Influence of phasic afferent information on phrenic neural output during hypercapnia

1988 ◽  
Vol 65 (2) ◽  
pp. 563-569 ◽  
Author(s):  
A. S. Menon ◽  
S. J. England ◽  
E. Vallieres ◽  
A. S. Rebuck ◽  
A. S. Slutsky
Keyword(s):  
Steady State ◽  
Spontaneous Breathing ◽  
Blood Gases ◽  
Constant Flow ◽  
Inspiratory Time ◽  
Afferent Information ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Time Average ◽  
Respiratory Generator

We measured the moving time average (MTA) of the phrenic neurogram before and after removal of phasic afferent information from the lungs, chest wall, and oscillations in blood gases by using constant-flow ventilation (CFV). Anesthetized dogs were studied at various levels of steady-state and progressive hypercapnia during spontaneous breathing and during CFV. When steady-state and progressive hypercapnia were compared, the frequency and height of the MTA phrenic neurogram were independent of the rate of induction of hypercapnia during each mode of ventilation. During spontaneous ventilation, the response to hypercapnia comprised mainly an increase in frequency with only a slight increase in the amplitude of the MTA phrenic waveform. During muscular paralysis and CFV, the responses were similar to those observed after vagotomy with mainly an increase in the amplitude and only a small increase in frequency. For both spontaneous breathing and CFV, increases in frequency were achieved mainly by a shortening in expiratory time with the inspiratory time remaining relatively constant. Our data support the concept of a centrally patterned respiratory generator, whose inherent pattern is modified by phasic feedback from peripheral receptors mainly of vagal origin.

Phrenic neural output during hypoxia in dogs: constant-flow ventilation vs. spontaneous breathing

1991 ◽  
Vol 70 (5) ◽  
pp. 2045-2051 ◽  
Author(s):  
S. S. Naqvi ◽  
A. S. Menon ◽  
B. E. Shykoff ◽  
A. S. Rebuck ◽  
A. S. Slutsky
Keyword(s):  
Spontaneous Breathing ◽  
Pattern Generation ◽  
Afferent Feedback ◽  
Respiratory Pattern ◽  
Constant Flow ◽  
Inspiratory Time ◽  
Amplitude Response ◽  
Expiratory Time ◽  
Neural Information ◽  
Anesthetized Dogs

We studied the effects of removing cyclic pulmonary afferent neural information on respiratory pattern generation in anesthetized dogs. Phrenic neural output during spontaneous breathing (SB) was compared with that occurring during constant-flow ventilation (CFV) at several levels of eucapnic hypoxemia. Hypoxia caused an increase in both the frequency and the amplitude of the moving time average (MTA) phrenic neurogram during both SB and CFV. The change in frequency as arterial saturation was reduced from 90 to 60% during SB was significantly higher than that during CFV [SB, 32.3 +/- 10.9 (SD) breaths/min; CFV, 10.3 +/- 5.8 breaths/min; P = 0.001]. By contrast, the increase in the amplitude of the MTA phrenic neurogram was smaller (SB, 0.62 +/- 0.68 units; CFV, 1.35 +/- 0.81 units; P = 0.01). The changes in frequency with hypoxia during both modes of ventilation resulted primarily from a shortening of expiratory time. Both inspiratory time and expiratory time were greater during CFV than during SB, but their change in response to hypoxia was not significantly different. We conclude that the amplitude response of the MTA phrenic neurogram to hypoxia is similar to that seen during hypercapnia; in the presence of phasic afferent feedback the MTA amplitude response is decreased and the frequency response is increased relative to the response observed in the absence of phasic afferents.

Catheter position and blood gases during constant-flow ventilation

1987 ◽  
Vol 62 (2) ◽  
pp. 513-519 ◽  
Author(s):  
A. S. Slutsky ◽  
A. S. Menon
Keyword(s):  
Steady State ◽  
Flow Rate ◽  
Blood Gases ◽  
Constant Flow ◽  
Arterial Blood Gases ◽  
Catheter Position ◽  
Flow Rates ◽  
Arterial Blood ◽  
Tracheal Carina ◽  
Co2 Elimination

We studied the effect of catheter position and flow rate on gas exchange during constant-flow ventilation (CFV) in eight anesthetized, paralyzed dogs. The distal tips of the insufflation catheters were positioned 0.5, 2.0, 3.5, and 5.0 cm from the tracheal carina. Flow rates were varied between 10 and 55 l/min and steady-state arterial blood gases were measured. At a given flow rate, arterial CO2 pressure (PaCO2) decreased as CFV was administered further into the lung up to a distance of 3.5 cm from the carina; there were no significant differences in PaCO2 at 3.5 and 5.0 cm. For a given catheter position, PaCO2 decreased with increasing flow rate up to a flow rate of 40 l/min. Further increases in flow rate had no significant effect on PaCO2. Arterial O2 pressure (PaO2) was relatively constant at all flow rates and catheter positions. We conclude that, up to a point, CO2 elimination can be improved by positioning the catheters further into the lung; advancing the catheters further than 3.5 cm from the carina may cause over-ventilation of specific lung regions resulting in a relative plateau in CO2 elimination and relatively constant PaO2's. Positioning the catheters further into the lung permits the use of lower flow rates, thus potentially minimizing the risk of barotrauma.

Effect of naloxone on ventilation in newborn rabbits

1981 ◽  
Vol 50 (4) ◽  
pp. 713-717 ◽  
Author(s):  
T. A. Hazinski ◽  
M. M. Grunstein ◽  
M. A. Schlueter ◽  
W. H. Tooley
Keyword(s):  
Blood Gases ◽  
Postnatal Life ◽  
Respiratory Drive ◽  
Arterial Blood Gases ◽  
Inspiratory Time ◽  
Ether Anesthesia ◽  
Respiratory Effect ◽  
Artery Cannulation ◽  
Arterial Blood ◽  
Before And After

Endorphins have been isolated from amniotic fluid and cord blood of mammals. To determine if these agents influence ventilation after birth, we measured ventilation (VE), tidal volume, inspiratory time, and respiratory frequency (f) in 19 rabbit pups before and after administration of naloxone (NLX), an endorphin antagonist. Tracheostomy and carotid artery cannulation were performed under light ether anesthesia. After 30-90 min for recovery the pups were placed in a body plethysmograph. Rectal temperature was kept at 37 +/- 0.5 degrees C. After 15 min of control measurements we infused saline, which had no respiratory effect. NLX (4 microgram/g) was then infused and measurements continued for 30 min. In 6 of 7 pups less than or equal to 4 days old, VE increased to 140-180% of control values and remained elevated for the remainder of the study period. Increased VE was due solely to increased f. By contrast, only 1 of 12 pups greater than or equal to 5 days old responded in this fashion. This difference was significant (P less than 0.005). Arterial blood gases were measured before and after NLX in 10 pups. In those pups who increased their ventilation after NLX, arterial CO2 tension fell and pH rose above pre-NLX values (P less than 0.05) for both variables). Blood gases of the group whose ventilation was uneffected remained unchanged. These results indicate that early in postnatal life endorphins probably modulate central respiratory drive in rabbits but that these agents become less important with maturation.

Constant-flow ventilation in pigs

1986 ◽  
Vol 61 (6) ◽  
pp. 2238-2242 ◽  
Author(s):  
P. Webster ◽  
A. S. Menon ◽  
A. S. Slutsky
Keyword(s):  
Steady State ◽  
Gas Exchange ◽  
Gas Flow ◽  
Blood Gases ◽  
Maximum Flow ◽  
Constant Flow ◽  
Catheter Position ◽  
Flow Rates ◽  
Co2 Partial Pressure ◽  
Flow Through

Constant-flow ventilation (CFV) is a ventilatory technique in which physiological blood gases can be maintained in dogs by a constant flow of fresh gas introduced via two catheters placed in the main-stem bronchi (J. Appl. Physiol. 53: 483–489, 1982). High-velocity gas exiting from the catheters can create uneven pressure differences in adjacent lung segments, and these pressure differences could lead to gas flow through collateral channels. To examine this hypothesis, we studied CFV in pigs, animals known to have a high resistance to collateral ventilation. In three pigs we examined steady-state gas exchange, and in six others we studied unsteady gas exchange at three flow rates (20, 35, and 50 l/min) and three catheter positions (0.5, 1.5, and 2.5 cm distal to the tracheal carina). During steady-state runs we were unable to attain normocapnia; the arterial CO2 partial pressure (PaCO2) was approximately 300 Torr at all flow rates and all catheter positions, compared with 20–50 Torr at similar flows and positions in dogs studied previously. The initial unsteady gas-exchange experiments indicated no consistent effect of catheter position or flow rate on the rate of rise of PaCO2. In three other pigs, the rates of rise of PaCO2 were compared with the rates observed with apneic oxygenation (AO). At the maximum flow and deepest position, the rate of rise of PaCO2 was lower during CFV than during AO. These data suggest that flow through collateral channels might be important in producing adequate gas transport during CFV; however, other factors such as airway morphometry and the effects of cardiogenic oscillations may explain the differences between the results in pigs and dogs.

Respiratory response to partial paralysis in anesthetized dogs

1984 ◽  
Vol 56 (6) ◽  
pp. 1583-1588 ◽  
Author(s):  
A. Oliven ◽  
E. C. Deal ◽  
S. G. Kelsen ◽  
N. S. Cherniack
Keyword(s):  
Motor Activity ◽  
Respiratory Muscle ◽  
Respiratory Muscles ◽  
Peak Activity ◽  
Inspiratory Time ◽  
Muscle Paralysis ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing ◽  
Partial Paralysis

The ability to maintain alveolar ventilation is compromised by respiratory muscle weakness. To examine the independent role of reflexly mediated neural mechanisms to decreases in the strength of contraction of respiratory muscles, we studied the effects of partial paralysis on the level and pattern of phrenic motor activity in 22 anesthetized spontaneously breathing dogs. Graded weakness induced with succinylcholine decreased tidal volume and prolonged both inspiratory and expiratory time causing hypoventilation and hypercapnia. Phrenic peak activity as well as the rate of rise of the integrated phrenic neurogram increased. However, when studied under isocapnic conditions, increases in the severity of paralysis, as assessed from the ratio of peak diaphragm electromyogram to peak phrenic activity, produced progressive increases in inspiratory time and phrenic peak activity but did not affect its rate of rise. After vagotomy, partial paralysis induced in 11 dogs with succinylcholine also prolonged the inspiratory burst of phrenic activity, indicating that vagal reflexes were not solely responsible for the alterations in respiratory timing. Muscle paresis was also induced with gallamine or dantrolene, causing similar responses of phrenic activity and respiratory timing. Thus, at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle partial paralysis results in a decrease in breathing rate without changing the rate of rise of respiratory motor activity. This is not dependent solely on vagally mediated reflexes and occurs regardless of the pharmacological agent used. These observations in the anesthetized state are qualitatively different from the response to respiratory muscle paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Salivary Flow Induction by Buccal Permucosal Pilocarpine in Anesthetized Beagle Dogs

1992 ◽  
Vol 71 (11) ◽  
pp. 1762-1767 ◽  
Author(s):  
M.L. Weaver ◽  
J.M. Tanzer ◽  
P.A. Kramer
Keyword(s):  
Steady State ◽  
Salivary Flow ◽  
Salivary Secretion ◽  
Reversed Phase ◽  
Use Of Data ◽  
Constant Rate ◽  
First Pass ◽  
Steady State Plasma Concentration ◽  
Anesthetized Dogs ◽  
Drug Solution

We tested whether permucosal delivery of pilocarpine nitrate could be used to elicit significant salivary secretion. Pilocarpine (pKa 6.6 at 37°C) was applied as solutions (pHs 5.6, 6.6, 7.6; 15 mg/mL) to the buccal mucosa (2.8 cm2) of 6 anesthetized dogs. Saliva was collected continuously from cannulated submandibular and parotid ducts and blood sampled during and after drug administration. Plasma pilocarpine levels were determined by reversed-phase HPLC. Absorption rates were determined by use of data from separate zero-order intravenous infusions to the same dogs. Pilocarpine was buccally absorbed at a constant rate of 72.9 ± 38.5 μg/kg/h following its application at pH 7.6. At this pH of the drug solution, the time to appearance of pilocarpine in blood plasma was 0.31 ± 0.08 h, and the time to appearance of salivary flow was 0.86 ± 0.32 h. A threshold dose of 32.9 ± 7.5 ug/kg was required to induce secretion with the pH 7.6 drug, the steady-state plasma concentration was 28.9 ± 19.3 ng/mL, and the steady-state submandibular flow rate was 0.14 ± 0.11 mL/ min/gland pair. Salivary flow induction was symmetrical and reached levels as high as 0.35 mL/min/submandibular gland pair without apparent tachyphylaxis. Results at pHs 5.6, 6.6, and 7.6 were consistent with the hypothesis that pilocarpine is primarily absorbed as un-ionized drug. The data indicate that transmucosal delivery of pilocarpine, avoiding "first pass" hepatic loss, may hold promise for the treatment of xerostomia.

Evidence against local neural mechanism for intestinal postprandial hyperemia

1983 ◽  
Vol 245 (3) ◽  
pp. H437-H446 ◽  
Author(s):  
R. A. Nyhof ◽  
C. C. Chou
Keyword(s):  
Oxygen Consumption ◽  
Oleic Acid ◽  
Neural Mechanism ◽  
Jejunal Mucosa ◽  
Vasoactive Substances ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Postprandial Hyperemia

The role of local intestinal nerves in the nutrient-induced intestinal hyperemia was investigated in jejunal segments of anesthetized dogs by comparing the hyperemic effect of intraluminal glucose and oleic acid solutions before and after mucosal anesthesia and infusions of methysergide, hexamethonium, and tetrodotoxin. Methysergide, hexamethonium, and tetrodotoxin all failed to alter either the vascular or metabolic responses to luminal placement of glucose or oleic acid. The increases in blood flow and oxygen uptake produced by glucose or oleic acid, however, were blocked or attenuated after exposing the mucosa to dibucaine. The effect was norepinephrine due to an altered vascular response to vasoactive substances as dibucaine did not alter vascular responses to isoproterenol or norepinephrine. Dibucaine, however, inhibited active transport and increased passive transport of glucose across rat intestinal sacs in vitro. Oxygen consumption of the canine jejunal mucosa was also inhibited by dibucaine in vitro. It seems that inhibition of the nutrient-induced intestinal hyperemia by dibucaine is due, at least in part, to its effect on oxygen consumption and glucose transport of the mucosal epithelial cells. Nutrient-induced hyperemia appears not to be neurally mediated but more closely related to metabolism.

Surfactant replacement partially restores the activity of pulmonary stretch receptors in surfactant-depleted cats

2006 ◽  
Vol 100 (2) ◽  
pp. 594-601 ◽  
Author(s):  
Richard Sindelar ◽  
Anders Jonzon ◽  
Andreas Schulze ◽  
Gunnar Sedin
Keyword(s):  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Lung Lavage ◽  
Lung Compliance ◽  
High Threshold ◽  
Inspiratory Time ◽  
Impulse Frequency ◽  
Surfactant Replacement ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

Single units of slowly adapting pulmonary stretch receptors (PSRs) were investigated in anesthetized cats during spontaneous breathing on continuous positive airway pressure (2–5 cmH2O), before and after lung lavage and then after instillation of surfactant to determine the PSR response to surfactant replacement. PSRs were classified as high threshold (HT) and low threshold (LT), and their instantaneous impulse frequency ( fimp) was related to transpulmonary pressure (Ptp) and tidal volume (Vt). Both the total number of impulses and maximal fimp of HT and LT PSRs decreased after lung lavage (55 and 45%, respectively) in the presence of increased Ptp and decreased Vt. While Ptp decreased markedly and Vt remained unchanged after surfactant instillation, all except one PSR responded with increased total number of impulses and maximal fimp (42 and 26%, respectively). Some HT PSRs ceased to discharge after lung lavage but recovered after surfactant instillation. The end-expiratory activity of LT PSRs increased or was regained after surfactant instillation. After instillation of surfactant, respiratory rate increased further with a shorter inspiratory time, resulting in a lower inspiratory-to-expiratory time ratio. Arterial pH decreased (7.31 ± 0.04 vs. 7.22 ± 0.06) and Pco2 increased (5.5 ± 0.7 vs. 7.2 ± 1.3 kPa) after lung lavage, but they were the same after as before instillation of surfactant (pH = 7.21 ± 0.08 and Pco2 = 7.6 ± 1.4 kPa) during spontaneous breathing. In conclusion, surfactant instillation increased lung compliance, which, in turn, increased the activity of both HT and LT PSRs. A further increase in respiratory rate due to a shorter inspiratory time after surfactant instillation suggests that the partially restored PSR activity after surfactant instillation affected the breathing pattern.

The Study of Dynamic Response to Acute Hemorrhage by Pulse Spectrum Analysis

2006 ◽  
Vol 34 (03) ◽  
pp. 449-460 ◽  
Author(s):  
Yu Hsin Chang ◽  
Chia I Tsai ◽  
Jaung Geng Lin ◽  
Yue Der Lin ◽  
Tsai Chung Li ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Spectrum Analysis ◽  
Pulse Spectrum ◽  
Acute Hemorrhage ◽  
Arterial Blood ◽  
Percentage Difference ◽  
Before And After

Traditional Chinese Medicine (TCM) holds that Blood and Qi are fundamental substances in the human body for sustaining normal vital activity. The theory of Qi, Blood and Zang-Fu contribute the most important theoretical basis of human physiology in TCM. An animal model using conscious rats was employed in this study to further comprehend how organisms survive during acute hemorrhage by maintaining the functionalities of Qi and Blood through dynamically regulating visceral physiological conditions. Pulse waves of arterial blood pressure before and after the hemorrhage were taken in parallel to pulse spectrum analysis. Percentage differences of mean arterial blood pressure and harmonics were recorded in subsequent 5-minute intervals following the hemorrhage. Data were analyzed using a one-way analysis of variance (ANOVA) with Duncan's test for pairwise comparisons. Results showed that, within 30 minutes following the onset of acute hemorrhage,the reduction of mean arterial blood pressure was improved from 62% to 20%. Throughout the process, changes to the pulse spectrum appeared to result in a new balance over time. The percentage differences of the second and third harmonics, which were related to kidney and spleen, both increased significantly than baseline and towards another steady state. Apart from the steady state resulting from the previous stage, the percentage difference of the 4th harmonic decreased significantly to another steady state. The observed change could be attributed to the induction of functional Qi, and is a result of Qi-Blood balancing activity that organisms hold to survive against acute bleeding.

Augmentation of phrenic neural activity by increased rates of lung inflation

1981 ◽  
Vol 50 (1) ◽  
pp. 149-161 ◽  
Author(s):  
A. I. Pack ◽  
R. G. DeLaney ◽  
A. P. Fishman
Keyword(s):  
Tidal Volume ◽  
Volume Change ◽  
Neural Activity ◽  
Negative Pressure ◽  
Spontaneous Breathing ◽  
Moving Average ◽  
Constant Flow ◽  
Lung Inflation ◽  
Negative Pressure Ventilation ◽  
Single Breath

Studies were conducted in anesthetized paralyzed dogs using a cycle-triggered constant-flow ventilator, which ventilated the animal in phase with the recorded phrenic neural activity. Intermittently tests were performed in which the animal was ventilated with a different airflow for a single breath. Increased airflows, within the range generated during spontaneous breathing, caused an increased rate of rise of the moving average phrenic neurogram and a shortening of the duration of the nerve burst. The magnitude of the increase in the rate of rise of the neurogram was related to the level of inspiratory airflow. Tests with brief pulses of airflow showed that an increase in the rate of rise of the phrenic neurogram could be produced without inflating the lung above the resting tidal volume of the animal. Similar results were obtained with negative-pressure ventilation and the effects were abolished by vagotomy. This vagally mediated augmentation of phrenic neural output may accelerate the inspiratory volume change in the lung during spontaneous breathing at hyperpneic levels.

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