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PubMed1998

[Changes of nitric oxide synthase in hypoxic pulmonary hypertension and the effect of L-arg and L-NAME on pulmonary circulation].

OBJECTIVE: To study the role of nitric oxide (NO) in Hypoxic pulmonary hypertension (HPH). METHODS: NADPH-d and immunohistochemistry were used to study the expression and localization of constructive and inducible nitric oxide synthase (cNOS iNOS) in the lungs of normoxia and HPH rats, at the same time, the effects of L-arginine (L-arg) and nitro-L-arginine-methyl-ester (L-NAME) on normoxic and hypoxic pulmonary circulation were investigated. RESULTS: NADPH-d positive expression was detected in the endothelium and smooth muscle cells (SMC) of large pulmonary vessels (PV) and in the epithelium and SMC of bronchi in the HPH group, but negative in the endothelium and SMC of small PV in normoxia. Hypoxia not only inhibited the expression of cNOS in the endothelium and SMC of PV and epithelium of bronchi, but also induced the expression of iNOS in the endothelium and SMC of PV and SMC of bronchi. Administration of L-NAME in normoxia had no effect on pulmonary circulation. The effect of administration of L-arg and L-NAME in hypoxia on right ventricular hypertrophy and remodeling of PV had no significance, compared with simple hypoxia. CONCLUSION: The inhibition of cNOS may contribute to the occurrence of HPH, but induced iNOS may depress the development of HPH.

Animals↗
PubMed1998

Pulmonary circulation demonstration using an isolated rat lung model.

We have developed a pulmonary circulation laboratory exercise that effectively illustrates basic concepts typically taught in a graduate physiology curriculum. The demonstration uses an isolated, perfused rat lung model to delineate the mechanisms by which pulmonary vascular resistance can be altered either passively or in an active manner by contraction or relaxation of vascular smooth muscle. The exercise further offers an opportunity to closely observe an experimental preparation commonly used to study the pulmonary circulation and allows students the opportunity to interpret the resulting physiological data. Student evaluations indicate that the demonstration was received with enthusiasm and provides an effective teaching tool for reinforcing concepts in pulmonary vascular physiology.

Animals↗
PubMed1981

Adaptation of the pulmonary circulation to extra-uterine life in the pig and its relevance to the human infant.

The normal structural and functional development of the pulmonary circulation has been studied in the pig, from fetal life to six months of age, with emphasis on the first 2 weeks. Pulmonary and systemic arterial pressures were measured in 50 animals, in 21 of which pulmonary vascular resistance was determined. After post mortem arterial injection, lung structure was analysed using quantitative morphometric techniques. Changes in the pulmonary circulation consisted of three overlapping phases: 1 Dilatation and recruitment of small arteries within the acinar region, beginning during the first 5 min and associated with a reduction in pulmonary arterial pressure. These changes continued during the first 24 h, associated with a loss of arterial muscle. 2 Between 24 h and 2 weeks, a significant reduction in the amount of arterial muscle was associated with a reduction in pulmonary: systemic vascular resistance ratio from 0.58 to 0.18. 3 Functionally, the pulmonary circulation appeared mature at rest by 2 weeks but growth and remodelling of the pulmonary arteries continued until an adult pattern was reached by 6 months of age.

Animals↗
PubMed1996

Human pulmonary circulation is an important site for both clearance and production of endothelin-1.

BACKGROUND: Animal studies suggest a major role of the pulmonary circulation in the clearance of circulating endothelin-1 (ET-1). The contribution of the human pulmonary circulation to plasma ET-1 clearance, however, has never been quantified. The absence of an AV gradient in plasma ET-1 has previously been interpreted as evidence that the lungs do not have a role in modulating circulating ET-1 levels. This study was designed to quantify and discern between pulmonary ET-1 clearance and production in humans. METHODS AND RESULTS: We studied 13 subjects by combining the multiple indicator-dilution technique with the measurement of immunoreactive ET-1 (irET-1). All patients had normal left ventricular ejection fractions (61 +/- 7%, mean +/- SD) and baseline hemodynamics. Mean pulmonary ET-1 extraction was 47 +/- 7%. The ET-1 extracted does not return to circulation and can be characterized by a sequestration rate constant: Kseq = 0.048 +/- 0.019 s-1. There was no significant difference between irET-1 levels from the pulmonary artery and aorta (0.61 +/- 0.29 and 0.68 +/- 0.33 pg/mL, respectively; P = .22); the normal lung consequently produces an amount of ET-1 that is quantitatively similar to the amount that has been extracted. CONCLUSIONS: The human lung is an important site for both clearance and production of ET-1. There is a normal physiological balance of ET-1 across the pulmonary circulation, which explains the absence of difference in AV ET-1 levels despite a 47 +/- 7% clearance. Reduced pulmonary clearance or increased production of this peptide may contribute to the increase in circulating levels found in various cardiovascular conditions.

Aged↗
PubMed2002

Chronic hypoxia causes angiogenesis in addition to remodelling in the adult rat pulmonary circulation.

Chronic hypoxia caused by migration of native sea-level dwellers to high altitude or chronic lung disease leads to the development of increased pulmonary vascular resistance and pulmonary hypertension. This altitude-induced hypertension offers no obvious benefit and may indeed be maladaptive. A major mechanism thought to contribute to the development of pulmonary hypertension is hypoxia-induced loss of small blood vessels, sometimes termed rarefaction or pruning. More recent evidence caused us to question this widely accepted concept including the potent angiogenic effect of chronic hypoxia in all other vascular beds and the demonstration that new vessels can form in the pulmonary circulation when stimulated by chronic infection and lung resection. We tested the hypothesis that chronic environmental hypoxia causes angiogenesis in the adult pulmonary circulation by using stereological techniques combined with confocal microscopy to examine the resultant changes in pulmonary vascular structure in rats. We found that chronic hypoxia resulted in increased total pulmonary vessel length, volume, endothelial surface area and number of endothelial cells in vivo. This is the first reported demonstration of hypoxia-induced angiogenesis in the mature pulmonary circulation, a structural adaptation that may have important beneficial consequences for gas exchange. These findings imply that we must revise the widely accepted paradigm that hypoxia-induced loss of small vessels is a key structural change contributing to the development of pulmonary hypertension in high altitude adaptation and chronic lung disease.

Animals↗
PubMed2001

Decrease in circulating hematopoietic progenitor cells by trapping in the pulmonary circulation.

BACKGROUND: When stem-cell grafts are infused into the venous circulation and stem/progenitor cells egress from BM, pulmonary capillary beds are the first microcirculation site that they encounter. This provides the potential for circulating progenitor cells to be trapped in the pulmonary circulation. METHODS: We compared the number of progenitor cells [CD34(+) cells, colony-forming unit-granulocyte-macrophage (CFU-GM), CD34(+) CD41(+) cells and CFU-megakaryocyte (CFU-meg)] and their expression of cell-adhesion molecules (CAM) in samples taken simultaneously from radial arteries and central veins of 21 patients following PBSC mobilization. RESULTS: The mean (+/- SD) frequency of progenitor cells in the radial arteries was reduced to 79% +/- 25% for CD34(+) cells, 73% +/- 27% for CFU-GM, 77% +/- 25% for CD34(+) CD41(+) cells and 70% +/- 29% for CFU-meg of the number in the central veins. This suggests that some progenitor cells might be trapped in the lung. No association between progenitor-cell expression of CAM and pulmonary trapping was observed. DISCUSSION: Our data demonstrate pulmonary trapping of PBSC during mobilization, suggesting a potential inhibitory effect on PBSC harvest and medullary trafficking following graft infusion. However, the impact associated with pulmonary PBSC trapping may be negligible in the clinical setting if sufficient cells are infused.

Antigens, CD34↗
PubMed2001

Effects of catecholamines on the pulmonary circulation in the ovine fetus.

High levels of circulating catecholamines are found in the fetus, and fetal stress and birth induce a marked surge in catecholamine secretion. Little is known about the role of catecholamines on the fetal pulmonary circulation. To determine the effects of catecholamines on the pulmonary vascular tone, we tested the hemodynamic response to norepinephrine and dopamine infusion in chronically prepared late-gestation fetal lambs. We found that norepinephrine infusion (0.5 microg. kg(-1). min(-1)) increased pulmonary artery pressure (PAP) by 10 +/- 1% (P < 0.01), left pulmonary artery blood flow by 73 +/- 14% (P < 0.01), and decreased pulmonary vascular resistance (PVR) by 33 +/- 6% (P < 0.01). The pulmonary vasodilator effect of norepinephrine was abolished after nitric oxide synthase inhibition. Dopamine infusion at 5 microg. kg(-1). min(-1) did not significantly change PVR. Conversely, dopamine infusion at 10 microg. kg(-1). min(-1) increased PAP (P < 0.01) and progressively increased PVR by 30 +/- 14% (P < 0.01). These results indicate that catecholamines may modulate basal pulmonary vascular tone in the ovine fetus. We speculate that catecholamines may play a significant role in the maintenance of the fetal pulmonary circulation and in mediating changes in the transitional pulmonary circulation.

Adrenergic alpha-Agonists↗
PubMed1990

[Pulmonary circulation in constrictive pericarditis].

Certain indices of pulmonary haemodynamics were determined at rest in 39 patients with constrictive pericarditis. The most frequent anomaly was raised value of total pulmonary resistance (in 82% of cases) and, in a lower percent, raised pulmonary vascular resistance. The systolic pressure in the pulmonary artery was raised in 30.8% of the patients, reaching values regarded as low or medium degree hypertension. In only 2 cases the systolic pressure in the pulmonary artery was 100 mm Hg or more. The systolic pressure in the pulmonary artery showed a slight positive correlation with the end-diastolic pressure in the left ventricle, and the subgroup with pulmonary hypertension had higher average values of the end-diastolic pressure in the left ventricle than patients with normal pressure in the pulmonary circulation (means = 21.0 +/- 5.7 vs 15.2 +/- 6.5 mm Hg). These results show a significant role of increased filling pressure of the left ventricle in the mechanism of pulmonary hypertension in patients with constrictive pericarditis.

Adolescent↗
PubMed1998

Carl J. Wiggers and the pulmonary circulation: a young man in search of excellence.

Oddly, Carl Wiggers (1883-1962), who is remembered for his work on the systemic circulation, may be considered the "American father of the pulmonary circulation." In nearly-20 papers published in the American Journal of Physiology between 1909 and 1925, he reported the first reliable pressure contours in the pulmonary artery, inquired into the relationship between respiration and pulmonary arterial pressure, examined right atrial and right ventricular function, and demonstrated how right and left heart dynamics relate to heart sounds. He also stimulated direct visualization of the lung microcirculation. Method and concept are inextricably linked in the progress of science. His contributions to the pulmonary circulation were based on his high-fidelity pressure and sound recording instruments, which he ultimately applied in the left heart. Wiggers' search for excellence in method brought him well-deserved fame in the systemic circulation, but the search began in the lung.

History, 20th Century↗
PubMed2003

Assessment of the anomalous pulmonary circulation by dynamic contrast-enhanced MR angiography in under four seconds.

The purpose of this study was to demonstrate the initial results of the dynamic contrast-enhanced MRA in under four seconds in the assessment of anomalous pulmonary circulation. We performed dynamic contrast enhanced MRA on ten patients with a temporal resolution of 2-3 sec for each phase. Five patients had pulmonary vascular anomaly and five patients had reconstructed pulmonary circulation. On nine patients catheter angiography was performed for the correlation. Dynamic contrast-enhanced MRA successfully demonstrated congenital pulmonary vascular anomalies and the pathway of anomalous pulmonary circulation in our series. With the improved temporal and spatial resolution, the dynamic contrast-enhanced MRA can be used in children and infants for the assessment of congenital vascular disease.

Child↗
PubMed1992

Uncoupling of atrial natriuretic peptide extraction and cyclic guanosine monophosphate production in the pulmonary circulation in patients with severe heart failure.

OBJECTIVES: This study was designed to evaluate the role of endogenous atrial natriuretic peptide in the pulmonary circulation in patients with chronic heart failure. BACKGROUND: Plasma atrial natriuretic peptide concentrations in patients with heart failure have been reported to be higher than those in normal subjects and to increase as the severity of heart failure progresses. Although endogenous atrial natriuretic peptide is thought to improve the condition of patients with heart failure by reducing preload and afterload, recent findings have indicated that a high plasma atrial natriuretic peptide level is a prognostic predictor in patients with heart failure. METHODS: To evaluate the pathophysiologic role of endogenous atrial natriuretic peptide in the pulmonary circulation, plasma atrial natriuretic peptide and cyclic guanosine monophosphate (cGMP) levels were determined in the main pulmonary artery and pulmonary capillary wedge region in 80 patients with chronic congestive heart failure (New York Heart Association functional classes II to IV). RESULTS: The plasma atrial natriuretic peptide level decreased significantly from the main pulmonary artery to the pulmonary capillary wedge region, whereas the plasma cGMP level increased significantly from the main pulmonary artery to the pulmonary capillary wedge region. In patients with mild chronic heart failure (n = 50), the plasma atrial natriuretic peptide level correlated with the cGMP level in the main pulmonary artery (gamma = 0.71, p less than 0.001). The atrial natriuretic peptide extraction level, calculated as (Atrial natriuretic peptide in the main pulmonary artery--Atrial natriuretic peptide in the pulmonary capillary wedge region) x Cardiac output x (1-hematocrit/100) (ng/min), also correlated with the cyclic guanosine monophosphate production level, calculated as (cGMP in the pulmonary capillary wedge region--cGMP in the main pulmonary artery) x Cardiac output x (1-hematocrit/100) (nmol/min) (gamma = 0.78, p less than 0.001). In contrast, such correlations were not found in patients with severe chronic heart failure (n = 30). In these patients, the atrial natriuretic peptide extraction level was significantly higher but there was no significant difference in the cGMP production level between the two groups (mild and severe chronic heart failure). Therefore, the molar ratio of cGMP production to atrial natriuretic peptide extraction in the pulmonary circulation was significantly lower in patients with severe chronic heart failure (88 +/- 16 vs. 480 +/- 41, p less than 0.001). CONCLUSIONS: These results indicate that down-regulation of atrial natriuretic peptide receptors coupled to guanylate cyclase may occur in the pulmonary vascular beds of patients with severe chronic heart failure.

Adolescent↗
PubMed1997

Pulmonary circulation at high altitude.

Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance is seen in normal subjects during hypoxic breathing at sea level, in acclimatized lowlanders and in high-altitude natives. Hypoxic pulmonary hypertension in all these circumstances is most generally moderate, except in high-altitude natives at exercise. Pulmonary hypertension may become severe during high-altitude pulmonary edema, during infantile or adult forms of subacute mountain sickness, and during chronic mountain sickness. Subacute and chronic mountain sickness may be associated with a right heart failure that would be the human counterpart of brisket disease described in cattle. Subjects susceptible to high-altitude pulmonary edema present with a slight increase in pulmonary vascular resistance at rest and at exercise, and often with an enhanced pulmonary vascular reactivity to hypoxia. However, compared to unselected controls, the overlap is great, so that noninvasive echo-Doppler studies of the pulmonary circulation at sea level are of little predictive value of tolerance to altitudes on an individual basis.

Acclimatization↗
PubMed1994

Ontogeny of NO activity and response to inhaled NO in the developing ovine pulmonary circulation.

To determine maturation-related changes in nitric oxide (NO) activity in the developing pulmonary circulation, we studied the hemodynamic effects of endogenous NO inhibition under basal conditions in the premature ovine fetus and the response to birth-related stimuli and exogenous NO in 30 fetal sheep at three different gestational ages. At 0.95 term, pulmonary vasodilation during inhaled NO (20 parts per million) was equivalent to the dilator response to 100% O2, but at 0.86 term vasodilation during inhaled NO was greater than the dilator response to 100% O2 (P < 0.05). At 0.78 term, left pulmonary arterial flow (QLPA) did not increase with exposure to either NO or 100% O2. Intrapulmonary infusion of nitro-L-arginine (L-NA) increased basal pulmonary vascular resistance 38% in the premature fetus at 0.78 term. L-NA treatment decreased the ventilation-induced rise in QLPA by 60% compared with controls (P < 0.05). Inhaled NO but not 100% O2 increased QLPA after L-NA treatment to levels achieved with ventilation alone in the controls. We conclude that in the premature pulmonary circulation (0.78 term) 1) basal pulmonary vascular resistance is modulated by endogenous NO, 2) pulmonary vasodilation at birth is partly mediated by endogenous NO activity, and 3) inhaled NO causes potent vasodilation.

Administration, Inhalation↗
PubMed1996

Differential role of endothelium-derived nitric oxide in the modulation of the systemic and pulmonary circulation in lambs.

We have studied the differential role of endothelium-derived nitric oxide (EDNO) in the regulation of the systemic and pulmonary circulations of the lamb. Hemodynamic effects of NG-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg i.v.), an inhibitor of NO synthesis, were determined in juvenile (6 +/- 1 weeks old) lambs, under conditions of basal and elevated vasomotor tone. Under basal conditions, L-NAME raised both systemic (SVR) and pulmonary vascular resistances (PVR) by 20-30% (increasing SVR from 0.318 +/- 0.013 to 0.385 +/- 0.015 mm Hg.min.ml-1.kg and PVR from 0.050 +/- 0.003 to 0.067 +/- 0.010 mm Hg.min.ml-1.kg). When tone was elevated in the pulmonary circulation with hypoxia (PVR was elevated by 60%, from 0.059 +/- 0.010 to 0.094 +/- 0.019 mm Hg.min.ml-1.kg), L-NAME treatment resulted in an augmented increase in PVR (PVR increased by greater than 50% to 0.140 +/- 0.024 mm Hg.min.ml-1.kg). However, when tone was elevated to a comparable degree in the systemic circulation with angiotensin infusion (SVR was elevated by 60%, from 0.432 +/- 0.065 to 0.065 to 0.634 +/- 0.113 mm Hg.min.ml-1.kg), the response to L-NAME was not augmented. Our data suggest that the role of EDNO in the modulation of the pulmonary circulation is dependent on the level of vasomotor tone, whereas its role in the systemic circulation is small and is independent of the level of vasomotor tone.

Animals↗
PubMed1998

Gadolinium chloride inhibition of pulmonary nitric oxide production and effects on pulmonary circulation in the rabbit.

Nitric oxide is an important regulator of pulmonary vascular resistance. Pulmonary nitric oxide formation is detectable in exhaled air and the synthesis is partly stretch-dependent. Gadolinium chloride (GdCl3) reduces pulmonary nitric oxide formation, possibly by interference with stretch-activated cellular calcium influx, but the effect on pulmonary circulation is not known. We therefore measured exhaled nitric oxide and pulmonary vascular resistance in anaesthetised rabbits, and compared the effects of GdCl3 with those of an nitric oxide-synthase inhibitor (L-N omega-nitro-arginine methyl ester, L-NAME). Both GdCl3 and L-NAME reduced nitric oxide in exhaled air and increased pulmonary vascular resistance. However, the increase in pulmonary vascular resistance was more pronounced with GdCl3 than with L-NAME. A 50% reduction of exhaled nitric oxide caused by either GdCl3 or L-NAME was accompanied by a 90% or 17% increase in pulmonary vascular resistance respectively. Inhaled nitric oxide (40 ppm) reduced pulmonary vascular resistance after L-NAME, but not after GdCl3 infusion. Infusion of glyceryltrinitrate reduced pulmonary vascular resistance after GdCl3 infusion. GdCl3 caused hypoxaemia, probably due to vasoconstriction since lung weight was unaltered. Thus GdCl3 can induce a marked increase in pulmonary vascular resistance, which partly may be caused by inhibition of pulmonary nitric oxide formation. Intact stretch-activated calcium channels may be important for maintenance of normal pulmonary vascular function.

Animals↗