppm in air) delivered to the lower trachea for 20-60 min. Bronchial C-fibers (BrCs) were the lung afferents most susceptible to ozone, the activity of 10 of 11 BrCs increasing from 0.2 +/- 0.2 to 4.6 +/- 1.3 impulses/s within 1-7 min of ozone exposure. Ten of 15 rapidly adapting receptors (RARs) were stimulated by ozone, their activity increasing from 1.5 +/- 0.4 to 4.7 +/- 0.7 impulses/s. Stimulation of RARs (but not of BrCs) appeared secondary to the ozone-induced reduction of lung compliance because it was abolished by hyperinflation of the lungs. Ozone had little effect on pulmonary C-fibers or slowly adapting pulmonary stretch receptors. Our results suggest that both BrCs and RARs contribute to the tachypnea and bronchoconstriction evoked by acute exposure to ozone when vagal conduction is intact and that BrCs alone are responsible for the vagally mediated tachypnea that survives vagal cooling to 7 degrees C.

Action Potentials↗
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↗