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.

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.

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

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

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 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.

Effects of sildenafil on hypoxic pulmonary vascular function in dogs

2006 ◽  
Vol 101 (4) ◽  
pp. 1085-1090 ◽  
Author(s):  
Pierre Fesler ◽  
Alberto Pagnamenta ◽  
Benoit Rondelet ◽  
François Kerbaul ◽  
Robert Naeije
Keyword(s):  
Arterial Pressure ◽  
Right Ventricular ◽  
Vascular Function ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Characteristic Impedance ◽  
Systemic Arterial Pressure ◽  
Pulmonary Vasodilators ◽  
Hydraulic Load ◽  
Pulmonary Arterial ◽  
Inhaled No

Sildenafil has been shown to be an effective treatment of pulmonary arterial hypertension and is believed to present with pulmonary selectivity. This study was designed to determine the site of action of sildenafil compared with inhaled nitric oxide (NO) and intravenous sodium nitroprusside (SNP), known as selective and nonselective pulmonary vasodilators, respectively. Inhaled NO (40 ppm), and maximum tolerated doses of intravenous SNP and sildenafil, (5 μg·kg−1·min−1 and 0.1 mg·kg−1·h−1), respectively, were administered to eight dogs ventilated in hypoxia. Pulmonary vascular resistance (PVR) was evaluated by pulmonary arterial pressure (Ppa) minus left atrial pressure (Pla) vs. flow curves, and partitioned into arterial and venous segments by the occlusion method. Right ventricular hydraulic load was defined by pulmonary arterial characteristic impedance (Zc) and elastance (Ea) calculations. Right ventricular arterial coupling was estimated by the ratio of end-systolic elastance (Ees) to Ea. Decreasing the inspired oxygen fraction from 0.4 to 0.1 increased Ppa − Pla at a standardized flow of 3 l·min−1·m−2 from 6 ± 1 to 18 ± 1 mmHg (mean ± SE). Ppa − Pla was decreased to 9 ± 1 by inhaled NO, 14 ± 1 by SNP, and 14 ± 1 mmHg by sildenafil. The partition of PVR, Zc, Ea, and Ees/Ea was not affected by the three interventions. Inhaled NO did not affect systemic arterial pressure, which was similarly decreased by sildenafil and SNP, from 115 ± 4 to 101 ± 4 and 98 ± 5 mmHg, respectively. We conclude that inhaled NO inhibits hypoxic pulmonary vasoconstriction more effectively than sildenafil or SNP, and sildenafil shows no more selectivity for the pulmonary circulation than SNP.

Atrial natriuretic factor attenuates the pulmonary pressor response to hypoxia

1988 ◽  
Vol 65 (5) ◽  
pp. 1975-1983 ◽  
Author(s):  
S. Adnot ◽  
P. E. Chabrier ◽  
C. Brun-Buisson ◽  
I. Viossat ◽  
P. Braquet
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Pressor Response ◽  
Systemic Arterial Pressure ◽  
Pulmonary Hemodynamics ◽  
Natriuretic Factor ◽  
Pulmonary Vasodilator ◽  
Pulmonary Arterial ◽  
Atrial Natriuretic

The influence of endogenous and exogenous atrial natriuretic factor (ANF) on pulmonary hemodynamics was investigated in anesthetized pigs during both normoxia and hypoxia. Continuous hypoxic ventilation with 11% O2 was associated with a uniform but transient increase of plasma immunoreactive (ir) ANF that peaked at 15 min. Plasma irANF was inversely related to pulmonary arterial pressure (Ppa; r = -0.66, P less than 0.01) and pulmonary vascular resistance (PVR; r = -0.56, P less than 0.05) at 30 min of hypoxia in 14 animals; no such relationship was found during normoxia. ANF infusion after 60 min of hypoxia in seven pigs reduced the 156 +/- 20% increase in PVR to 124 +/- 18% (P less than 0.01) at 0.01 microgram.kg-1.min-1 and to 101 +/- 15% (P less than 0.001) at 0.05 microgram.kg-1.min-1. Cardiac output (CO) and systemic arterial pressure (Psa) remained unchanged, whereas mean Ppa decreased from 25.5 +/- 1.5 to 20.5 +/- 15 mmHg (P less than 0.001) and plasma irANF increased two- to nine-fold. ANF infused at 0.1 microgram.kg-1.min-1 (resulting in a 50-fold plasma irANF increase) decreased Psa (-14%) and reduced CO (-10%); systemic vascular resistance (SVR) was not changed, nor was a further decrease in PVR induced. No change in PVR or SVR occurred in normoxic animals at any ANF infusion rate. These results suggest that ANF may act as an endogenous pulmonary vasodilator that could modulate the pulmonary pressor response to hypoxia.

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