[Pulmonary circulation and the right- and left-ventricular function in chronic interstitial pulmonary fibrosis of unknown etiology. III. Function of the left ventricle].
Explore the source record for details and available documents.
Blood Pressure↗
SEARCH · Search PubMed
Results for “PULMONARY CIRCULATION”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Effects of prostaglandins B2 and B1 on the pulmonary circulation in the intact dog.
The effects of prostaglandins (PG) B2 and B1 on the pulmonary circulation were studied in the intact spontaneously breathing dog under conditions of controlled blood flow using right heart and transseptal catheterization techniques to isolate and perfuse the left lower lung lobe. Infusion of PGB2 and PGB1 into the left lower lung lobe increased lobar arterial and lobar venous pressure but had no significant effect on left atrial pressure. PGB2 and PGB1 increased pressure gradients between the lobar artery and lobar small vein and between the lobar small vein and the left atrium. PGB2 and PGB1 increased isometric tension in isolated helical segments of lobar vein (3-5 mm diameter) but had little or no effect on lobar arterial segments of the same size. These results indicate that in the intact dog prostaglandins of the B series increase pulmonary vascular resistance by constricting lobar veins and to a lesser extent vessels upstream to lobar small veins, presumably small lobar arteries. PGB2 and PGB1 both produced large increases in pulmonary vascular resistance in the dog with PGB2 being about 10 times as potent as PGB1. It is concluded that PGB2 is one of the most potent pressor substances in the canine pulmonary vascular bed.
Animals↗
Removal of adenosine from the rabbit pulmonary circulation, in vivo and in vitro.
The contributions of pulmonary endothelial and blood cells to the removal of adenosine during a single passage through the rabbit pulmonary circulation were investigated. In the isolated, blood-free perfused rabbit lung in situ, single pass pulmonary removal of [3H]-adenosine injected into the pulmonary artery was accomplished by a low-affinity, saturable process yielding apparent Michaelis-Menten constants of Km = 498 +/- 36 microM and Vmax = 39 +/- 4 mumol/min per lung. Similar experiments in the intact, anesthetized animal, in vivo revealed a rapid, high-affinity removal of [3H]adenosine from plasma with apparent Michaelis-Menten constants of Km = 3.3 +/- 0.5 microM and Vmax = 6.5 +/- 2.4 mumol/min per lung. However, complete recovery of the injected adenosine was achieved upon lysing of cells from blood collected during a single transpulmonary passage of the substrate, indicating that blood cells were responsible for adenosine removal in vivo. The rate of disappearance of adenosine from plasma, observed by incubating the substrate with whole rabbit blood in vitro, was comparable to that found in vivo. We conclude that although, in the absence of circulating blood, rabbit lung is able to extract adenosine in vitro, this mechanism is of little significance in vivo where blood cells appear to be primarily responsible for such removal.
Adenosine↗
Effect of changing lung liquid volume on the pulmonary circulation of fetal lambs.
During fetal life the lung develops as a liquid-filled structure with low blood flow compared with postnatal life. We studied the effects of liquid expansion of the fetal lung by measuring vascular conductance in perfused lungs in situ and arterial diameters in excised lungs of fetal lambs. Pulmonary vascular conductance invariably rose as the lung was deflated from its initial volume; maximal deflation to residual volume increased conductance 122%. With reexpansion, conductance fell progressively, culminating in cessation of flow at lung volumes of twice the initial volume. These changes persisted after vagotomy and thoracic sympathectomy and therefore were mechanical in character. Lung expansion from residual volume initially expanded 300- to 500-micron arteries but compressed arteries greater than 1,500 micron. Further expansion reduced the caliber of all arteries. Thus increasing lung liquid volume progressively constricts the pulmonary circulation in the fetus. Because the fetal pulmonary vascular resistance-lung volume relationship differs from that of the U-shaped form found in adult lungs, concepts based on the adult pulmonary circulation are not appropriate for liquid-filled fetal lungs.
Animals↗
Carbon monoxide and pulmonary circulation in an ovine model.
The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.
Animals↗
Enhanced beta-adrenergic-receptor responsiveness in hypoxic neonatal pulmonary circulation.
The influence of alveolar hypoxia on pulmonary vascular adrenergic receptors was studied in conscious newborn lambs. In control animals, pulmonary vessels were directly constricted by epinephrine and norepinephrine, but were unaffected by isoproterenol. Pulmonary resistance (PVR) was also unaffected by propranolol, thus implying minimal beta-receptor activity under normoxic conditions. Hypoxia raised PVR but also modified the pulmonary vascular responses to catecholamines: isoproterenol became a dilator, whereas the constrictor effects of epinephrine and norepinephrine were abolished. Although beta-blockade did not alter base-line PVR, propranolol increased the constrictor response to hypoxia, implying that hypoxia increases beta-adrenergic activity or reactivity in the pulmonary circulation. Consistent with this hypothesis are the following: 1) in alpha-blocked lambs, epinephrine was without local effects during normoxia, but caused vasodilation during hypoxia; 2) the absent constrictor response to epinephrine during hypoxia is fully restored by propranolol; and 3) although alpha-blockade blunts the hypoxic constrictor response, the full response is restored when beta-blockade is added. These results indicate that the hypoxic constrictor response is partially opposed by increased beta-mediated vasodilation. These enhanced beta-receptor effects are due, at least in part, to increased beta-receptor reactivity of unknown mechanism.
Animals↗
[Pathophysiological reactions of the pulmonary circulation in airway and lung diseases].
Hypoxic pulmonary vasoconstriction (HPV) is a physiological phenomenon in healthy lungs and a regulatory mechanism in alveolar hypoventilation by which blood flow is diverted from poorly ventilated areas to better ventilated alveolar regions. Maintained alveolar hypoxia (related either to respiratory diseases or to high altitude) results in a persistent activation of HPV. The latter mechanism is involved in the development of pulmonary vasoconstriction and right heart failure (Cor pulmonale) in chronic airway diseases. Compared to other species, especially the bovine and the porcine lung is highly susceptible to develop pulmonary hypertension because of anatomical and physiological pecularities. Consequently, therapeutic support of the heart is indicated in cattle and pigs suffering from respiratory diseases. In contrast, non-selective vasodilators are not recommended because they override the compensatory effect of hypoxic vasoconstriction and impair pulmonary gas exchange.
Animals↗
Dose optimization for dynamic time-resolved contrast-enhanced 3D MR angiography of pulmonary circulation.
OBJECTIVE: The aim of this study was to optimize contrast media dose for assessment of pulmonary circulation with dynamic time-resolved contrast-enhanced 3D MR angiography. SUBJECTS AND METHODS. Twenty healthy volunteers (20-38 years old; mean [+/- SD], 27.2 +/- 4.5 years) were examined prospectively using turbo fast low-angle shot MR angiography (TR/TE, 2.4/1.04). Ten consecutive coronal 3D slabs with a frame rate of 3.2-sec duration were acquired during injection of contrast media at a rate of 4 mL/sec. Signal intensities were measured in various vessels and pulmonary parenchyma. Maximum signal-intensity enhancement (DeltaSI(max)) and time to peak enhancement were calculated. Depiction of pulmonary vessels and pulmonary parenchyma was scored according to an image quality score. RESULTS: Central pulmonary arteries were well visualized at all tested doses. Segmental arteries, however, were blurry with 0.025 or 0.05 mmol/kg; image quality was improved at 0.1 mmol/kg of gadoterate meglumine (p < 0.05). Image quality did not further improve at 0.2 mmol/kg (p = not significant). Values for DeltaSI(max) in the pulmonary trunk were 38.9 +/- 9.7, 64.1 +/- 9.1, 79.7 +/- 12.2, and 96 +/- 6.0 at 0.025, 0.5, 0.1, and 0.2 mmol/kg of gadoterate meglumine, respectively. Pulmonary parenchyma showed almost no enhancement at 0.025 and 0.5 mmol/kg of gadoterate meglumine (DeltaSI(max) = 1.6 +/- 1.1 and 1.6 +/- 1.2, respectively), but better visualization was shown with 0.1 and 0.2 mmol/kg of gadoterate meglumine (DeltaSI(max) = 2.9 +/- 0.8 and 6.7 +/- 2.1, respectively). Time from peak enhancement in pulmonary arteries to peak enhancement in veins was independent of dose. CONCLUSION: A dose of 0.1 mmol/kg of gadolinium chelate allows depiction of pulmonary arteries and qualitative assessment of pulmonary parenchyma. Thus, 0.1 mmol/kg can be recommended for dynamic contrast-enhanced 3D MR angiography.
Adult↗
Influence of the pulmonary circulation on adrenaline pharmacokinetics during cardiopulmonary resuscitation.
The influence of the pulmonary circulation on the pharmacokinetics and -dynamics of endogenously released, and intravenously injected (10 micrograms kg-1), and endobronchially (e.b.) administered (100 micrograms kg-1) adrenaline was investigated in an animal cardiopulmonary-resuscitation (CPR) model. During resuscitation 80% of endogenously released and i.v. adrenaline was eliminated before reaching the arterial circulation, whereas arterial availability of adrenaline was higher than mixed-venous availability in the e.b.-medicated animals. Success of resuscitation seemed to depend on maximum adrenaline concentrations and drug availability in arterial blood. Although the average amount of endogenously released adrenaline was calculated to be equivalent to an i.v. bolus of 8 micrograms kg-1, additional i.v. or e.b. adrenaline medication resulted in higher arterial plasma concentrations, improved circulation during CPR, and better resuscitability. It is concluded that, even without a specific pulmonary metabolism, a drastic decrease in blood flow can lead to significant arterio-venous gradients in plasma concentrations and availability of a drug with a very high clearance like adrenaline.
Administration, Inhalation↗
Chronic lung injury in preterm lambs: abnormalities of the pulmonary circulation and lung fluid balance.
Chronic lung disease of early infancy, or bronchopulmonary dysplasia, is a frequent complication of prolonged mechanical ventilation after premature birth. Pulmonary hypertension and edema are common features of this condition, which is often attributed to long-term, repetitive overinflation of incompletely developed lungs. The overall objective of this work was to examine the effects on the pulmonary circulation and lung fluid balance of different ventilation strategies using large versus small inflation volumes in an animal model of bronchopulmonary dysplasia. We studied 16 newborn lambs that were delivered prematurely (124+/-3 d gestation, term = 147 d) by cesarean section and mechanically ventilated for 3 to 4 wk. Ten lambs were ventilated at 20 breaths/min, yielding a tidal volume of 15+/-5 mL/kg, and six lambs were ventilated at 60 breaths/min, yielding a tidal volume of 6+/-2 mL/kg. All lambs received surfactant at birth and had subsequent surgery for closure of the ductus arteriosus and catheter placement to allow serial measurements of pulmonary vascular resistance and lung lymph flow. Chronic lung injury, documented by serial chest radiographs and postmortem pathologic examination, developed in all lambs irrespective of the pattern of assisted ventilation. Pulmonary vascular resistance, which normally decreases during the month after birth at term, did not change significantly from the first to the last week of study. Lung lymph flow, an index of net transvascular fluid filtration, increased with time in lambs that were ventilated at 20 breaths/min, but not in lambs ventilated at 60 breaths/min. Lymph protein concentration decreased with time, indicative of increased fluid filtration pressure, without evidence of a change in lung vascular protein permeability. Postmortem studies showed interstitial lung edema, increased pulmonary arteriolar smooth muscle and elastin, decreased numbers of small pulmonary arteries and veins, and decreased capillary surface density in distal lung of chronically ventilated lambs compared with control lambs that were killed either 1 d (same postconceptional age) or 3 wk (same postnatal age) after birth at term. Thus, chronic lung injury from prolonged mechanical ventilation after premature birth inhibits the normal postnatal decrease in pulmonary vascular resistance and leads to lung edema from increased fluid filtration pressure. These abnormalities of the pulmonary circulation may contribute to the abnormal respiratory gas exchange that often exists in infants with bronchopulmonary dysplasia.
Animals↗
Inhibition of 20-HETE abolishes the myogenic response during NOS antagonism in the ovine fetal pulmonary circulation.
Mechanisms that maintain high pulmonary vascular resistance (PVR) and oppose vasodilation in the fetal lung are poorly understood. In fetal lambs, increased pulmonary artery pressure evokes a potent vasoconstriction, suggesting that a myogenic response contributes to high PVR in the fetus. In adult systemic circulations, the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) has been shown to modulate the myogenic response, but its role in the fetal lung is unknown. We hypothesized that acute increases in pulmonary artery pressure release 20-HETE, which causes vasoconstriction, or a myogenic response, in the fetal lung. To address this hypothesis, we studied the hemodynamic effects of N-methylsufonyl-12,12-dibromododec-11-enamide (DDMS), a specific inhibitor of 20-HETE production, on the pulmonary vasoconstriction caused by acute compression of the ductus arteriosus (DA) in chronically prepared fetal sheep. An inflatable vascular occluder around the DA was used to increase pulmonary artery pressure under three study conditions: control, after pretreatment with nitro-L-arginine (L-NA; to inhibit shear-stress vasodilation), and after combined treatment with both L-NA and a specific 20-HETE inhibitor, DDMS. We found that DA compression after L-NA treatment increased PVR by 44 +/- 12%. Although intrapulmonary DDMS infusion did not affect basal PVR, DDMS completely abolished the vasoconstrictor response to DA compression in the presence of L-NA (44 +/- 12% vs. 2 +/- 4% change in PVR, L-NA vs. L-NA + DDMS, P < 0.05). We conclude that 20-HETE mediates the myogenic response in the fetal pulmonary circulation and speculate that pharmacological inhibition of 20-HETE might have a therapeutic role in neonatal conditions characterized by pulmonary hypertension.
Amides↗
Initial results and medium-term follow-up of stent implantation of patent ductus arteriosus in duct-dependent pulmonary circulation.
OBJECTIVES: This study was designed to assess the safety, efficacy, medium-term outcome, and complications of patent ductus arteriosus (PDA) stenting in duct-dependent pulmonary circulation. BACKGROUND: Patent ductus arteriosus stenting has been proposed as an alternative to surgical shunt on account of postoperative morbidity and complications of surgical shunting. METHODS: Between April 2000 and February 2003, 69 patients with duct-dependent pulmonary circulation underwent cardiac catheterization with the intent of PDA stenting as first palliative procedure. Patients with critical pulmonary stenosis and pulmonary atresia with intact ventricular septum post-radiofrequency valvotomy who had PDA stenting were excluded. Thirteen more patients were excluded because of branch pulmonary artery (PA) stenosis. The follow-up was by clinical examination, echocardiography, and repeat cardiac catheterization at six to nine months following the procedure. RESULTS: Patent ductus arteriosus stenting was successful in 51 patients (91.1%) and failed in 5 patients (8.9%). The mean narrowest PDA diameter was 1.9 +/- 0.6 mm. The mean procedure and fluoroscopy time were 95.7 min and 29.4 min, respectively. In one patient the stent dislodged and migrated to the left femoral artery and another patient developed transient intravascular hemolysis. There was no procedure-related mortality. Three patients (5.9%) died one day to two months after the procedure. At follow-up (3.2 months to 2.4 years), 8 patients developed significant stent stenosis requiring reintervention. Seven patients developed worsening of preexisting branch PA stenosis. The freedom from reintervention was 89% and 55% at 6 months and 1 year, respectively. CONCLUSIONS: Patent ductus arteriosus stenting is an attractive alternative to surgical shunt in a majority of patients with duct-dependent circulation. An absolute contraindication to this technique is the presence of branch pulmonary stenosis.
Child, Preschool↗
Who was the first to describe pulmonary circulation?
On occasion of the 425th anniversary of the publication of M.R. COLOMBO's De re anatomica, the author assesses this work and discusses the priority problems arising in connection with the description of pulmonary circulation. The life and activity of COLOMBO's contemporary, MICHAEL SERVETUS is also discussed. The conclusion is drawn that priority must go to SERVETUS who in 1553 gave the first description of pulmonary circulation.
Anatomy↗
Failure of cryopreserved homograft valved conduits in the pulmonary circulation.
BACKGROUND: This study evaluates our experience with the cryopreserved homograft valved conduit used for reconstruction of the pulmonary circulation in patients with congenital heart disease. METHODS AND RESULTS: Between July 1, 1985, and December 31, 1990, 219 patients had cryopreserved homograft extracardiac valved conduits placed in the pulmonary circuit. Average age at operation was 7.2 years. Of these, 132 patients had a pulmonary homograft, and 87 had an aortic homograft. Twenty-four patients (11%) died in hospital. Hospital survivors (n = 195) have been followed an average of 29.8 months (SD, +/- 18.4 months). Fourteen patients died during follow-up, almost all related to the complexity of their original cardiac malformation. Thirty-two patients (15%) have required reoperation for conduit-related problems. Actuarial freedom from conduit reoperation is 55 +/- 12% at 5 years. The most common indication for reoperation was calcific stenosis (n = 27). Other indications for reoperation were pseudoaneurysm (n = 2), conduit infection (n = 2), and pulmonary insufficiency (n = 1). Reoperation rate for patients with aortic homografts (16 of 87) compared with that for pulmonary homografts (16 of 132) was not significantly different by the actuarial method. CONCLUSIONS: Long-term function of cryopreserved homograft valved conduits in the pulmonary circulation is disappointing.
Actuarial Analysis↗
[The radiological diagnosis of the hemodynamic situation in the pulmonary circulation in chronic obstrictive ventilation disorders].
Hemodynamic consequences, especially in view of a developing pulmonary hypertension are essential factors regarding the course and prognosis of an obstructive airflow disturbance. The characteristic roentgen symptoms of pulmonary vascular changes in a group of patients are collected and statistically evaluated to find those symptoms correlating best with the results of cardiac catheterisation. The importantce of using not a single symptom but characteristic groups of symptoms for the radiological diagnosis of pulmonary hypertension is stressed. Radiological signs of increased pulmonary pressure do not directly correlate to the degree of direct measurements, false positive radiological reports need not be expected. Positive radiological symptoms indicate irreversible anatomical changes in pulmonary circulation. For the individual patient the pulmonary arterial pressure by cardiac catheterisation alone is not sufficient for the diagnosis and prognosis of this case as in obstructive air-way disturbance two definitely different types of diseases, namely type A (emphysema) and type B (bronchitis) with divergent hemodynamic consequences must be distinguished. For this differentiation the radiological evaluation of the anatomical situation is essential.
Aged↗
[Radiologic diagnosis of the hemodynamic situation in the pulmonary circulation in chronic obstructive ventilatory disorders].
Hemodynamic consequences, especially in view of a developing pulmonary hypertension are essential factors regarding the course and prognosis of an obstructive airflow disturbance. The characteristic roentgen symptoms of pulmonary vascular changes in a group of patients are collected and statistically evaluated to find those symptoms correlating best with the results of cardiac catheterisation. The importance of using not a single symptom but characteristic groups of symptoms for the radiological diagnosis of pulmonary hypertension is stressed. Radiological signs of increased pulmonary pressure do not directly correlate to the degree of measurements, false positive radiological reports need not be expected. Positive radiological symptoms indicate irreversible anatomical changes in pulmonary circulation. For the individual patient the pulmonary arterial pressure by cardiac catheterisation alone is not sufficient for the diagnosis and prognosis of this case as in obstructive air-way disturbance two definitely different types of diseases, namely type A (emphysema) and type B (bronchitis) with divergent hemodynamic consequences must be distinguished. For this differentiation the radiological evaluation of the anatomical situation is essential.
Adult↗
Stenting the neonatal arterial duct in duct-dependent pulmonary circulation: new techniques, better results.
OBJECTIVES: The goal of this study was to assess a new approach to stent the arterial duct in neonates with a duct-dependent pulmonary circulation. BACKGROUND: Previous attempts to stent the neonatal arterial duct were unsatisfactory. Learning from these failures, we speculated that covering the complete length of the duct with current low-profile stents might avoid previous problems. METHODS: Ten neonates with duct-dependent pulmonary circulations through a short straight duct were treated with stent implantation. The duct was crossed with an atraumatic 0.014-inch wire. A low-profile premounted coronary stent (outer diameter <4F, length 13 to 24 mm, diameter 3.0 to 4.0 mm) was positioned within the duct, not protected by a sheath; care was taken to cover the complete length of the duct from the aortaductal junction until well within the pulmonary trunk. RESULTS: All stents could safely be deployed with adequate pulmonary flow at early- and medium-term follow-up. There were no procedure-related complications; one patient died early from sepsis. All patients had adequate relief of cyanosis for at least three to four months. During follow-up, the pulmonary vasculature bed had grown without distortion. Acute occlusion of a stented duct was not observed. Ductal flow progressively decreased slowly over several months by luminal narrowing, until the stented duct had either become redundant or was dilated/restented or until elective staged surgery was performed. CONCLUSIONS: With current technology, complete stenting of a short straight duct is a safe and effective palliation, allowing adequate growth of the pulmonary arteries.
Cardiac Surgical Procedures↗
Changes in pulmonary circulation in severe bronchopulmonary dysplasia.
Eight patients with severe bronchopulmonary dysplasia underwent cardiac catheterisation. Seven had a pulmonary vascular resistance greater than 3 mm Hg.l-1 min.m2 (mean 8.9, range 2.2-13.8). All had raised intrapulmonary shunts (mean 25.6%, range 5.4-50%, normal less than 5%). Two had a high alveolar dead space, and two had unsuspected congenital heart disease. Epoprostenol (prostacyclin), but not 100% oxygen, caused a significant fall in pulmonary vascular resistance. Death was associated with a high pulmonary vascular resistance and a high shunt. Morphometric studies in three cases showed normal numbers of airways, but increased thickness of bronchial muscle. The numbers of alveoli were reduced and the walls thickened. There was increased medial thickness in small pulmonary arteries with distal extension of muscle. In the oldest child some vessels were obliterated by fibrosis. We speculate that measurements of pulmonary vascular resistance and shunt may have prognostic value; that a trial of pulmonary vasodilators other than oxygen might be worthwhile in patients with poor prognosis; and that abnormalities of the pulmonary circulation contribute to the difficulties of managing patients with bronchopulmonary dysplasia.
Blood Pressure↗