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At least 415 records · Page 23Linked to original sources
PubMed1985

Pulmonary circulation in low cardiac output syndrome following open heart surgery.

The pulmonary circulation of 41 patients with low cardiac output syndrome (LOS) in the recovery period following open heart surgery was studied. Cardiac indices (CI) of these patients in LOS was 1.64 +/- 0.28 (Mean +/- SD) L/min X m2 and increased to 2.60 +/- 0.50 L/min X m2 after the stabilization of hemodynamic conditions. Mean pulmonary arterial pressure, pulmonary arteriolar resistance index (PARI) and total pulmonary resistance index (TPRI) in the condition of LOS were very high and significantly decreased after recovery from LOS, although the mean left atrial pressure showed no significant change. The correlation coefficient (r) between CI and PARI was found to be -0.574. High Pao2 with reductions of alveolar-arterial oxygen tension difference (A-aDo2) and physiological pulmonary shunt ratio (Qs/Qt) in LOS significantly decreased concomitant with significant increases in both A-aDo2 and Qs/Qt after the stabilization of the hemodynamic condition. Moderate correlations were obtained between CI and Pao2 (r = -0.478), and high correlations were established between CI and physiological pulmonary shunt flow (Qps) (r = 0.747). These studies showed that pulmonary vasoconstriction was playing a major role in the elevation of pulmonary vascular resistance in LOS, which eventually leads to the reduction of intrapulmonary shunting.

Aortic Valve↗
PubMed1993

Bronchial hyperreactivity in patients with moderate pulmonary circulation overload.

The clinical course of congestive heart failure (CHF) and mitral valve stenosis (MVS) is accompanied by episodes of dyspnea, wheezing, and cough, symptoms also observed in patients with bronchial hyperreactivity. However, it is still controversial whether bronchial hyperreactivity is demonstrable in patients with chronic overload of the pulmonary circulation. In order to examine the effects of CHF on the respiratory function, we performed pulmonary function tests, titrated bronchial acetylcholine provocations, and left and right heart catheterization in 21 patients with impaired left ventricular function (mean ejection fraction, 37 percent, NYHA class 3), 5 patients with MVS, and 17 control patients with coronary artery disease (mean ejection fraction, 63 percent). Bronchial hyperresponsiveness was defined as an obstructive response to increased doses of inhaled acetylcholine. A 20 percent fall in forced expiratory volume in the first second (FEV1), a 100 percent increase in total airway resistance (Rtot), and a 60 percent reduction of pulmonary conductance (SGtot) were considered positive. Patients with impaired left ventricular function showed significantly higher airway resistance, and lower airway conductance at the maximal tolerated acetylcholine dose compared with control patients. Patients with MVS had a significant lower airway conductance. The induced bronchial obstruction was completely reversible upon inhalation of a beta 2-mimetic. We conclude that chronic overload of the pulmonary circulation is accompanied by bronchial hyperreactivity that may augment the symptoms of dyspnea in patients with CHF and MVS.

Acetylcholine↗
PubMed2001

NO and prostaglandin interactions during hemodynamic stress in the fetal ovine pulmonary circulation.

Nitric oxide (NO) and prostacyclin (PGI(2)) are potent fetal pulmonary vasodilators, but their relative roles and interactions in the regulation of the perinatal pulmonary circulation are poorly understood. We compared the separate and combined effects of nitric oxide synthase (NOS) and cyclooxygenase (COX) inhibition during acute hemodynamic stress caused by brief mechanical compression of the ductus arteriosus (DA) in chronically prepared fetal lambs. Nitro-L-arginine (L-NNA; NOS antagonist), meclofenamate (Mec; COX inhibitor), combined drugs (L-NNA-Mec), or saline (control) was infused into the left pulmonary artery (LPA) before DA compression. In controls, DA compression decreased pulmonary vascular resistance (PVR) by 43% (P < 0.01). L-NNA, but not Mec, treatment completely blocked vasodilation and caused a paradoxical increase in PVR (+31%; P < 0.05). The effects of L-NNA-Mec and L-NNA on PVR were similar. To determine if the vasodilator effect of PGI(2) is partly mediated by NO release, we studied PGI(2)-induced vasodilation before and after NOS inhibition. L-NNA treatment blocked the PGI(2)-induced rise in LPA blood flow by 73% (P < 0.001). We conclude that NO has a greater role than PGs in fetal pulmonary vasoregulation during acute hemodynamic stress and that PGI(2)-induced pulmonary vasodilation is largely mediated by NO release in the fetal lung.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

[Thromboembolism of the general and pulmonary circulation (according to data from the Office of Pathological Anatomy of the Latvian Republic for 1976-1983)].

Thromboembolism was found in 1060 (11.9%) of 8926 retrospectively studied autopsies. Thromboembolism of the lesser (pulmonary) circulation was the most frequent (7.3%), the domination of females was noted (62.8%). Peak in both males and females was within the age group of 70 to 79 years. The most frequent source of the pulmonary circulation thromboembolism was the lower limb veins. Thromboembolism of the pulmonary (31.9%) and greater (61%) circulation was most frequently observed in the ischemic heart disease. Monthly variations were not statistically significant.

Adult↗
PubMed1990

Distensibility and pressure-flow relationship of the pulmonary circulation. I. Single-vessel model.

To ascertain the relative contributions of vascular distensibility and nonhomogeneous behavior within the pulmonary circulation to the distinctive nonlinear relationship between inflow pressure (Pin) and flow [pressure-flow (P-F) relationship] and between Pin and outflow pressure (Pout) at constant flow (Pin-Pout relationship), we developed a multibranched model in which the elastic behavior of, and forces acting on, individual branches can be varied independently. The response of the multibranched model is described in the companion article (J. Appl. Physiol. 68: 1514-1527, 1990). Here we describe the methods used and the responses of single components of the larger model. Perivascular pressure is modeled as a function of intravascular and transpulmonary pressures (Pv and Ptp, respectively) and vessel length as a function of lung volume. These and the relationship between vascular area (A) and transmural pressure (Ptm) were modeled primarily from the dog data of Smith and Mitzner (J. Appl. Physiol. 48: 450-467, 1980). Vasomotor tone is modeled as a radial collapsing pressure (Pt) in the same plane as Ptm. In view of lack of information about the relationship between Pt and A for a given active state, different patterns were assumed that span a wide range of possible relationships. The P-F and Pin-Pout relationships of single vessels were very similar to those reported for the entire intact circulation. Of note, the slope of the Pin-Pout relationship in the low Pout range (0-5 Torr) was very low (less than 0.25) and increased gradually with Pout toward unity. Vasomotor tone caused an apparent parallel shift in the P-F relationship in the physiological flow range of the dog (2-8 l/min) regardless of the pattern used to model the Pt vs. A relationship; different patterns affected the P-F relationship only over the low flow range before the parallel shift was established.

Animals↗
PubMed1991

Mechanism of action of platelet activating factor in the pulmonary circulation: an investigation using a novel isotopic system in rabbit isolated lung.

1. Rabbit isolated lungs were perfused via the pulmonary artery with Tyrode solution containing 4.5% Ficoll and 0.1% bovine serum albumin at a constant rate of 20 ml min-1. Lung perfusate was drawn for alternating 5 min periods from two reservoirs, one containing 125I-albumin and the other unlabelled albumin to wash out the intravascular label. Microvascular 125I-albumin leakage was determined from the count remaining at the end of the washout phase with an external gamma scintillation probe. In addition, perfusion pressure was monitored continuously. Each experiment comprised 6 cycles over a total period of 60 min. 2. Infusion of platelet activating factor (PAF, 3 nmol min-1 for 10 min) resulted in microvascular 125I-albumin leakage, whereas lyso-PAF was without effect. During PAF infusions there was also an increase in perfusion pressure. Both the permeability and pressor effects of PAF were inhibited by the PAF antagonist L-652731. 3. Infusion of the thromboxane analogue U-46619 (0.6 nmol min-1 for 10 min) caused an increase in perfusion pressure but protein accumulation was not significantly different from that observed with control infusions. 4. Bolus injections of PAF (1 nmol) caused increases in perfusion pressure which were reduced by indomethacin, dazmegrel and BW 755C. Bolus injections of PAF, repeated at 30 min intervals caused reproducible pressor responses; however, repeated injections at 60 min intervals resulted in augmented responses. This augmentation did not occur in the presence of indomethacin. 5. Retrograde perfusion of PAF via the pulmonary vein induced increased perfusion pressure and microvascular 125I-albumin leakage. The observed increase in leakage when compared with forward perfusion suggests that PAF produces predominantly arteriolar constriction i.e. proximal to the site of leakage during forward perfusion. 6. These results indicate that PAF is a vasoconstrictor in the rabbit pulmonary circulation and augmented responses occur with repeated injections at 60 min intervals. Cyclo-oxygenase inhibition abolished this vascular hyperresponsiveness induced by PAF. PAF also caused protein accumulation in the lungs. Both these actions of PAF appear to be receptor-mediated because they were inhibited by PAF antagonists. Another pulmonary vasoconstrictor, U-46619 did not cause protein accumulation suggesting that the extravasation of protein with PAF is not merely secondary to changes in vascular tone.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1981

Radiotelemetry of direct blood pressure measurements in the arterial and pulmonary circulation.

Radiotelemetry of direct blood pressure measurements in the arterial and pulmonary circulation is assessed in most practical situations of everyday life and sport activities. Comparison of radiotelemetric data with values estimated by practitioners, students and doctors of internal medicine demonstrates a general underestimation of everyday physical and emotional stress, whereas car driving is heavily overestimated. A wide difference is also found in swimming, isometric exercise and the cold phase of the sauna bath.

Aerospace Medicine↗
PubMed1980

[The influence of hypobaric hypoxia upon the hemodynamics of the pulmonary circulation (author's transl)].

The influence of hypobaric hypoxia at the pulmonary gaseous exchange and the hemodynamics of the pulmonary circulation was tested by 12 healthy subjects at the age from 33 to 47 years. They were submitted to a basis investigation with determination of VC, VE, VO2, VCO2, Hb, PO2A/a, pH, HR, ECG, PVd, PAp, HZV, RL. These investigations were followed by stress examination by means of the bicycle ergometry in four rectangular steps during conditions of normoxia and of hypobaric hypoxia in a low-pressure chambre at 66.5 kPa (500 Torr) each of 6 min duration. During the influence of hypoxia a PO2a-decrease in a sense of partial insufficiency could be already observed at rest during conditions of a decreased alveolar oxygen-partial-pressure. At the same time was found a significant increase of the systolic peripheral and the diastolic pulmonary arterial pressure. At the increasing step by step ergometric exercise during conditions of the hypoxia stress were growing significance evidence of different reactions of the pulmonary and cardiocirculatory parameters occurred.

Adult↗
PubMed1999

Nitric oxide and endothelin-1 in coronary and pulmonary circulation.

Since the discovery of the vasorelaxant properties of nitric oxide and the vasoconstrictor effect of endothelin-1, there have been many studies of the distribution and functional significance of these agents in various vascular beds. In the coronary and pulmonary circulation nitric oxide and endothelin-1 actions have been largely investigated in terms of an imbalance between the opposing effects of these vasoactive agents leading to pathophysiological conditions. This article review functional and immunocytochemical studies with emphasis on the ultrastructural localization of nitric oxide synthase and endothelin-1 in the coronary and pulmonary vascular beds. Localization of nitric oxide synthase (type III or I or II) has been shown in endothelial cells, smooth muscle, and perivascular nerves of the coronary and pulmonary vascular beds and in the neurons, nerve fibers, and the small granule-containing cells within cardiac ganglia. Endothelin-1 was mainly localized in subpopulations of coronary and pulmonary endothelial cells. These immunocytochemical studies provide information about the sources of nitric oxide and endothelin-1 that contribute to the vasomotor control of cardiac and pulmonary circulation under normal and pathophysiological conditions.

Animals↗
PubMed1978

Uptake and inactivation of prostaglandin E2 methyl analogues in the rat pulmonary circulation.

1 The fate of (15S)-15-methyl prostaglandin E(2) methyl ester and 16,16-dimethyl prostaglandin E(2) in the pulmonary circulation of rat isolated lungs was compared with that of prostaglandin E(2) by means of bioassay.2 Calculated on the basis of height of response of the assay tissues, the inactivation of prostaglandin E(2) was 96 +/- 1%, of 15-methyl prostaglandin E(2) methyl ester, 53 +/- 6% and of 16,16-dimethyl prostaglandin E(2), 50 +/- 4%.3 Responses of the hamster stomach strip to the prostaglandin E(2) analogues passing through the pulmonary circulation were prolonged and slower in onset than those to the analogue given directly to the tissue. No such difference was observed with prostaglandin E(2).4 Bromocresol green, bromothymol blue, bromocresol purple and thymol blue (10(-5) M) all inhibited the inactivation of the three prostaglandins studied, as did diphloretin phosphate (1.5 x 10(-6) M). All five inhibitors also reversed the shape change in response seen after transpulmonary injection of 16-16-dimethyl prostaglandin E(2).5 We conclude that the inactivation of the methyl analogues is due to uptake, as they are not substrates for prostaglandin dehydrogenase.6 The lung may act as a depot for some compounds taking them up from the pulmonary vessels and later releasing them slowly into the systemic circulation.

Animals↗
PubMed1988

Temporal response of the fetal pulmonary circulation to pharmacologic vasodilators.

To determine the temporal response of the fetal pulmonary circulation to pharmacologic vasodilators and to assess vasoreactivity following vasodilation, we infused either acetylcholine, histamine, or bradykinin directly into the left pulmonary artery of 21 chronically prepared fetal sheep. Blood flow (Q) to the left lung was measured by electromagnetic flow transducer. Left pulmonary artery infusion of acetylcholine at 1.5 micrograms.min-1 for 2 hr produced an increase in Q from 59 +/- 8 ml.min-1 to a peak of 113 +/- 10 ml.min-1 at 20 min into the infusion (P less than 0.001). After the peak at 20 min, Q steadily declined toward baseline to 66 +/- 7 ml.min-1 at the end of the 2-hr infusion period (P less than 0.01). Q in the 1/2-hr period following infusion was significantly less than the baseline period (47 +/- 6; P less than 0.04) with no change in pulmonary artery pressure. Similar patterns were seen with 2-hr infusions of histamine (150 ng.min-1) and bradykinin (100 ng.min-1). After a 2-hr infusion of one of the agents, a repeat infusion with that agent or a different one resulted in a diminished response. We conclude that fetal pulmonary vasodilation in response to local infusion of acetylcholine, histamine, or bradykinin is not sustained over a 2-hr period, and that following 2-hr exposure to vasodilators, pulmonary vascular resistance is increased and pulmonary vasoreactivity to pharmacologic vasodilators is decreased.

Acetylcholine↗
PubMed1982

Pulmonary circulation of the llama at high and low altitudes.

We have studied the pulmonary circulation of three closely related animals, the llama, alpaca, and guanaco. The mean pulmonary arterial pressure of 12 llamas and one alpaca indigenous to high altitude in the Andes was found to be slightly but significantly higher than that of three llamas and three guanacos born and bred at low altitude in England. On the other hand, the medial thickness of the muscular pulmonary arteries and the relative weights of the two ventricles were the same in three llamas and one alpaca at high altitude as they were in one llama and two guanacos at low altitude. It is concluded that the pulmonary vasoconstrictive response to hypoxia, while present, is greatly reduced in this species and it is suggested that this may have taken place by evolutionary adaptation.

Altitude↗
PubMed1997

Differential effects of nitric oxide synthase modulation on porcine systemic and pulmonary circulation in vivo.

OBJECTIVE: To study and compare the effects of inhibiting endothelial nitric oxide synthase on systemic and pulmonary circulation in an in vivo model. DESIGN: Prospective, randomized, controlled study. SETTING: Laboratory for experimental surgery at a university medical center. SUBJECTS: Seventeen anesthetized, mechanically ventilated pigs. INTERVENTIONS: To produce a stable and continuous stimulation of endothelial nitric oxide synthase, an infusion of acetylcholine was given to one group of animals (n = 5) in a dose that decreased mean arterial pressure by 15%. After 45 mins, N(G)-monomethyl-L-arginine (L-NMMA) was given in a dose of 3 mg/kg for 5 mins in order to inhibit the enzyme. A second dose of 10 mg/kg was given 30 mins later. L-arginine was then given in a dose of 100 mg/kg to reverse the inhibition. One group of animals (n = 6) received a single dose of indomethacin (2.5 mg/kg) 15 mins after the start of acetylcholine infusion. L-NMMA and L-arginine were then given. In a control group (n = 5), the effects of L-NMMA and L-arginine were studied without acetylcholine. Circulatory parameters were monitored and resistance indices were calculated via arterial, central venous, and pulmonary artery catheters. MEASUREMENTS AND MAIN RESULTS: In control animals, 3 and 10 mg/kg of L-NMMA induced an increase in mean arterial pressure of 14% and 25%, respectively, with similar increases in systemic vascular resistance. Mean pulmonary arterial pressure increased by 22% and 48%, respectively. Acetylcholine lowered mean arterial pressure by 15% and did not affect the relative changes induced by L-NMMA. Acetylcholine had no effect on pulmonary resting tone but enhanced the pulmonary hypertension and increase in resistance induced by L-NMMA. This enhancement was abolished by indomethacin, which produced systemic hypertension while no effect on pulmonary pressure was seen. CONCLUSIONS: A basal release of nitric oxide contributes to the maintenance of normal vascular tone in the anesthetized pig. Stimulation of endothelial nitric oxide synthase by acetylcholine did not result in any further pulmonary vasodilation as was seen in the systemic circulation. Inhibition of nitric oxide synthase had a greater effect on pulmonary pressure than on systemic pressure. However, this difference was abolished by the administration of indomethacin. Increased nitric oxide release or acetylcholine itself seems to stimulate the production of a vasoconstricting prostanoid in the pulmonary circulation.

Acetylcholine↗
PubMed1995

Time varying loading of the pulmonary circulation: a model to describe hemodynamic observations in the stiff left atrial syndrome.

OBJECTIVE: To develop a mathematical model that could explain the following observations: that right heart failure can develop in association with no other cardiac abnormality than a severe reduction in the compliance of the left atrium; and that patients with this syndrome have systolic pulmonary hypertension with left atrial v waves in the absence of either mitral regurgitation or left ventricular dysfunction. DESIGN: A model of the pulmonary circulation was designed with a time varying terminal hydraulic load, which was varied between a noncompliant left atrium during systole and a compliant left ventricle/left atrium combination during diastole. Using representative parameters and a pulmonary arterial flow wave as input, pressures in the pulmonary artery and left atrium and right ventricular power output were calculated. RESULTS: Pulmonary arterial and left atrial systolic pressures are increased as left atrial compliance is reduced. The time varying change in terminal load results in an increase in systolic pressures, whereas diastolic pressures remain normal. A decrease in left atrial compliance increases both the nonpulsatile and pulsatile components of pulmonary input impedance, whereas only the nonpulsatile component of right ventricular power output is increased. CONCLUSIONS: The time varying pulmonary load model of the pulmonary circulation, in the presence of a reduced left atrial compliance results in pulmonary, and left atrial pressures similar to those observed in patients with the stiff left atrial syndrome. The resulting increase in right ventricular power output could be an important factor in the development of right heart failure.

Aged↗