scholarly journals Pulmonary Vasoconstrictive and Bronchoconstrictive Responses to Anaphylaxis Are Weakened via β2-adrenoceptor Activation by Endogenous Epinephrine in Anesthetized Rats

2011 ◽  
Vol 114 (3) ◽  
pp. 614-623 ◽  
Author(s):  
Wei Zhang ◽  
Toshishige Shibamoto ◽  
Yuhichi Kuda ◽  
Chieko Ohmukai ◽  
Yasutaka Kurata
Keyword(s):  
Arterial Pressure ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Aortic Blood Flow ◽  
Sprague Dawley ◽  
Adrenoceptor Antagonist ◽  
Sprague Dawley Rats ◽  
Ici 118,551 ◽  
Pulmonary Arterial

Background Patients treated with propranolol, a nonselective β-adrenoceptor antagonist, have increased incidence and severity of anaphylaxis. We determined whether β1- or β2-adrenoceptor antagonist modulated pulmonary vasoconstriction and bronchoconstriction in rat anaphylactic hypotension. Methods Anesthetized ovalbumin-sensitized male Sprague-Dawley rats were randomly allocated to the following pretreatment groups (n = 7/group): (1) sensitized control (nonpretreatment), (2) propranolol, (3) the selective β2-adrenoceptor antagonist ICI 118,551, (4) the selective β1-adrenoceptor antagonist atenolol, and (5) adrenalectomy. Shock was induced by an intravenous injection of the antigen. Mean arterial pressure, pulmonary arterial pressure, left atrial pressure, central venous pressure, portal venous pressure, airway pressure, and aortic blood flow were continuously measured. Results In either sensitized control or atenolol-pretreated rats, mean arterial pressure and aortic blood flow decreased substantially, whereas pulmonary arterial pressure and airway pressure did not increase soon after antigen injection. In contrast, in rats pretreated with either propranolol, ICI 118,551, or adrenalectomy, airway pressure significantly increased by 14 cm H2O, and pulmonary arterial pressure by 7.5 mmHg after antigen injection. At 2.5 min after antigen injection, the plasma concentration of epinephrine increased 14-fold in the sensitized rats except for the adrenalectomy group. Portal venous pressure after antigen injection increased by 16 mmHg similarly in all sensitized rats. All of the sensitized control group and two of the atenolol group were alive for 60 min after antigen injection, whereas all rats of the propranolol, ICI 118,551, and adrenalectomy groups died within 50 min after antigen injection. Conclusions The pulmonary vasoconstrictive and bronchoconstrictive responses to systemic anaphylaxis were weakened via β2-adrenoceptor activation by epinephrine endogenously released from the adrenal gland in the anesthetized Sprague-Dawley rats.

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

Comparative responses to endothelin 2 and sarafotoxin 6b in systemic vascular bed of cats

1990 ◽  
Vol 258 (5) ◽  
pp. H1550-H1558
Author(s):  
R. K. Minkes ◽  
P. J. Kadowitz
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Vasodilator Activity ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
Dose Dependent ◽  
Higher Doses

Cardiovascular responses to endothelin 2 (ET-2) and sarafotoxin 6b (S6b) were investigated in the cat. ET-2 (0.1-1 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP), whereas S6b (0.1-1 nmol/kg iv) only decreased AP. Central venous pressure (CVP), cardiac output (CO), and pulmonary arterial pressure (PAP) were increased. ET-2 produced biphasic changes in systemic vascular resistance (SVR), whereas S6b decreased SVR at the two lower doses and caused a biphasic change at the 1 nmol/kg dose. The effects of ET-1 and ET-2 were similar, whereas the effects of S6b were similar to ET-3. ET-2 and S6b had small effects on right ventricular contractile force and caused transient increases in heart rate. Distal aortic blood flow was increased in response to all doses of both peptides, whereas increases in carotid blood flow were observed only in response to the higher doses of ET-2 and S6b. ET-2 produced dose-dependent decreases in superior mesenteric artery (SMA) blood flow, whereas decreases in SMA flow in response to S6b were observed only at the 1 nmol/kg dose. Renal blood flow was decreased significantly only at the higher doses of ET-2 and S6b. The present data show that ET-2 and S6b can produce both vasodilation and vasoconstriction in the systemic and regional vascular beds of the cat and demonstrate previously unrecognized vasodilator activity in response to S6b. It is concluded that ET-2 and S6b produce complex cardiovascular responses in the anesthetized cat.

Pulmonary venous pressure increases during alveolar hypoxia in isolated lungs of newborn pigs

1992 ◽  
Vol 73 (2) ◽  
pp. 552-556 ◽  
Author(s):  
C. D. Fike ◽  
M. R. Kaplowitz
Keyword(s):  
Airway Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Co2 Gas ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Newborn Pigs ◽  
Isolated Lungs

The purpose of this study was to determine whether pulmonary venous pressure increases during alveolar hypoxia in lungs of newborn pigs. We isolated and perfused with blood the lungs from seven newborn pigs, 6–7 days old. We maintained blood flow constant at 50 ml.min-1.kg-1 and continuously monitored pulmonary arterial and left atrial pressures. Using the micropuncture technique, we measured pressures in 10 to 60-microns-diam venules during inflation with normoxic (21% O2–69–74% N2–5–10% CO2) and hypoxic (90–95% N2–5–10% CO2) gas mixtures. PO2 was 142 +/- 21 Torr during normoxia and 20 +/- 4 Torr during hypoxia. During micropuncture we inflated the lungs to a constant airway pressure of 5 cmH2O and kept left atrial pressure greater than airway pressure (zone 3). During hypoxia, pulmonary arterial pressure increased by 69 +/- 24% and pressure in small venules increased by 40 +/- 23%. These results are similar to those obtained with newborn lambs and ferrets but differ from results with newborn rabbits. The site of hypoxic vasoconstriction in newborn lungs is species dependent.

Hypoxic pulmonary vasoconstriction during steady and pulsatile flow in ferrets

1984 ◽  
Vol 57 (1) ◽  
pp. 205-212 ◽  
Author(s):  
T. J. Gregory ◽  
M. L. Ellsworth ◽  
J. C. Newell
Keyword(s):  
Arterial Pressure ◽  
Steady Flow ◽  
Pulsatile Flow ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Flow Curves ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Pulsatile Perfusion

We examined the effects of hypoxia and pulsatile flow on the pressure-flow relationships in the isolated perfused lungs of Fitch ferrets. When perfused by autologous blood from a pump providing a steady flow of 60 ml/min, the mean pulmonary arterial pressure rose from 14.6 to 31.3 Torr when alveolarPO2 was reduced from 122 to 46 Torr. This hypoxic pressor response was characterized by a 10.1-Torr increase in the pressure-axis intercept of the extrapolated pressure-flow curves and an increase in the slope of these curves from 130 to 240 Torr X l–1 X min. With pulsatile perfusion from a piston-typepump, mean pulmonary arterial pressure increased from 17.5 to 36.3 Torr at the same mean flow.Thishypoxic pressor response was also characterized by increases in the intercept pressure and slope of thepressure-flow curves. When airway pressure was raised during hypoxia, the intercept pressure increased further to 25 +/- 1 Torr with a further increase in vascular resistance to 360 Torr X l–1 X min. Thus, in contrast to the dog lung, in the ferret lung pulsatile perfusion does not result in lower perfusion pressures during hypoxia when compared with similar mean levels of steady flow. Since the effects of high airway pressure and hypoxia are additive, they appear to act at or near the same site in elevating perfusion pressure.

scholarly journals Comparative Study of Capillary Filtration Coefficient (Kfc) Determination by a Manual and Automatic Perfusion System. Step by Step Technique Review

2019 ◽  
pp. 901-908
Author(s):  
C.C. Bravo-Reyna ◽  
G. Torres-Villalobos ◽  
N. Aguilar-Blas ◽  
J. Frías-Guillén ◽  
J.R. Guerra-Mora
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Ischemia Reperfusion ◽  
Venous Pressure ◽  
Filtration Coefficient ◽  
Perfusion System ◽  
Gold Standard Method ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Arterial

The purpose of calculating the capillary filtration coefficient is to experimentally evaluate edema formation in models of pulmonary ischemia-reperfusion injury. For many years, the obtaining of this coefficient implies a series of manual maneuvers during ex-vivo reperfusion of pulmonary arterial pressure, venous pressure and weight, as well as the calculation of the Kfc formula. Through automation, the calculation of capillary filtration coefficient could be easier and more efficient. To describe an automatic method designed in our laboratory to calculating the capillary filtration coefficient and compare with traditional determination of capillary filtration coefficient as gold standard method. An automatic three valve perfusion system was constructed, commanded by a mastery module connected to a graphical user interface. To test its accuracy, cardiopulmonary blocks of Wistar rats were harvested and distributed in manual (n=8) and automated (n=8) capillary filtration coefficient determination groups. Physiological parameters as pulmonary arterial pressure, pulmonary venous pressure, weight and capillary filtration coefficient were obtained. Results: Capillary filtration coefficient, pulmonary arterial pressure, venous arterial pressure shown no statistical significance difference between the groups. The automated perfusion system for obtaining Kfc was standardized and validated, giving reliable results without biases and making the process more efficient in terms of time and personal staff.

A New Look at Pulmonary Edema

Physiology ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 150-153 ◽  
Author(s):  
GA Laine ◽  
SJ Allen ◽  
JP Williams ◽  
J Katz ◽  
JC Gabel ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Critically Ill Patients ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Colloid Osmotic Pressure ◽  
Fluid Accumulation ◽  
Fatal Complication ◽  
Therapeutic Measures ◽  
Pulmonary Arterial

Fluid accumulation within the lungs is a potentially fatal complication in critically ill patients. Sepsis and increased microvascular permeability are often implicated as the cause. This article shows that edema can be prevented by lowering systemic venous pressure (to permit pulmonary lymph to drain), by lowering pulmonary arterial pressure, and by maintaining plasma colloid osmotic pressure. It points out the importance of understanding the basic physiology behind pulmonary edema and therapeutic measures.

Lowered pulmonary arterial pressure prevents edema after endotoxin in sheep

1987 ◽  
Vol 63 (3) ◽  
pp. 1008-1011 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
J. Katz ◽  
J. C. Gabel ◽  
G. A. Laine
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Dry Weight ◽  
Base Line ◽  
Capillary Membrane ◽  
Significant Difference ◽  
Pulmonary Arterial ◽  
The Difference

Escherichia coli endotoxin causes increased capillary membrane permeability and increased pulmonary arterial pressure (PAP) in sheep. If the pulmonary hypertension extends to the level of the microvasculature, then the increased microvascular pressure may contribute to the pulmonary edema caused by endotoxin. We tested the hypothesis that reducing the pulmonary hypertension would reduce the amount of edema caused by endotoxin. Twelve sheep were chronically instrumented with catheters to measure PAP, left atrial pressure, and central venous pressure. The sheep were divided into two groups. One group (E) of six sheep received an intravenous infusion of 4 micrograms/kg of E. coli endotoxin. The second group (E + SNP) received the same dose of endotoxin as well as a continuous infusion of sodium nitroprusside (SNP) to reduce PAP. Three hours after the endotoxin infusions, the sheep were terminated and the extravascular fluid-to-blood-free dry weight ratios of the lungs were determined (EVF). The base-line PAP was 17.5 +/- 2.7 mmHg. A two-way analysis of variance demonstrated a significant difference (P less than 0.01) in PAP between the E and E + SNP groups. Although PAP in each group varied as a function of time, the difference between the two groups did not. The mean PAP for the E + SNP group (20.9 +/- 1.5 mmHg) was lower than the E group PAP of 27.3 +/- 2.1 mmHg after the endotoxin spike. Furthermore, the E + SNP group EVF (3.9 +/- 0.2) was significantly less than the EVF of the E group (4.7 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary hypertension after postlavage lung injury in rabbits: possible role of polymorphonuclear leukocytes

1991 ◽  
Vol 71 (5) ◽  
pp. 1990-1995 ◽  
Author(s):  
R. Burger ◽  
A. C. Bryan
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Lung Lavage ◽  
High Frequency Ventilation ◽  
Mean Airway Pressure ◽  
Pulmonary Arterial

Previous studies showed that repeated lung lavage leads to a severe lung injury with very poor gas exchange, a substantial protein leak into the alveoli with hyaline membrane formation, pulmonary hypertension, and migration of granulocytes (PMN) into the alveolar spaces. Depletion of PMN leads to a better gas exchange and a markedly decreased protein leak with only scanty hyaline membranes. In this study we show that there is sustained pulmonary hypertension after the lung lavage, but in PMN-depleted rabbits there is no postlavage increase in pulmonary arterial pressure. Changing the shunt fraction by manipulating mean airway pressure still leads to a hypoxic vasoconstriction with increase of pulmonary arterial pressure. Thus, after lung lavage, pulmonary reactivity to hypoxia is still preserved. Comparisons between high-frequency ventilation and conventional mechanical ventilation at the same mean airway pressures showed that equal mean airway pressure in these two very different modes of ventilation do not translate into the same mean functional lung volumes.

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