Respiratory effects of brief baroreceptor stimuli in the anesthetized dog

1985 ◽  
Vol 59 (4) ◽  
pp. 1258-1265 ◽  
Author(s):  
E. L. Dove ◽  
P. G. Katona

To quantify the immediate isocapnic respiratory response to baroreceptor stimulation, pressure in the isolated externally perfused carotid sinuses (CS) of 24 vagotomized alpha-chloralose-anesthetized dogs was increased selectively during either inspiration or expiration as a step (from time of onset to end of respiratory phase) or a pulse (500 ms). The rise time (150 ms), base-line pressure (80 mmHg), and stimulus magnitude (40 mmHg) were similar for the two stimuli. The time of stimulus onset (delay), expressed as a percent of control time of inspiration (TI) or expiration (TE), was varied. TI, TE, and tidal volume (VT) were expressed as percent changes from control. Stimuli delivered early in inspiration lengthened TI [23.5 +/- 6.4% (SE) for step and 11.7 +/- 6.3% for pulse stimuli at 5% delay] more effectively than late stimuli. VT was essentially unaltered. In contrast, step stimuli delivered during expiration caused a lengthening of TE (32.7 +/- 6.3% at 5% delay) that did not depend on the delay (up to 75%). Very late (85%) pulse stimuli lengthened TE (15.2 +/- 5.7%) more effectively than early stimuli. For both stimuli, the expiratory VT was unaltered. When the responses are compared before and after separation of the blood supply of the carotid bodies from the CS region and when they are compared before and after inhibition of reflex systemic hypotension by ganglionic blockade, the observed responses were shown to be due solely to CS baroreceptor stimulation and not to alterations in carotid body blood flow or reflex changes in systemic cardiovascular variables.

1975 ◽  
Vol 39 (2) ◽  
pp. 235-241 ◽  
Author(s):  
R. Lemen ◽  
J. G. Jones ◽  
P. D. Graf ◽  
G. Cowan

“Closing volume” (CV) was measured by the single-breath oxygen (SBO2) test in six dogs (alloxan group) before and after alloxan 100–200 mg/kg iv) was injected. CV increased significantly (P less than 0.05) from 32 +/- 3.2% (base line) to 45 +/- 3.5 % in period 1 (0–30 min after alloxan), but vital capacity (VC), respiratory system pressure volume (PV) curves, and alveolar plateau slopes did not change. No radiologic evidence of pulmonary edema was demonstrated in two dogs studied in period 1. CV decreased to 20 +/- 3.9% during period 2 (30–80 min after alloxan) and was associated with tracheal frothing, decreased VC, changes in the PV curve, and alveolar plateau slope, as well as histologic evidence of severe pulmonary edema. CV was 29 +/- 3.0%, and there were no changes in VC, PV curves, or alveolar plateau slopes in 6 other dogs studied for 2 h (control group). CV increased during period 1 before pulmonary edema could be demonstrated by changes in VC, PV curves, or radiography, but in period 2 lung function was so altered that CV by the SBO2 technique gave no useful information.


1989 ◽  
Vol 67 (3) ◽  
pp. 1150-1156 ◽  
Author(s):  
D. Georgopoulos ◽  
S. G. Holtby ◽  
D. Berezanski ◽  
N. R. Anthonisen

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.


1985 ◽  
Vol 249 (2) ◽  
pp. H249-H254
Author(s):  
G. J. Grover ◽  
H. R. Weiss

This study was performed to determine if the partially occluded myocardium could maintain its O2 supply-to-consumption ratio during atrial pacing. In 14 open-chest anesthetized dogs, the left anterior descending coronary artery was occluded to 50% of base-line flow, and in half of the dogs the hearts were paced to 50% above base-line heart rate. Blood flows were determined by use of microspheres before and after occlusion, and O2 supply-consumption variables were determined by use of microspectrophotometry. After occlusion in control and paced groups, blood flow was depressed in the ischemic region compared with the nonischemic region. In paced animals, blood flows in all regions were significantly higher compared with their respective values in nonpaced animals. After pacing, mean O2 consumption was 34% higher (53% in the occluded region) compared with control animals. The O2 supply-to-consumption ratio was similar in the occluded region of paced animals compared with the same region in controls. This ratio was lower in ischemic regions of both groups compared with their respective nonischemic regions. This indicates that, despite a reduced O2 supply-to-consumption ratio in the ischemic area, an unutilized reserve of flow exists.


1975 ◽  
Vol 228 (2) ◽  
pp. 470-476 ◽  
Author(s):  
Lloyd TC

Anesthetized dogs were pump perfused in a system that held systemic arterial pressure constant. Pulmonary arterial beds were pressurized, and the induced transient falls of systemic vascular resistance (SVR) were measured. An approximately linear relationship between percent fall of SVR and pulmonary artery pressure was obtained. Left atria and pulmonary venous beds were pressurized using square-pulse, staircase, and ramp wave forms, and changes in SVR were measured. The effect of varying the interval between stimuli was appraised. An approximately linear relationship was obtained for responses to square-wave left atrial forcing pressure (Pla). With staircase forcing, the change of SVR per unit change of Pla depended upon prestimulus Pla. With ramp forcing, responses increased approximately linearly with respect to the logarithm of the rate of pressure rise. Responses to square-wave stimulation varied directly with respect to the interstimulus interval. This study shows that left atrial-pulmonary vein baroreflexes are capable of producing substantial short-term falls of SVR, and that the response depends upon stimulus pressure, rate of pressure change, base-line pressure, and pressure history.


1981 ◽  
Vol 51 (5) ◽  
pp. 1314-1319 ◽  
Author(s):  
J. Kaplan ◽  
G. C. Smaldone ◽  
H. A. Menkes ◽  
D. L. Swift ◽  
R. J. Traystman

A new technique using a monodispersed aerosol of histamine delivered to sublobar bronchi through a flexible fiber-optic bronchoscope was used to study the role of the vagus nerve and the effect of anesthesia in the response of collateral channels to exogenous histamine. Studies were performed in paralyzed dogs anesthetized with pentobarbital sodium or alpha-chloralose. Challenges with histamine aerosol were delivered to separate bronchi in each animal before and after bilateral cervical vagotomy. Resistance through collateral channels increased in a reproducible manner following histamine challenge. Vagotomy resulted in no significant change in base-line resistance through collateral channels. The response of collateral channels to exogenous histamine aerosol was not significantly affected by vagotomy or the type of anesthesia used. We conclude that vagal reflexes do not play a significant role in the response of collateral channels to exogenous histamine.


1981 ◽  
Vol 240 (2) ◽  
pp. H262-H273
Author(s):  
T. R. Harris ◽  
K. A. Overholser ◽  
R. G. Stiles

We have extended earlier studies on coronary vascular permeability-surface area (PS) for [14C]sucrose to include observations of the transcoronary flow resistance before and after partial occlusion of the left anterior descending coronary artery. Multiple-tracer (MT) studies were conducted on 13 anesthetized dogs by inserting an isotope mixture (125I-albumin, 51Cr-red blood cells, [14C]sucrose, 3HOH) into a cannula connecting the carotid and the left anterior descending coronary artery. Analysis of blood sampled from the coronary sinus allowed calculation of PS, extravascular 3HOH volume (VT), and extravascular [14C]sucrose volume (VS). Flow reduction significantly reduced VT and VS and increased PS/VT relative to base line. Coronary resistance distal to the obstruction (R) decreased significantly immediately after flow reduction but then, over the low-flow period, increased significantly above this initial low-flow value. The mean R during reduced flow normalized to R immediately after flow reduction (Ri) correlated significantly with PS/VT during ischemia. Because R/Ri is not correlated with VT alone, we speculate that capillary permeability alterations may play a role in the deterioration of myocardial perfusion during ischemia.


1982 ◽  
Vol 243 (3) ◽  
pp. F253-F259 ◽  
Author(s):  
B. J. Tucker ◽  
O. W. Peterson ◽  
M. G. Ziegler ◽  
R. C. Blantz

Renal and systemic adrenergic system responses were examined and compared under conditions of Inactin, a barbiturate, and alpha-chloralose anesthesia in hydropenic Munich-Wistar rats. Base-line plasma norepinephrine and other catecholamine levels were higher in Inactin-anesthetized rats. Norepinephrine was infused to raise blood pressure 15-20 mmHg above base line and plasma norepinephrine was again significantly higher with Inactin. In another group, angiotensin II was infused into the cerebral lateral ventricle in both Inactin- and alpha-chloralose-anesthetized rats, a method of stimulating centrally activated adrenergic output. After central stimulation, mean arterial pressure increased only in alpha-chloralose-anesthetized rats. Micropuncture studies examining systemic and glomerular hemodynamics were performed in alpha-chloralose- and Inactin-anesthetized rats before and after the infusion of phentolamine, an alpha-adrenergic antagonist. Infusion of phentolamine decreased mean arterial pressure to a significantly greater extent in the Inactin-anesthetized rats, suggesting a greater base-line systemic alpha-adrenergic activity with Inactin anesthesia. However, renal afferent and efferent arteriolar resistances were not significantly different after phentolamine, and any trend for resistances to decrease could be explained by autoregulation. Inactin increases systemic adrenergic activity, but renal vascular resistances are not significantly affected by this increased activity.


1985 ◽  
Vol 59 (6) ◽  
pp. 1986-1990 ◽  
Author(s):  
A. N. Freed ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes

We studied the effects of the flow of dry air on collateral tone in the lung periphery. A bronchoscope was wedged in sublobar segments of anesthetized dogs, and measurements of collateral resistance (Rcs) were recorded before and after flow was increased from 200 to 2,000 ml/min for a 5-min period. Five minutes after exposure was completed, Rcs increased by an average of 117 +/- 25.2% (SE) over control. Maximum Rcs occurred 5 min after the challenge was concluded and required 48 +/- 10.5 min to return to base line. When flow rate was held constant and exposure period varied, Rcs increased with increased stimulus duration. With exposure times held constant, the response of the collateral system was positively associated with changes in stimulus strength (flow rate). No refractory period was observed with repetitive challenges. Finally, when dry air (delivered at 22 degrees C) and conditioned air (i.e., delivered at 28 degrees C; relative humidity = 80%) challenges were alternated in the same wedged segment, dry air produced a mean increase in Rcs of 93.2%, whereas challenge with warm moist air increased Rcs only 33.5%. Regardless of which challenge was presented first, dry air consistently produced a greater constrictor response. This response is similar to that observed in cold air- and exercise-induced asthma and indicates that the lung periphery in dogs, like larger airways in asthmatic subjects, has the potential to increase tone when exposed to dry air. Peripheral airways in dogs thus constitute a model that can be used for the investigation of exercise-induced asthma.


1989 ◽  
Vol 257 (5) ◽  
pp. R1147-R1153 ◽  
Author(s):  
A. J. Minisi ◽  
M. Dibner-Dunlap ◽  
M. D. Thames

Phenylephrine infusion (PE) has been used to raise arterial pressure (BP) in order to investigate reflex responses mediated by sinoaortic baroreflexes (SAB). Increases in cardiac filling pressures have been reported during PE. Our experiments determined whether PE selectively activates SAB without activation of vagal cardiopulmonary baroreflexes (CPR). We measured changes in mean BP, mean pulmonary arterial pressure (PAP), and renal sympathetic nerve activity (RSNA) during PE in alpha-chloralose-anesthetized dogs before and after sinoaortic denervation (SAD; n = 10), selective vagotomy (n = 9), or SAD and vagotomy (n = 4). PE elevated both BP and PAP in all dogs studied. In dogs with SAB and CPR intact, RSNA was reflexively inhibited (% change RSNA: -76.3 +/- 4.7). In SAD dogs, inhibition of RSNA was significantly attenuated but not abolished (% change RSNA: -27.5 +/- 11.8). This inhibition after SAD correlated closely with increases in PAP. Small BP changes (10 mmHg) were associated with insignificant changes in PAP and RSNA. Volume expansion after SAD produced changes in PAP and RSNA similar to those produced by PE. After selective vagotomy, the sensitivity (% change RSNA/mmHg change BP) of the reflex elicited by PE was significantly decreased (-2.7 +/- 0.03 pre vs. -1.8 +/- 0.12 post; P = 0.01). PE failed to change RSNA after combined SAD and vagotomy. We conclude that vagal CPR contribute to reflex inhibition of RSNA during PE except when elevations of BP are small.


1987 ◽  
Vol 63 (5) ◽  
pp. 1829-1836 ◽  
Author(s):  
P. Hanly ◽  
A. Sienko ◽  
R. B. Light

Acute bilateral Pseudomonas aeruginosa pneumonia was induced in 10 anesthetized dogs, after which five dogs received intravenous indomethacin (2 mg/kg) (indomethacin group), whereas five others were infused with saline (2 ml/kg) (control group). Plasma levels of 6-ketoprostaglandin F1 alpha(6-keto-PGF1 alpha) and thromboxane B2 (TxB2), stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), respectively, were measured by radioimmunoassay. Although TxB2 levels were not different before and after inoculation in either group, 6-keto-PGF1 alpha levels increased from their base-line value in each animal as pneumonia developed (indomethacin group: less than 100 to 330 +/- 90 pg/ml; control group: less than 100 to 630 +/- 300 pg/ml). Both prostaglandins fell to less than 100 pg/ml in each dog after indomethacin infusion, whereas they remained elevated in the control group after infusion of normal saline. Perfusion of consolidated lung regions (Qp/QT), measured with radioactive microspheres and expressed as a percent of total pulmonary blood flow, was dramatically reduced after indomethacin (35 +/- 3 to 16 +/- 1%) with consequent improvement in pulmonary shunt (Qs/QT: 30 +/- 8 to 18 +/- 6%) and arterial O2 tension (PaO2: 123 +/- 25 to 274 +/- 77 Torr). These parameters remained unchanged or deteriorated further in the control group after infusion of saline. Three additional dogs with Pseudomonas pneumonia were studied in which the indomethacin-induced reduction in Qp/QT was substantially but not completely reversed by intravenous infusion of PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)


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