Effect of vagotomy and vagal stimulation on lung mechanics and circulation

1963 ◽  
Vol 18 (5) ◽  
pp. 881-887 ◽  
Author(s):  
H. J. H. Colebatch ◽  
D. F. J. Halmagyi
Keyword(s):  
Arterial Pressure ◽  
Vagal Stimulation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Lung Mechanics ◽  
Respiratory Pattern ◽  
Peripheral Airway ◽  
Inspiratory Resistance ◽  
Cervical Vagotomy ◽  
Pulmonary Arterial

In sheep, anesthetized and intubated, bilateral cervical vagotomy produced no change in lung compliance (Cl), reduced inspiratory resistance to airflow, increased expiratory resistance to airflow, and changed the pattern of breathing. Electrical stimulation of the peripheral end of the cut vagus nerve produced an immediate increase in lung volume due to an increase in inspiratory tonus, a fall in Cl, an increase in resistance to airflow, and a decrease in heart rate and systemic arterial pressure. Pulmonary arterial pressure remained unchanged; pulmonary arterial resistance increased. These effects were blocked by atropine. The lung mechanics changes were partly reversed spontaneously, completely reversed by forced inflation, and potentiated by prostigmine. The effects on lung mechanics suggest that vagal stimulation in the sheep mainly affects the peripheral airways producing airway closure, and indicates the possibility of a nervous mechanism for the control of the number of ventilated lung units. compliance; total pulmonary resistance; inspiratory; tonus; peripheral airway reaction; respiratory pattern Submitted on December 6, 1962

Mechanism and pharmacology of endotoxin shock in sheep

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
Author(s):  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Arterial Oxygen Saturation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Arterial Oxygen ◽  
Marked Rise ◽  
Pulmonary Arterial ◽  
Pressure Fall

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

Cardiorespiratory effects of rapid saline infusion in normal man

1975 ◽  
Vol 38 (5) ◽  
pp. 786-775 ◽  
Author(s):  
A. L. Muir ◽  
D. C. Flenley ◽  
B. J. Kirby ◽  
M. F. Sudlow ◽  
A. R. Guyatt ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Control Period ◽  
Lung Compliance ◽  
Saline Infusion ◽  
Tidal Range ◽  
Closing Volume ◽  
Rapid Infusion ◽  
Pulmonary Arterial

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

Vasomotor waves of arterial blood pressure after cessation of cardiopulmonary bypass in man

Perfusion ◽  
1990 ◽  
Vol 5 (4) ◽  
pp. 261-266
Author(s):  
V. Vainionpää ◽  
A. Hollme'n ◽  
J. Timisjärvi
Keyword(s):  
Blood Pressure ◽  
Cardiopulmonary Bypass ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Heart Patients ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Epicardial Pacing

The occurrence of vasomotor waves during cardiopulmonary bypass (CPB) is a recognized phenomenon. The lesser known oscillation of arterial pressure after cessation of CPB was observed in 18 open-heart patients. The duration of an oscillatory wave was 13.5±5.0 seconds, the amplitude 6.1 ±2.6mmNg and the mean arterial pressure 76.5± 10.7mmHg. Inter-and also intraindividual variations in frequency and amplitude of the oscillation, however, did occur. In 13 patients, this oscillation occurred during ventricular epicardial pacing. The oscillation continued until the end of the operation in eight patients; in others, the oscillation was of shorter duration. An oscillation of pulmonary arterial pressure (PAP) was simultaneously observed in nine patients (eight with pacemaker) and central venous pressure (CVP) oscillation in eight patients (all with pacemaker). The duration of a wave was the same as in systemic arterial pressure and the amplitudes were 1.5-3.0mmHg in PAP and 1.0-2.0mmHg in CVP. These arterial vasomotor waves, seen here after CPB, largely resemble those observed during perfusion in man and also the Mayerwaves explored in experimental animals. The pacing rhythm seems to favourthe appearance of those blood pressure oscillations.

Upstream pressure for systemic to pulmonary flow from bronchial circulation in dogs

1987 ◽  
Vol 63 (2) ◽  
pp. 485-491 ◽  
Author(s):  
P. G. Agostoni ◽  
M. E. Deffebach ◽  
W. Kirk ◽  
S. Lakshminarayan ◽  
J. Butler
Keyword(s):  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Driving Pressure ◽  
Upstream Site ◽  
Bronchial Circulation ◽  
Pulmonary Flow ◽  
Upstream Pressure ◽  
Pulmonary Arterial ◽  
Bidirectional Flow

Systemic to pulmonary flow from bronchial circulation, important in perfusing potentially ischemic regions distal to pulmonary vascular obstructions, depends on driving pressure between an upstream site in intrathoracic systemic arterial network and pulmonary vascular bed. The reported increase of pulmonary infarctions in heart failure may be due to a reduction of this driving pressure. We measured upstream element for driving pressure for systemic to pulmonary flow from bronchial circulation by raising pulmonary venous pressure (Ppv) until the systemic to pulmonary flow from bronchial circulation ceased. We assumed that this was the same as upstream pressure when there was flow. Systemic to pulmonary flow from bronchial circulation was measured in left lower lobes (LLL) of 21 anesthetized open-chest dogs from volume of blood that overflowed from pump-perfused (90–110 ml/min) pulmonary vascular circuit of LLL and was corrected by any changes of LLL fluid volume (wt). Systemic to pulmonary flow from bronchial circulation upstream pressure was linearly related to systemic arterial pressure (slope = 0.24, R = 0.845). Increasing Ppv caused a progressive reduction of systemic to pulmonary flow from bronchial circulation, which stopped when Ppv was 44 +/- 6 cmH2O and pulmonary arterial pressure was 46 +/- 7 cmH2O. A further increase in Ppv reversed systemic to pulmonary flow from bronchial circulation with blood flowing back into the dog. When net systemic to pulmonary flow from bronchial circulation by the overflow and weight change technique was zero a small bidirectional flow (3.7 +/- 2.9 ml.min-1 X 100 g dry lobe wt-1) was detected by dispersion of tagged red blood cells that had been injected.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhaled nitric oxide partially reverses hypoxic pulmonary vasoconstriction in the dog

1994 ◽  
Vol 76 (3) ◽  
pp. 1350-1355 ◽  
Author(s):  
J. A. Romand ◽  
M. R. Pinsky ◽  
L. Firestone ◽  
H. A. Zar ◽  
J. R. Lancaster
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Vasomotor Tone ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmonary vasomotor tone decreases pulmonary arterial pressure (Ppa). We conducted this study to better characterize the hemodynamic effects induced by NO inhalation during hypoxic pulmonary vasoconstriction in 11 anesthetized ventilated dogs. Arterial and venous systemic and pulmonary pressures and aortic flow probe-derived cardiac output were recorded, and nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) were measured. The effects of 5 min of NO inhalation at 0, 17, 28, 47, and 0 ppm during hyperoxia (inspiratory fraction of O2 = 0.5) and hypoxia (inspiratory fraction of O2 = 0.16) were observed. NO inhalation has no measurable effects during hyperoxia. Hypoxia induced an increase in Ppa that reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO induced an immediate (< 30 s) decrease in Ppa and calculated pulmonary vascular resistance (P < 0.05 each) but did not return either to baseline hyperoxic values. Increasing the concentration of NO to 74 and 145 ppm in two dogs during hypoxia did not induce any further decreases in Ppa. Reversing hypoxia while NO remained at 47 ppm further decreased Ppa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systemic arterial pressure. MetHb remained low, and NO-Hb was unmeasurable. We concluded that NO inhalation only partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective to the pulmonary circulation.

Comparative responses to endothelin-2 and sarafotoxin 6b in the pulmonary vascular bed of the cat

1991 ◽  
Vol 69 (2) ◽  
pp. 211-214 ◽  
Author(s):  
R. K. Minkes ◽  
B. D. Nossaman ◽  
P. Kvamme ◽  
P. J. Kadowitz
Keyword(s):  
Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Significant Activity ◽  
Constant Flow ◽  
Carboxy Terminus ◽  
Flow Conditions ◽  
Vascular Bed ◽  
Natural Flow ◽  
Pulmonary Arterial ◽  
Pulmonary Vascular Bed

Pulmonary vascular responses to endothelin-2 and sarafotoxin 6b were investigated in the feline pulmonary vascular bed under natural flow and constant flow conditions. Injections of endothelin-2 and sarafotoxin 6b in a dose of 0.3 nmol/kg iv increased pulmonary arterial and left atrial pressures and cardiac output, and caused a biphasic change in calculated pulmonary vascular resistance. Endothelin-2 caused a biphasic change in systemic arterial pressure, while sarafotoxin 6b only decreased arterial pressure. Under constant flow conditions in the intact-chest cat, injections of endothelin-2 and sarafotoxin 6b in doses of 0.1–1 nmol into the perfused lobar artery increased lobar arterial pressure in a dose-related manner but were less potent than the thromboxane A2 mimic, U46619. An ET analog with only the Cys1–Cys15 disulfide bond and an amidated carboxy terminus had no significant activity in the pulmonary vascular bed. The present data show that endothelin-2 and sarafotoxin 6b have significant vasoconstrictor activity in the pulmonary vascular bed of the cat.Key words: pulmonary circulation, endothelin-2, sarafotoxin 6b.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

A Study of Prostaglandins and Prostaglandin Antagonists in Relation to Anaphylaxis in Calves

1974 ◽  
Vol 52 (5) ◽  
pp. 942-951 ◽  
Author(s):  
J. F. Burka ◽  
P. Eyre
Keyword(s):  
Arterial Pressure ◽  
Broad Spectrum ◽  
Systemic Arterial Pressure ◽  
Protective Effects ◽  
Systemic Anaphylaxis ◽  
Superfusion System ◽  
Transient Rise ◽  
Diethylcarbamazine Citrate ◽  
Pulmonary Arterial ◽  
Prostaglandin Antagonists

Actions of prostaglandins (PG) E1, E2, and F2α on the cardiovascular–respiratory systems of anesthetized calves were studied in conjunction with the effects of a series of prostaglandin antagonists on acute systemic anaphylaxis. Meclofenamate, acetylsalicylic acid (ASA), phenylbutazone, and indomethacin, all inhibitors of PG synthesis, were particularly effective in protecting calves from anaphylactic cardiovascular shock. Meclofenamate showed "broad spectrum" antagonism of the mediators of anaphylaxis. Indomthacin and ASA eliminated the biphasic fall in systemic arterial pressure, suggesting that prostaglandins may be involved, together with biogenic amines, in the early stages of anaphylaxis. SC-19220, polyphloretin phosphate, and diethylcarbamazine citrate (DECC) had little or no inhibitory effects against exogenous prostaglandins and afforded only weak protection against systemic anaphylaxis. "Broad spectrum" inhibition of amine and PG receptors, as well as inhibition of slow-reacting substance of anaphylaxis formation and release, may account for part of the protective effects of DECC. A blood-bathed superfusion system suggested participation by PG F2α in bovine anaphylaxis. Cardiovascular–respiratory changes induced by exogenous prostaglandins in calves suggest that PG F2α may be responsible for the transient rise in systemic arterial pressure and increase in pulmonary arterial pressure in anaphylaxis, whereas PG E1 and E2 may be participating in the primary fall in systemic arterial pressure.

Influence of nitroglycerin on splanchnic capacity and splanchnic capacity-cardiac output relationship

1994 ◽  
Vol 76 (1) ◽  
pp. 112-119 ◽  
Author(s):  
M. A. Morse ◽  
D. L. Rutlen
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Carotid Sinus ◽  
Systemic Arterial Pressure ◽  
Intravascular Volume ◽  
Portal Flow ◽  
Portal Vein Pressure ◽  
Cervical Vagotomy

It has been postulated, but not tested directly, that nitroglycerin's venodilatory effects attenuate cardiac output. Thus, the present study examined the importance of changes in splanchnic capacity, as assessed by scintigraphy, in the regulation of cardiac output during nitroglycerin administration in 16 anesthetized pigs under conditions of carotid sinus denervation and cervical vagotomy. With nitroglycerin administration (0.5 mg/min i.v.) for 5 min, systemic arterial pressure decreased from 115 +/- 7 to 95 +/- 7 mmHg (P < 0.0001), portal vein pressure decreased from 9.0 +/- 0.5 to 8.5 +/- 0.5 mmHg (P < 0.0001), portal flow increased from 637 +/- 49 to 668 +/- 60 ml/min (P = 0.09), and transhepatic resistance decreased from 7.5 +/- 1.5 to 6.5 +/- 1.0 mmHg.min.l-1 (P < 0.01), but cardiac output was unchanged (1,929 +/- 126 to 1,890 +/- 138 ml/min). Total splanchnic intravascular volume (VI) increased 1.6 +/- 1.0% (P < 0.05, 14 +/- 10 ml). This increase was due to an increment in extrahepatosplenic (mesenteric) VI (12.9 +/- 1.9%, P < 0.0001), since splenic VI decreased (9.6 +/- 2.8%, P < 0.0001) and hepatic VI did not change. After splenectomy, nitroglycerin infusions at doses of 0.5 and 2 mg/min were associated with increases in total splanchnic VI of 3.7 +/- 1.2% (P < 0.0001, 30 +/- 10 ml) and 7.6 +/- 1.7% (P < 0.001, 59 +/- 10 ml) due entirely to increases in mesenteric volume of 9.9 +/- 2.7% (P < 0.0001) and 16.5 +/- 1.9% (P < 0.0001), respectively, but cardiac output was unchanged at the end of infusion at either dose.(ABSTRACT TRUNCATED AT 250 WORDS)

A canine model of neurogenic pulmonary edema

1985 ◽  
Vol 59 (3) ◽  
pp. 1019-1025 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
Alpha Chloralose

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

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