Involvement of the fastigial nuclei in vagally mediated respiratory responses

1997 ◽  
Vol 82 (6) ◽  
pp. 1853-1861 ◽  
Author(s):  
Fadi Xu ◽  
Donald T. Frazier
Keyword(s):  
External Jugular Vein ◽  
Vagal Afferents ◽  
Mechanical Stimuli ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Before And After ◽  
The Right ◽  
Bilateral Lesions ◽  
Respiratory Reflexes ◽  
Respiratory Responses

Xu, Fadi, and Donald T. Frazier. Involvement of the fastigial nuclei in vagally mediated respiratory responses. J. Appl. Physiol. 82(6): 1853–1861, 1997.—Previous studies have demonstrated that the cerebellum, especially the fastigial nucleus (FN), is capable of modulating respiratory responses to chemical and mechanical stimuli. Because there is evidence to show projections from vagal afferents to the FN, the goal of this study was to determine the role of the FN in the respiratory reflexes elicited by activation of vagal afferents. Experiments were performed in anesthetized (chloralose), paralyzed, and artificially ventilated cats with an occipital exposure of the cerebellum. Administration of capsaicin (Cap; 5–10 μg/kg) via the right external jugular vein at the end of inspiration and application of lung inflation (LI; 10 cmH2O) during inspiration were carried out to stimulate nonmyelinated and myelinated vagal afferents, respectively. The phrenic neurogram was recorded as an index of the respiratory motor output. Control cardiorespiratory variables [expiratory duration (Te), arterial blood pressure] and their immediate responses to stimuli were compared before and after bilateral lesions of the FN. The results showed the following. 1) Cap injection and LI resulted in a dramatic increase in Te (apnea). 2) FN lesions did not significantly alter the control Te; however, the apneic duration induced by Cap injection was prolonged. 3) Neither FN lesions nor cerebellectomy affected the apneic duration that resulted from application of LI. 4) Cold blockade of the vagi (6–8°C) eliminated the respiratory responses elicited by LI but not Cap injection; vagotomy abolished the responses to both stimuli. 5) FN lesions did not change the control ABP or its responses to either LI or Cap injection. It is concluded that the FN is involved in vagally mediated respiratory reflexes elicited by activation of nonmyelinated (C-fiber) vagal afferents.

Ozone enhances excitabilities of pulmonary C fibers to chemical and mechanical stimuli in anesthetized rats

1998 ◽  
Vol 85 (4) ◽  
pp. 1509-1515 ◽  
Author(s):  
Ching-Yin Ho ◽  
Lu-Yuan Lee
Keyword(s):  
Low Dose ◽  
Acute Exposure ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Baseline Activity ◽  
Tracheal Pressure ◽  
C Fiber

Acute exposure to ozone (O3) enhances pulmonary chemoreflex response to capsaicin, and an increased sensitivity of bronchopulmonary C-fiber afferent endings may be involved. The present study was aimed at determining the effect of O3 on the responses of pulmonary C fibers to chemical and mechanical stimuli. A total of 31 C fibers were studied in anesthetized, open-chest, and vagotomized rats. During control, right atrial injection of a low dose of capsaicin abruptly evoked a short and mild burst of discharge [0.77 ± 0.28 impulses (imp)/s, 2-s average]. After acute exposure to O3 (3 parts/million for 30 min), there was no significant change in arterial blood pressure, tracheal pressure, or baseline activity of C fibers. However, the stimulatory effect of the same dose of capsaicin on these fibers was markedly enhanced (6.05 ± 0.88 impulses/s; P < 0.01) and prolonged immediately after O3 exposure, and returned toward control in 54 ± 6 min. Similarly, the pulmonary C-fiber response to injection of a low dose of lactic acid was also elevated after O3 exposure. Furthermore, O3 exposure significantly potentiated the C-fiber response to constant-pressure (tracheal pressure = 30 cmH2O) lung inflation (control: 0.19 ± 0.07 imp/s; after O3: 1.12 ± 0.26 imp/s; P < 0.01). In summary, these results show that the excitabilities of pulmonary C-fiber afferents to lung inflation and injections of chemical stimulants are markedly potentiated after acute exposure to O3, suggesting a possible involvement of these afferents in the O3-induced changes in breathing pattern and chest discomfort in humans.

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion

2002 ◽  
Vol 93 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Hydrogen Ion ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Hydrogen Ions ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Blood Ph ◽  
C Fiber

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO2-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO2-enriched gas mixture (15% CO2, balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 ± 0.01 to 7.17 ± 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25–1.0 μg/kg) was significantly increased from 3.07 ± 0.70 impulses/s at control to 8.48 ± 1.52 impulses/s during HPC ( n = 27; P < 0.05), and this enhanced response returned to control within ∼10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4–8 μg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36–1.82 mmol · kg−1 · min−1 for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO2 is mediated through the action of hydrogen ions on the C-fiber sensory terminals.

The effect of nimodipine on intracranial pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Mark N. Hadley ◽  
Robert F. Spetzler ◽  
Mary S. Fifield ◽  
William D. Bichard ◽  
John A. Hodak
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Systemic Blood Pressure ◽  
Artery Occlusion ◽  
Content Type ◽  
Arterial Blood ◽  
Increased Risk ◽  
Before And After ◽  
The Right ◽  
Cerebral Artery Occlusion

✓ Nimodipine was administered by intravenous infusion to six male baboons before, during, and after 6 hours of middle cerebral artery occlusion. Intracranial pressure (ICP) and systemic blood pressure were monitored continuously. An epidural balloon was inflated at regular intervals at three levels of arterial CO2 tension (25, 35, and 50 mm Hg) before and after the administration of nimodipine, and volume-pressure curves were generated. In every case, curves generated after intravenous nimodipine infusion were lower and shifted more to the right than the same set of curves generated before nimodipine administration, regardless of the baseline ICP. The reduction in ICP following nimodipine infusion was not due to a reduction in mean arterial blood pressure and was statistically significant at all three levels of pCO2 (p < 0.01). These results suggest that, in the presence of elevated ICP due to cerebral infarction, there is no increased risk of exacerbating intracranial hypertension with the addition of nimodipine.

Lung inflation evokes reflex dilation of microvessels in rat skeletal muscle

1990 ◽  
Vol 258 (4) ◽  
pp. H939-H945 ◽  
Author(s):  
J. Yu ◽  
A. M. Roberts ◽  
I. G. Joshua
Keyword(s):  
Skeletal Muscle ◽  
Femoral Nerve ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Vagal Afferents ◽  
Physiological Salt Solution ◽  
Vagus Nerves ◽  
Lung Inflation ◽  
Index Of Microcirculatory Resistance ◽  
The Right

Lung inflation can reflexively decrease peripheral resistance, but effects on the microcirculation have not been determined. In this study, we examined the effects of lung inflation on microvessels in skeletal muscle. In anesthetized spontaneously breathing rats, the right cremaster muscle with intact circulation and innervation was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles (3As) were displayed by television microscopy and measured as an index of microcirculatory resistance. In other experiments, sympathetic activity (in the genital femoral nerve) to the cremaster was recorded. Lung inflation decreased systemic blood pressure by 32 +/- 3 mmHg and increased 3A diameter by approximately 23% (P less than 0.05, n = 17). The increase was abolished by cutting the cervical vagus nerves or the right genital femoral nerve. Furthermore, inflation decreased sympathetic nerve activity by 47.6 +/- 11.3% (P less than 0.05, n = 5) before vagotomy but not after. Dilation in response to inflation was also abolished by phentolamine or guanethidine. These results suggest that stimulation of vagal afferents by inflation reflexively decreases microvascular resistance by withdrawal of sympathetic tone.

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate

1989 ◽  
Vol 257 (3) ◽  
pp. R595-R598 ◽  
Author(s):  
K. G. Cornish ◽  
M. W. Barazanji ◽  
T. Yong ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Nonhuman Primate ◽  
Volume Expansion ◽  
Maximum Sensitivity ◽  
Response Curves ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Before And After ◽  
The Right

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

scholarly journals Ultrasound evaluation of piglet diaphragm function before and after fatigue

1997 ◽  
Vol 83 (5) ◽  
pp. 1654-1659 ◽  
Author(s):  
Keith C. Kocis ◽  
Peter J. Radell ◽  
Wayne I. Sternberger ◽  
Jane E. Benson ◽  
Richard J. Traystman ◽  
...  
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Blood Gases ◽  
Mean Velocity ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Diaphragm Function ◽  
Ultrasound Evaluation ◽  
Before And After ◽  
The Right

Kocis, Keith C., Peter J. Radell, Wayne I. Sternberger, Jane E. Benson, Richard J. Traystman, and David G. Nichols. Ultrasound evaluation of piglet diaphragm function before and after fatigue. J. Appl. Physiol. 83(5): 1654–1659, 1997.—Clinically, a noninvasive measure of diaphragm function is needed. The purpose of this study is to determine whether ultrasonography can be used to 1) quantify diaphragm function and 2) identify fatigue in a piglet model. Five piglets were anesthetized with pentobarbital sodium and halothane and studied during the following conditions: 1) baseline (spontaneous breathing); 2) baseline + CO2 [inhaled CO2 to increase arterial[Formula: see text] to 50–60 Torr (6.6–8 kPa)]; 3) fatigue + CO2 (fatigue induced with 30 min of phrenic nerve pacing); and 4) recovery + CO2 (recovery after 1 h of mechanical ventilation). Ultrasound measurements of the posterior diaphragm were made (inspiratory mean velocity) in the transverse plane. Images were obtained from the midline, just inferior to the xiphoid process, and perpendicular to the abdomen. M-mode measures were made of the right posterior hemidiaphragm in the plane just lateral to the inferior vena cava. Abdominal and esophageal pressures were measured and transdiaphragmatic pressure (Pdi) was calculated during spontaneous (Sp) and paced (Pace) breaths. Arterial blood gases were also measured. Pdi(Sp) and Pdi(Pace) during baseline + CO2 were 8 ± 0.7 and 49 ± 11 cmH2O, respectively, and decreased to 6 ± 1.0 and 27 ± 7 cmH2O, respectively, during fatigue + CO2. Mean inspiratory velocity also decreased from 13 ± 2 to 8 ± 1 cm/s during these conditions. All variables returned to baseline during recovery + CO2. Ultrasonography can be used to quantify diaphragm function and identify piglet diaphragm fatigue.

Mechanisms of Respiratory Responses to Vasodilator Drugs Urecholine (Carbaminoyl Beta-Methylcholine) and Nitroglycerine

1957 ◽  
Vol 189 (1) ◽  
pp. 123-128 ◽  
Author(s):  
Robert T. Schopp ◽  
Thomas M. Gilfoil ◽  
William B. Youmans
Keyword(s):  
Blood Pressure ◽  
Sodium Cyanide ◽  
Respiratory Response ◽  
Vasodilator Drugs ◽  
Arterial Blood ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Alpha Chloralose ◽  
Respiratory Stimulation ◽  
Respiratory Responses

The effects on respiratory rate and amplitude following intravenous injection of the vasodilator drugs, Urecholine (carbaminoyl-beta-methylcholine) and nitroglycerine were determined in dogs before and after bilateral vagotomy and isolation of the carotid sinuses. The animals were anesthetized with sodium pentothal followed by alpha-chloralose (70 mg/kg). Following the procedures for denervation of sino-aortic pressoreceptors and carotid and aortic chemoreceptors the animals showed no respiratory response to 1–2 mg sodium cyanide. It was found that the respiratory stimulation which occurs during the fall in blood pressure induced by injection of Urecholine or nitroglycerine frequently persists after sino-aortic denervation. The respiratory stimulation in the denervated animals in response to nitroglycerine was reduced or prevented in individual experiments by counteracting the fall in arterial blood pressure by means of a pressure-regulating device. It is concluded that in the dosage used nitroglycerine, and possibly also Urecholine, exert their effects on respiration indirectly by causing alterations in blood pressure or blood flow rather than through any specific action on the respiratory center.

Effect of unilateral and bilateral auditory cortex lesions on the discrimination of vocalizations by Japanese macaques

1986 ◽  
Vol 56 (3) ◽  
pp. 683-701 ◽  
Author(s):  
H. E. Hefner ◽  
R. S. Heffner
Keyword(s):  
Auditory Cortex ◽  
Right Hemisphere ◽  
Japanese Macaque ◽  
Great Difficulty ◽  
Japanese Macaques ◽  
Detectable Effect ◽  
Before And After ◽  
Species Specific ◽  
The Right ◽  
Bilateral Lesions

Ten Japanese macaques were trained to discriminate between two types of Japanese macaque coo vocalizations before and after auditory cortex ablation. Five of the animals were tested following left unilateral ablation, whereas the other five were tested following right unilateral ablation. After postoperative testing, symmetrical lesions were made in the remaining hemisphere in two animals from each group and the effect of bilateral lesions was assessed. The animals were tested using a shock avoidance procedure. Unilateral ablation of left auditory cortex consistently resulted in an initial impairment in the ability to discriminate between the vocalizations with the animals regaining normal performance in 5-15 sessions. In contrast, right unilateral ablation had no detectable effect on the discrimination. Bilateral auditory cortex ablation rendered the animals permanently unable to discriminate between the coos. Although the monkeys could learn to discriminate the coos from noise and from 2- and 4-kHz tones, they had great difficulty in discriminating between the coos and tones in the same frequency range as the coos (i.e., 500 Hz and 1 kHz). The initial impairment following left unilateral lesions indicates that the ability to perceive species-specific vocalizations is lateralized to the left hemisphere. The observation that bilateral lesions abolish the discrimination indicates that the recovery in the left lesion cases was the result of the right hemisphere mediating the discrimination.

Hepatic Congestion Induced by Partial Occlusion of the Hepatic Veins in Healthy Dogs

1968 ◽  
Vol 26 ◽  
pp. 116-117
Author(s):  
F. R. Dawoud ◽  
J. J. Ghidoni
Keyword(s):  
Hepatic Vein ◽  
Jugular Vein ◽  
Light And Electron Microscopy ◽  
Vena Cava ◽  
Middle Lobe ◽  
External Jugular Vein ◽  
Hepatic Veins ◽  
Hepatic Congestion ◽  
Before And After ◽  
The Right

The inferior vena cava and hepatic veins of twenty randomly selected normal dogs (22-27 kg) were exposed through a right transthoracic, transdiaphragmatic incision. The small hepatic vein from the middle lobe of the liver was routinely ligated. After the hepatic vein draining the left 3 lobes of the liver was catheterized from the right external jugular vein, a tape was passed around that hepatic vein. The pressure in the intrahepatic part of the hepatic vein was measured and recorded before and after reducing the main left hepatic vein to the size of the catheter by tying the tape. The catheter was cut short and inserted into the jugular vein to establish limited hepatic drainage through a lumen of known and constant cross section; the catheters were accessible for additional pressure measurements. The animals were killed according to a predetermined schedule at 1, 3, 7, and 15 days. Specimens for light and electron microscopy were taken from the congested and uncongested lobes of the liver. Tissues were fixed in cold cacodylate buffered 5% glutaraldehyde and postfixed with osmium. Tissue blocks were rapidly dehydrated and embedded in a mixture of Maraglas, D.E.R. 732, and DDSA.

Sign in / Sign up

Export Citation Format

Share Document