Respiratory changes induced by prolonged laryngeal stimulation in awake piglets

1986 ◽  
Vol 61 (3) ◽  
pp. 1018-1024 ◽  
Author(s):  
D. F. Donnelly ◽  
G. G. Haddad
Keyword(s):  
Blood Pressure ◽  
Partial Pressure ◽  
Minute Ventilation ◽  
Young Animal ◽  
Whole Body ◽  
Electrode Placement ◽  
Base Line ◽  
Stimulus Period ◽  
Arterial Partial Pressure ◽  
Arterial Blood

To examine the role of the laryngeal reflex in modulating cardiorespiratory function, we stimulated the superior laryngeal nerves (SLN) bilaterally in unanesthetized, chronically instrumented piglets (n = 10, age 5–14 days). The SLN were placed in cuff electrodes and wires were exteriorized in the neck for stimulation. A cannula placed in the aorta was used for blood pressure recording and arterial blood sampling. During each experiment, 1–2 days after surgery, ventilation was recorded using whole-body plethysmography, and electroencephalogram and electrocardiogram were recorded after acute subcutaneous electrode placement. After base-line recordings, the SLN were electrically stimulated for 1 h. During this period, mean respiratory frequency decreased by 40–75% and apneas of 10–15 s were regularly interspersed between single breaths or clusters of breaths. Periods of breathing were always associated with opening of the eyes and generally with head and body movements, an awakening that occurred every 10–15 s. At 1 h into the stimulus period, minute ventilation had decreased by 57 +/- 7% (mean +/- SE), arterial partial pressure of O2 (PaO2) by 68 +/- 3 Torr, and arterial partial pressure of CO2 (PaCO2) had increased by 19 +/- 2 Torr. Throughout the entire stimulus period, mean blood pressure and average heart rate were maintained within 12% of base line. We suggest that: low-threshold SLN afferents exert primarily respiratory effects and only minor cardiovascular effects; breathing during laryngeal reflex activation is sustained by an arousal system; and the laryngeal reflex does not pose an imminent threat to the unanesthetized, awake, young animal.

Arterial and Mixed Venous Kinetics of Desflurane and Sevoflurane, Administered Simultaneously, at Three Different Global Ventilation to Perfusion Ratios in Piglets with Normal Lungs

2021 ◽  
Author(s):  
Moritz Kretzschmar ◽  
James E. Baumgardner ◽  
Alf Kozian ◽  
Thomas Hachenberg ◽  
Thomas Schilling ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Minute Ventilation ◽  
Arterial Partial Pressure ◽  
Arterial Blood ◽  
Partial Pressures ◽  
Inhaled Anesthetic ◽  
Kinetics Of ◽  
Normal Lungs ◽  
Mixed Venous

Background Previous studies have established the role of various tissue compartments in the kinetics of inhaled anesthetic uptake and elimination. The role of normal lungs in inhaled anesthetic kinetics is less understood. In juvenile pigs with normal lungs, the authors measured desflurane and sevoflurane washin and washout kinetics at three different ratios of alveolar minute ventilation to cardiac output value. The main hypothesis was that the ventilation/perfusion ratio ( .VA/.Q  ) of normal lungs influences the kinetics of inhaled anesthetics. Methods Seven healthy pigs were anesthetized with intravenous anesthetics and mechanically ventilated. Each animal was studied under three different .VA/.Q conditions: normal, low, and high. For each .VA/.Q condition, desflurane and sevoflurane were administered at a constant, subanesthetic inspired partial pressure (0.15 volume% for sevoflurane and 0.5 volume% for desflurane) for 45 min. Pulmonary arterial and systemic arterial blood samples were collected at eight time points during uptake, and then at these same times during elimination, for measurement of desflurane and sevoflurane partial pressures. The authors also assessed the effect of .VA/.Q on paired differences in arterial and mixed venous partial pressures. Results For desflurane washin, the scaled arterial partial pressure differences between 5 and 0 min were 0.70 ± 0.10, 0.93 ± 0.08, and 0.82 ± 0.07 for the low, normal, and high .VA/.Q conditions (means, 95% CI). Equivalent measurements for sevoflurane were 0.55 ± 0.06, 0.77 ± 0.04, and 0.75 ± 0.08. For desflurane washout, the scaled arterial partial pressure differences between 0 and 5 min were 0.76 ± 0.04, 0.88 ± 0.02, and 0.92 ± 0.01 for the low, normal, and high .VA/.Q conditions. Equivalent measurements for sevoflurane were 0.79 ± 0.05, 0.85 ± 0.03, and 0.90 ± 0.03. Conclusions Kinetics of inhaled anesthetic washin and washout are substantially altered by changes in the global  .VA/.Q   ratio for normal lungs. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

scholarly journals Observations on some cardiopulmonary effects of midazolam, xylazine and a midazolam / ketamine combination in the goat

1999 ◽  
Vol 70 (3) ◽  
Author(s):  
G.F. Stegmann
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Partial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Minute Volume ◽  
Partial Pressure Of Oxygen ◽  
Arterial Partial Pressure ◽  
Arterial Blood ◽  
Change In Mean

Xylazine, midazolam and a midazolam / ketamine combination were administered to 6 goats in a randomised 3-way block design. All goats received all treatments with at least a 7-day interval between treatments. Statistically significant (P < 0.05) changes were observed in some of the measured cardiopulmonary variables for xylazine and midazolam/ ketamine. Xylazine administration resulted in statistically significant decreases in minute volume, arterial partial pressure of oxygen, heart rate andmeanarterial blood pressure. The increase in arterial partial pressure of carbon dioxide was not statistically significant. For the midazolam / ketamine combination, the decrease in tidal volume was statistically significant, but not the decrease in minute volume and increase in arterial partial pressure of carbon dioxide. The decrease in the arterial partial pressure of oxygen was also statistically significant. The mean arterial blood pressure for the combination was statistically significantly higher compared to xylazine. The changes in cardiopulmonary variables after midazolam administration were not statistically significant, such as tidal and minute volume, arterial partial pressure of oxygen and carbon dioxide. However, clinically significant effects such as hypoventilation and hypoxia were observed after its administration. The change in mean arterial blood pressure was minimal.

Acute hypoxemia stimulates atrial natriuretic factor secretion in vivo

1988 ◽  
Vol 255 (2) ◽  
pp. H295-H300 ◽  
Author(s):  
A. J. Baertschi ◽  
J. M. Adams ◽  
M. P. Sullivan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Atrial Natriuretic Factor ◽  
Minute Ventilation ◽  
Base Line ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Arterial Po2

The hypothesis was tested that acute hypoxemia may be a physiological stimulus for atrial natriuretic factor (ANF) secretion in anesthetized, spontaneously breathing rabbits. Base-line plasma ANF (range from 29.8 to 219 pg/ml; mean +/- SE = 87.0 +/- 14.1 pg/ml; n = 16 rabbits) was negatively correlated with base-line arterial PO2 (r = -0.759; P less than 0.01) but not with PCO2, pH, mean arterial blood pressure, central venous pressure (CVP), minute ventilation, heart rate, or type of anesthetics used. Acute hypoxemia (arterial PO2 22.3-44.3 mmHg) lasting 10 min increased plasma ANF levels over base line by 69.2 +/- 47.7 (SE) pg/ml at 6 min and 87.5 +/- 46.8 (SE) pg/ml at 9 min (P less than 0.01; n = 9). The increase in arterial pH and minute ventilation and the decrease of arterial PCO2 paralleled the changes in plasma ANF. Mean arterial blood pressure, CVP, and heart rate did not change significantly. ANF responses to hypoxemia (range from 4.4 to 423 pg/ml) correlated with base-line CVP (r = 0.761; P less than 0.01) and base-line ANF (r = 0.523; P less than 0.05) but with no other measured variable. Although the mediators of hypoxemia-induced release of ANF need to be explored further, this study raises the possibility that ANF might be involved in the adaptation to hypoxemia.

Cardiovascular and metabolic responses to temperature in Coluber constrictor

1987 ◽  
Vol 253 (2) ◽  
pp. R222-R227 ◽  
Author(s):  
J. N. Stinner
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Stroke Volume ◽  
Minute Ventilation ◽  
Marked Change ◽  
Effect Of Temperature ◽  
Metabolic Demand ◽  
Thermal Dependence ◽  
Arterial Blood ◽  
Coluber Constrictor

The cardiovascular adjustments associated with elevated metabolic demand caused by rising body temperature were investigated in Coluber constrictor. From 16 to 35 degrees C, O2 consumption increased roughly ninefold. Systemic blood flow, determined by the Fick method, increased approximately 4.5-fold and arteriovenous O2 difference increased approximately 2-fold. Heart rate steadily increased over the temperature range examined. At the cooler temperatures stroke volume also increased but, above approximately 25 degrees C, stroke volume declined with rising temperature. The changes in stroke volume may result from the direct effect of temperature on myocardial contractility. The thermal dependence of blood convection requirement in C. constrictor is similar to changes in air convection requirement determined in a previous study. Consequently the minute ventilation-to-perfusion ratio appears to be independent of temperature, at least from 20 to 35 degrees C. Systemic arterial blood pressure increases with rising body temperature due to the rise in cardiac output, whereas vascular resistance declines. Blood pressure in snakes disturbed by the investigator is roughly two times higher than in resting animals at all temperatures studied. This marked change in blood pressure suggests an "alarm reaction" mediated by the sympathetic nervous system.

scholarly journals Heat stress alters hemodynamic responses during the Valsalva maneuver

2010 ◽  
Vol 108 (6) ◽  
pp. 1591-1594 ◽  
Author(s):  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Phase Ii ◽  
Valsalva Maneuver ◽  
Late Phase ◽  
Thermal Conditions ◽  
Whole Body ◽  
Hemodynamic Responses ◽  
Arterial Blood

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

Suctioning and Cerebral Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Base Line ◽  
Arterial Blood

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.

Abstract P102: Liver Acquitted, Fat Indicted: Hepatic Chemerin Knockdown Does Not Reduce Blood Pressure While Whole-body Knockdown Does

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
David J Ferland ◽  
Bridget Seitz ◽  
Emma S Darios ◽  
Janice M Thompson ◽  
Steve T Yeh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Reduce Blood Pressure ◽  
Blood Pressure Regulation ◽  
Whole Body ◽  
Pressure Regulation ◽  
Perivascular Adipose Tissue ◽  
Subcutaneous Injections ◽  
Arterial Blood ◽  
Phosphate Buffered Saline

Chemerin is an inflammatory adipokine positively associated with hypertension and obesity with the majority of chemerin thought to derive from the liver and adipose tissue. The contributions of liver-derived chemerin to plasma chemerin levels and blood pressure regulation are unknown. We compared whole-body vs liver chemerin inhibition using antisense oligonucleotides (ASO) with liver-restricted activity (GalNAc) or liver and fat activity (Gen 2.5). We hypothesized that in normotensive male SD rats, circulating chemerin is predominately liver-derived and regulates blood pressure. A scrambled ASO control and phosphate-buffered saline (PBS) were used as controls and radiotelemetry was used to monitor blood pressure. Baseline mean arterial blood pressure (MAP) was recorded for one week, beginning 5 days after surgery to establish a baseline. ASOs were given weekly by subcutaneous injections for four weeks. Two days after the final injection, animals were sacrificed for tissue RT-PCR and plasma chemerin measurements using Western analysis. Gen 2.5 chemerin ASO treatments (compared to PBS control) reduced chemerin mRNA in liver, retroperitoneal fat, and mesenteric perivascular adipose tissue (mPVAT) by 99.5% ± 0.1%, 95.2% ± 0.3%, and 69% ± 2%, respectively, and plasma chemerin was reduced to undetectable levels. GalNAc chemerin ASO treatments (compared to PBS control) reduced chemerin mRNA in liver by 97.9% but had no effect on chemerin expression in retroperitoneal fat and mPVAT; plasma chemerin was reduced by 90% ± 5%. Gen 2.5 chemerin ASO treatment reduced MAP, which reached a nadir of 7 ± 2.1 mmHg 48 – 72 hours after each dose compared to the scrambled ASO controls. By contrast, MAP was unchanged in animals receiving the GalNAc chemerin ASO. Thus, although most circulating chemerin is liver-derived, plasma chemerin does not play a role in blood pressure regulation. This study suggests that while chemerin is still generally associated with increased blood pressure, circulating chemerin levels cannot directly predict this effect. In addition, local effects of chemerin from fat may explain this discrepancy and support chemerin’s association with both hypertension and obesity.

Role of adrenal catecholamines during forced submergence in ducks

1991 ◽  
Vol 261 (6) ◽  
pp. R1364-R1372 ◽  
Author(s):  
A. M. Lacombe ◽  
D. R. Jones
Keyword(s):  
Blood Pressure ◽  
Partial Pressure ◽  
Heart Rates ◽  
Peripheral Vasoconstriction ◽  
Arterial Partial Pressure ◽  
Arterial Ph ◽  
Venous Infusion ◽  
Lactate Levels

Maximum underwater tolerance (UTmax) of chronically adrenalectomized ducks (ADX, 5.3 +/- 0.3 min) and chronically adrenal-denervated ducks (DNX, 7.2 +/- 0.2 min) was significantly lower than sham-operated controls (SH-ADX, 10 +/- 0.8 min; SH-DNX, 12.2 +/- 0.5 min). After 4 min forced submergence, heart rates of ADX (62 +/- 16 beats/min) and DNX (31 +/- 2 beats/min) ducks were significantly higher than in their respective sham-operated controls (23 +/- 3 and 17 +/- 2 beats/min), although their blood pressure was significantly lower. Arterial partial pressure of O2, arterial O2 content, arterial pH, and lactate levels in DNX ducks (42 +/- 2 mmHg, 4.5 +/- 0.8 ml O2/100 ml blood, 7.233 +/- 0.016, 3.1 +/- 0.3 mM, respectively) were significantly lower than in SH-DNX ducks after 5 min forced submergence (53 +/- 1 mmHg, 6.8 +/- 0.4 ml O2/100 ml blood, 7.301 +/- 0.007, 4.8 +/- 0.4 mM, respectively). Venous infusion of catecholamines in ADX and DNX ducks during forced submergence significantly increased UTmax. It is suggested that adrenal catecholamines increase tolerance to underwater submersion by enhancing peripheral vasoconstriction, thus preserving the O2 stores for the heart and brain. Other adrenal products could also be involved.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

Ventilatory failure during loaded breathing: the role of central neural drive

1988 ◽  
Vol 65 (1) ◽  
pp. 249-255 ◽  
Author(s):  
J. F. Watchko ◽  
T. A. Standaert ◽  
D. E. Mayock ◽  
G. Twiggs ◽  
D. E. Woodrum
Keyword(s):  
Minute Ventilation ◽  
Respiratory Muscles ◽  
Muscle Performance ◽  
Emg Activity ◽  
Base Line ◽  
Force Frequency ◽  
Peripheral Muscle ◽  
Arterial Blood ◽  
Loaded Breathing ◽  
Ventilatory Failure

Minute ventilation (VE), arterial blood gases, diaphragmatic electromyogram (EMG) activity, centroid frequency (Fc) and peak inspiratory airway pressures (Paw) were measured in five unanesthetized tracheostomized infant monkeys during various intensities of inspiratory resistive loaded breathing (IRL) until either 1) ventilatory failure occurred (failed trial) or 2) normocapnia was sustained for 1 h (successful trial). During successful trials VE and arterial PCO2 (PaCO2) were sustained at base-line levels, and an increase in peak integrated diaphragmatic EMG activity and peak inspiratory Paw occurred. In contrast, during ventilatory failure runs, VE decreased and PaCO2 rose compared with their respective base-line values. The fall in VE occurred secondary to a significant decline in breathing frequency. Tidal volume was sustained at base-line levels during all trials (both successful and failed groups). Inspiratory Paw's and peak moving time average EMG were sustained at elevated levels during ventilatory failure runs, suggesting that the respiratory muscles did not fail as pressure generators. Furthermore, the EMG Fc did not change from base line during either successful or failed trials. These data suggest that peripheral muscle fatigue did not occur, although in the absence of a more direct test of muscle performance, i.e., a force-frequency curve, we cannot rule out the possibility that a component of peripheral failure contributed to our results. Ventilatory failure during severe IRL in the infant monkey was most clearly associated with an alteration in the respiratory center timing mechanism, i.e., such failure was a function of a decline in respiratory frequency.

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