Pulmonary microvascular response to prostacyclin (PGI2) infusion in unanesthetized sheep

1982 ◽  
Vol 52 (5) ◽  
pp. 1338-1342 ◽  
Author(s):  
R. Gunther ◽  
C. Zaiss ◽  
R. H. Demling
Keyword(s):  
Cardiac Output ◽  
Aortic Pressure ◽  
Base Line ◽  
Fluid Exchange ◽  
Protein Ratio ◽  
Microvascular Response ◽  
Pulmonary Arterial ◽  
Pulmonary Microcirculation ◽  
Rebound Increase ◽  
Mean Aortic Pressure

We studied the effect of prostacyclin (PGI2) infusion and cessation of infusion on the pulmonary microcirculation. We used lung lymph flow (QL) and the lymph to plasma protein ratio as sensitive indices of net fluid (QF) and protein flux (CP). After a 4-h base line period, we infused PGI2 (0.2 micrograms . kg(-1).min(-1) into eight unanesthetized sheep for 2 h. We monitored vascular pressures and lymph during infusion and for another 18 h after PGI2. During infusion, QL and cardiac output increased by 75 and 50%, respectively, over base line, whereas the lymph-to-plasma ratio (L/P) remained constant for both albumin and globulin. This resulted in a significant increase in both fluid and protein flux. Pulmonary vascular pressures remained unchanged, whereas mean aortic pressure decreased. The increase in QF and CP was felt to be due to an increase in the surface area of fluid exchange vessels rather than increased permeability. After infusion, cardiac output rapidly returned to base line, whereas mean QL remained increased by 70% over base line for 2–8 h. Mean L/P decreased from 0.65 to 0.53. Pulmonary arterial pressure and pulmonary vascular resistance increased. The increase in QL and decrease in L/P indicate a rebound increase in pulmonary microvascular pressure in the postperfusion period.

Cerebral blood flow and evoked potentials during Cushing response in sheep

1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Evoked Potentials ◽  
Aortic Pressure ◽  
Base Line ◽  
Auditory Evoked Responses ◽  
Cushing Response

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

Elevated pulmonary lymph flow and protein content during status epilepticus in sheep

1982 ◽  
Vol 52 (1) ◽  
pp. 91-95 ◽  
Author(s):  
R. P. Simon ◽  
L. L. Bayne ◽  
R. F. Tranbaugh ◽  
F. R. Lewis
Keyword(s):  
Driving Force ◽  
Left Atrial ◽  
Cervical Spinal Cord ◽  
Lymph Flow ◽  
Base Line ◽  
Albumin Concentration ◽  
Plasma Albumin ◽  
Protein Ratio ◽  
Pulmonary Arterial ◽  
Plasma Albumin Concentration

The pathophysiology of postictal pulmonary edema was investigated by inducing seizures with bicuculline in nine paralyzed, halothane-anesthetized sheep and measuring of pulmonary lymphatic flow, pulmonary arterial and left atrial pressures, and lymph and plasma albumin concentration. Pulmonary microvascular pressure and transcapillary albumin conductance were calculated. Seizures transiently (less than 15 min) elevated microvascular pressure in all animals; lymph flow increased greater than twofold in response to the increased hydrostatic driving force. However, the elevation in lymph flow, with a stable lymph-to-plasma protein ratio and doubled transcapillary albumin conductance, persisted for the duration of the experiment, more than 3 h after microvascular pressure returned to base line. These changes were neurally mediated because they were blocked by cervical spinal cord transection in four additional animals.

Vasodilator reserve in respiratory muscles during maximal exertion in ponies

1986 ◽  
Vol 60 (5) ◽  
pp. 1571-1577 ◽  
Author(s):  
M. Manohar
Keyword(s):  
Blood Flow ◽  
Maximal Exercise ◽  
Respiratory Muscles ◽  
Aortic Pressure ◽  
Whole Body ◽  
Adenosine Infusion ◽  
Base Line ◽  
Triceps Brachii ◽  
Vasodilator Reserve ◽  
Mean Aortic Pressure

Eight healthy adult grade ponies were studied at rest as well as during maximal exertion carried out with and without adenosine infusion (3 microM X kg-1 X min-1 into the pulmonary artery) on a treadmill to compare levels of blood flow in respiratory muscles with those in other vigorously working muscles and to ascertain whether there remained any unutilized vasodilator reserve in respiratory muscles of maximally exercising ponies. Radionuclide-labeled 15-micron-diam microspheres, injected into the left ventricle, were used to study tissue blood flows. During maximal exertion, there were increases above base-line values in heart rate (336%), mean aortic pressure (41%), cardiac output (722%), and arterial O2 content (56%). The whole-body O2 consumption was 123 +/- 11 ml X min-1 X kg-1, and the stride/respiratory frequency of the galloping ponies was 138 +/- 4/min. With adenosine infusion during maximal exertion, mean aortic pressure decreased (P less than 0.05), but none of the above variables was different from maximal exercise alone. During maximal exertion, blood flow in the adrenal glands, myocardium, respiratory, and limb muscles increased, whereas that in the kidneys decreased and the cerebral perfusion remained unaltered. With adenosine infusion during maximal exercise, renal vasoconstriction intensified, whereas adrenal and coronary beds exhibited further vasodilatation. During maximal exertion, blood flow in the equine diaphragm (265 +/- 36 ml X min-1 X 100 g-1) was not different from that in the gluteus medius (253 +/- 36) and biceps femoris (233 +/- 29); both are principal muscles of propulsion in the equine subjects) or the triceps brachii (227 +/- 26) muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparative effects of arachidonic acid, bisenoic prostaglandins, and an endoperoxide analog on the canine pulmonary vascular bed

1977 ◽  
Vol 55 (6) ◽  
pp. 1369-1377 ◽  
Author(s):  
Philip J. Kadowitz ◽  
Ernst W. Spannhake ◽  
Stan Greenberg ◽  
Larry P. Feigen ◽  
Albert L. Hyman
Keyword(s):  
Cardiac Output ◽  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Pulmonary Arterial Pressure ◽  
Superior Vena ◽  
Vena Cava ◽  
Aortic Pressure ◽  
Pulmonary Arterial

The effects of bolus injections of the postaglandin precursor, arachidonic acid, and PGD2, PGF2α, PGE2, and the PGH2 analog ((15S)-hydroxyl-9α,11α(epoxymethano)-prosta-5Z-dienoic acid) were compared on the pulmonary circulation in the intact spontaneously breathing pentobarbital-anesthetized dog. Arachidonic acid increased pulmonary arterial pressure, decreased aortic pressure, and increased cardiac output when injected into the superior vena cava or right atrium. PGE2, like arachidonic acid, increased pulmonary arterial pressure and cardiac output and decreased aortic pressure, whereas PGF2α and PGD2 increased pulmonary arterial pressure but did not affect cardiac output or aortic pressure when injected into the superior vena cava or right atrium. The PGH2 analog increased pulmonary arterial pressure and to a lesser extent, aortic pressure, without affecting cardiac output. None of these substances changed left atrial or right atrial pressure. The cardiopulmonary effects of arachidonic acid were blocked by indomethacin whereas the rise in pulmonary arterial pressure in response to the bisenoic prostaglandins and the analog were enhanced by the cyclooxygenase inhibitor. These data suggest that the increase in pulmonary vascular resistance in response to arachidonic acid may be due to conversion of the precursor into vasoactive intermediates and products such as bisenoic prostaglandins whereas the decrease in systemic vascular resistance is probably due to the formation of PGE2 and other peripheral vasodilator substances.

Effect of progressive exercise on lung fluid balance in sheep

1988 ◽  
Vol 64 (5) ◽  
pp. 2125-2131 ◽  
Author(s):  
J. H. Newman ◽  
B. J. Butka ◽  
R. E. Parker ◽  
R. J. Roselli
Keyword(s):  
Cardiac Output ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Progressive Exercise ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

The purpose of this study is to determine the roles of cardiac output and microvascular pressure on changes in lung fluid balance during exercise in awake sheep. We studied seven sheep during progressive treadmill exercise to exhaustion (10% grade), six sheep during prolonged constant-rate exercise for 45–60 min, and five sheep during hypoxia (fraction of inspired O2 = 0.12) and hypoxic exercise. We made continuous measurements of pulmonary arterial, left atrial, and systemic arterial pressures, lung lymph flow, and cardiac output. Exercise more than doubled cardiac output and increased pulmonary arterial pressures from 19.2 +/- 1 to 34.8 +/- 3.5 (SE) cmH2O. Lung lymph flow increased rapidly fivefold during progressive exercise and returned immediately to base-line levels when exercise was stopped. Lymph-to-plasma protein concentration ratios decreased slightly but steadily. Lymph flows correlated closely with changes in cardiac output and with calculated microvascular pressures. The drop in lymph-to-plasma protein ratio during exercise suggests that microvascular pressure rises during exercise, perhaps due to increased pulmonary venous pressure. Lymph flow and protein content were unaffected by hypoxia, and hypoxia did not alter the lymph changes seen during normoxic exercise. Lung lymph flow did not immediately return to base line after prolonged exercise, suggesting hydration of the lung interstitium.

Bradykinin pathway is involved in acute hemodynamic effects of enalaprilat in dogs with heart failure

1996 ◽  
Vol 270 (6) ◽  
pp. H1985-H1992 ◽  
Author(s):  
F. Barbe ◽  
J. B. Su ◽  
T. T. Guyene ◽  
B. Crozatier ◽  
J. Menard ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Enzyme Inhibitors ◽  
Renin Angiotensin System ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Aortic Pressure ◽  
Hemodynamic Effects ◽  
Converting Enzyme Inhibitors ◽  
Hoe 140 ◽  
Mean Aortic Pressure

To determine the role of the renin-angiotensin system and the bradykinin pathway in the mechanism of action of angiotensin-converting enzyme inhibitors in heart failure, the acute effects of enalaprilat (1 mg/kg) were compared with those of a renin inhibitor (ciprokiren, 1 mg/kg i.v.) in 10 chronically instrumented conscious dogs with heart failure induced by right ventricular pacing (3 wk, 240 beats/min). The effects of enalaprilat and ciprokiren on bradykinin infusion (3, 10, and 30 micrograms/min) and the effects of enalaprilat in the presence of the bradykinin B2 receptor antagonist Hoe-140 (10 micrograms/kg i.v.) were also examined. Both inhibitors significantly decreased mean aortic pressure and increased cardiac output. However, enalaprilat induced significantly greater hemodynamic effects than ciprokiren (mean aortic pressure, -13 +/- 3 vs. -6 +/- 1 mmHg; cardiac output, 0.4 +/- 0.1 vs. 0.15 +/- 0.1 l/min). Bradykinin infusion led to dose-dependent decreases in mean aortic pressure and increases in cardiac output that were not modified by pretreatment with ciprokiren but were potentiated 10-fold by enalaprilat. Hoe-140 significantly reduced the hemodynamic effects of enalaprilat. Thus endogenous bradykinin is involved in the acute hemodynamic effects of enalaprilat in experimental heart failure.

Leukotriene B4 increases pulmonary transvascular filtration by a neutrophil-independent mechanism

1990 ◽  
Vol 68 (3) ◽  
pp. 1260-1264 ◽  
Author(s):  
C. A. Burgess ◽  
B. K. McCandless ◽  
J. A. Cooper ◽  
A. B. Malik
Keyword(s):  
Leukotriene B4 ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Protein Clearance ◽  
Endothelial Monolayers ◽  
Pulmonary Hemodynamic ◽  
Microvascular Response ◽  
Pulmonary Arterial

We examined the role of circulating granulocytes in the pulmonary microvascular response to leukotriene B4 (LTB4) by prior depletion of circulating granulocytes using hydroxyurea. LTB4 (2 micrograms/kg injection followed by infusion of 2 micrograms/kg over 15 min) produced transient increases in pulmonary arterial pressure and pulmonary vascular resistance, indicating that neutrophils were not required for the pulmonary hemodynamic effects of LTB4. Infusion of LTB4 in granulocyte-depleted sheep also resulted in transient increases in pulmonary lymph flow (QL) with no significant change in the lymph-to-plasma protein concentration ratio (L/P), findings similar to those in control animals. In vitro studies indicated that LTB4 (10(-7) or 10(-9) M) produced a transient adherence of neutrophils to cultured pulmonary artery endothelial monolayers. Maximal responses occurred at 10 min after the addition of LTB4 to the endothelial cell-neutrophil coculture system, and the adherence decreased to base line within 60 min. LTB4 infusion in sheep also produced a transient uptake of autologous 111In-oxine-labeled neutrophils. The results indicate that LTB4-mediated increase in pulmonary transvascular protein clearance (QL x L/P) is independent of circulating granulocytes.

Modulation by endogenous opioids of pulmonary vasoconstrictor response to acute lung injury

1988 ◽  
Vol 64 (5) ◽  
pp. 1823-1828 ◽  
Author(s):  
A. T. Scardella ◽  
J. A. Neubauer ◽  
N. H. Edelman ◽  
T. V. Santiago
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Endogenous Opioids ◽  
Pulmonary Perfusion ◽  
Base Line ◽  
Injured Lung ◽  
Pulmonary Arterial

The effects of endogenously generated opioids on distribution of pulmonary perfusion (as assessed by radiolabeled microspheres) and overall gas exchange in acute acid-induced lung injury were studied. In 14 anesthesized dogs, sufficient acid was given to one lung to double shunt fraction (Qs/Qt) from 14.2 +/- 0.8 to 32.4 +/- 2.6% (SE). This resulted in a significant decrease in Po2 from 495 +/- 9 to 136 +/- 21 Torr, cardiac output from 2.47 +/- 0.27 to 1.46 +/- 0.15 1/min, and blood pressure from 139 +/- 3 to 116 +/- 5 mmHg and a significant rise in pulmonary arterial pressure from 9.6 +/- 0.8 to 14.9 +/- 0.8 mmHg. After acid instillation, microsphere distribution to the injured lung segments decreased to 50% of the base-line value. At the same time, microsphere distribution in the normal segments increased to 160% of base line. In 7 of the 14 dogs the effects of naloxone (1 mg/kg) given after lung injury were compared with the other 7 animals that were given saline. Naloxone administration caused a significant redistribution of regional pulmonary perfusion such that microsphere distribution in the injured lung segments increased by a factor of 2 at 35 min compared with the animals given saline. Consistent with this finding, Qs/Qt in the naloxone group increased to 34.7 +/- 5.0% at 35 min, whereas that of the saline group decreased to 28.2 +/- 2.5%. The difference between the two groups was significant at 35 min. These changes occurred without further alterations in cardiac output, pulmonary arterial pressure, or systemic blood pressure in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of platelet-activating factor antagonist SRI 63-441 on endotoxemia in sheep

1988 ◽  
Vol 65 (6) ◽  
pp. 2624-2631 ◽  
Author(s):  
C. N. Sessler ◽  
F. L. Glauser ◽  
D. Davis ◽  
A. A. Fowler
Keyword(s):  
Late Phase ◽  
Platelet Activating Factor ◽  
Aortic Pressure ◽  
Transient Rise ◽  
Paf Receptor ◽  
Pulmonary Arterial ◽  
Early Rise ◽  
Arterial Po2 ◽  
Mean Aortic Pressure

We investigated whether platelet-activating factor (PAF) mediates endotoxin-induced systemic and pulmonary vascular derangements by studying the effects of a selective PAF receptor antagonist, SRI 63-441, during endotoxemia in sheep. Endotoxin infusion (1.3 micrograms/kg over 0.5 h) caused a rapid, transient rise in pulmonary arterial pressure (Ppa) from 16 +/- 3 to 36 +/- 10 mmHg (P less than 0.001) and pulmonary vascular resistance (PVR) from 187 +/- 84 to 682 +/- 340 dyn.s.cm-5 (P less than 0.05) at 0.5 h, followed by a persistent elevation in Ppa to 22 +/- 3 mmHg and in PVR to 522 +/- 285 dyn.s.cm-5 at 5 h in anesthetized sheep. Arterial PO2 (PaO2) decreased from 341 +/- 79 to 198 +/- 97 (P less than 0.01) and 202 +/- 161 Torr at 0.5 and 5 h, respectively (inspired O2 fraction = 1.0). SRI 63-441, 20 mg.kg-1.h-1 infused for 5 h, blocked the early rise in Ppa and PVR and fall in PaO2, but had no effect on the late phase pulmonary hypertension or hypoxemia. Endotoxin caused a gradual decrease in mean aortic pressure, which was unaffected by SRI 63-441. Infusion of SRI 63-441 alone caused no hemodynamic alterations. In follow-up studies, endotoxin caused an increase in lung lymph flow (QL) from 3.8 +/- 1.1 to 14.1 +/- 8.0 (P less than 0.05) and 12.7 +/- 8.6 ml/h at 1 and 4 h, respectively. SRI 63-441 abolished the early and attenuated the late increase in QL.(ABSTRACT TRUNCATED AT 250 WORDS)

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