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PubMed1997

[Effect of different hypoxic duration on changes of pulmonary circulation].

In order to assess the relationship between the hypoxic duration and pulmonary hypertension, we investigated the pulmonary hemodynamics and right ventricular hypertrophy and pulmonary vascular structure changes in rats with hypoxic exposure for 1 day to 3 weeks. After hypoxic treatment, the pulmonary artery pressure of rats increased in 3 days, and it was up to peak at 2 weeks later. The weight of right ventricle of rats significantly increased after 1 week. The endothelium of pulmonary vascular of rats became swollen in 3 days, and then increased in extracellular matrix deposition. Vessel wall thickening was found in 1 week hypoxic rats, and it was very significant in 3 week hypoxic rats. The results suggest that the duration of hypoxic treatment is related to the change of pulmonary circulation in 3 weeks in rats.

Animals↗
PubMed2002

Occurrence of dopaminergic (D(2)) receptors within the rabbit pulmonary circulation.

The pharmacological characteristics and the microanatomical localization of dopamine D(2)-like receptors, or more correctly spiroperidol binding sites, in the rabbit pulmonary circulation were studied using combined marker binding and light microscopy autoradiography with [((3))H]-spiroperidol (spiperone) as marker. The marker was bound to the samples of the pulmonary artery in a manner consistent with the labelling of dopamine D(2)-like receptors with an equilibrium dissociation constant (K(d)) of about 2.4+/-0.07 nmol/l and a maximum density of binding sites of 65+/-4.5 fmol/mg tissue. Samples of bronchial artery show the same results as those of the pulmonary artery. In contrast, binding experiments made with samples of rabbit lung (capillary of the microcirculation), of pulmonary veins and/or of bronchial veins did not allow the evaluation of specific binding.Autoradiography, observed with light microscopy, showed the development of specific silver grains within the whole wall of extraparenchymal branches of the pulmonary artery and/or of the bronchial artery. Development of silver grains was inhibited by compounds active on the dopamine receptors. The greater sensitivity to displacement by domperidone, haloperidol, and bromocriptine than to displacement by N-propyl-nor-apomorphine, quinpirole and clozapine suggests that the binding sites observed in extraparenchymal, large and medium-sized branches of the rabbit pulmonary and bronchial arteries belong, likely, to the dopamine D(2) receptor subtype. Quantitative analysis of images let us count the amount of these receptors in many samples of the pulmonary and/or bronchial arteries.

Animals↗
PubMed1987

The process of gas exchange in the pulmonary circulation incorporating the contribution of axial diffusion.

A mathematical model is made to describe the process of gas exchange in the pulmonary circulation incorporating the contribution of axial diffusion. The model takes into account the transport mechanisms of molecular diffusion, convection and facilitated diffusion due to the presence of haemoglobin as a carrier of the gases. The mathematical formulation leads to a coupled system of non-linear elliptic partial differential equations. A numerical scheme is described to solve such a system. It is found that the axial diffusion does not have an appreciable effect on the transport of the species in the blood.

Diffusion↗
PubMed1999

Effect of adenosine on pulmonary circulation of rabbits.

The effect and mechanism of action of adenosine on the pulmonary circulation of rabbits were studied. Adenosine (10(-5)-10(-3) M) produced a concentration-dependent decrease in pulmonary arterial tension of precontracted pulmonary arterial rings. Removal of endothelium (denuded) augmented the adenosine-induced vasodilation in the pulmonary arterial rings. Theophylline (5 x 10(-5) M), an adenosine receptor antagonist, reduces the vasodilation induced by adenosine in intact and denuded rings. Pretreatment of the pulmonary rings with the cyclooxygenase inhibitor indomethacin (5 x 10(-6) M) significantly attenuated the adenosine-induced relaxation in denuded but not in the intact pulmonary arterial rings. Methylene blue (5 x 10(-5) M), a guanylate cyclase inhibitor, significantly reduced the relaxation induced by adenosine in both the intact and the denuded arterial rings. Adenosine significantly attenuated the pressor responses of serotonin and acetylcholine in the intact and denuded rabbit's pulmonary arterial rings. The results of this study indicate that adenosine induces pulmonary vasodilation and that functional endothelium is not required to evoke this dilation. In addition, guanylate cyclase activity and the generation of cGMP is essential for adenosine to induce vasodilation in the rabbit lung. Furthermore, the results of this study may suggest that adenosine could be used to reduce the severity of pulmonary hypertension and possibly pulmonary edema.

Adenosine↗
PubMed1999

Analysis of endotoxin effects on the intact pulmonary circulation.

OBJECTIVE: The mechanism of sustained alterations in pulmonary hemodynamics during endotoxin shock remains unclear. To gain more detailed knowledge we used the four-element windkessel model as a descriptor of the pulmonary circuit. METHODS: Consecutive changes in characteristic resistance (R1), vascular compliance (C), input resistance (R2) and inductance (L) were continuously assessed following injection of endotoxin in 6 anaesthetised pigs, and were compared with the corresponding values measured in a similar group of sham-operated animals. RESULTS: Endotoxin challenge resulted in a biphasic pulmonary artery pressure response. Blood flow decreased progressively from 2.8 +/- 0.2 l/min to 2 +/- 0.2 l/min. Ohmic pulmonary vascular resistance (PVR) increased gradually from 0.2 +/- 0.04 to 0.76 +/- 0.1 mm Hg s ml-1. The early increase in PAP (from 14 +/- 2 to 27 +/- 4 mm Hg) was mediated by changes in both R1 (from 0.04 +/- 0.01 to 0.06 +/- 0.01 mm Hg s ml-1) and R2 (from 0.16 +/- 0.04 to 0.61 +/- 0.2 mm Hg s ml-1). These responses, in turn, altered the proximal vascular compliance. A subsequent increase in PAP (from 27 +/- 2 to 32 +/- 3 mm Hg) paralleled the specific decline in distal pulmonary vasculature compliance from 0.84 +/- 0.1 to 0.65 +/- 0.1 ml/mmHg. Analysis of the time course of PVR did not allow us to distinguish between vasoconstriction and stiffening of the vascular tree as mechanisms accounting for PAP changes. CONCLUSIONS: Endotoxemia leads to pulmonary hypertension, which is a result of constriction of proximal pulmonary arteries during the early phase, whereas the late phase is characterised by a decline in distal pulmonary vasculature compliance.

Animals↗
PubMed2003

Effects of pulmonary artery remodeling on pulmonary circulation after lung volume reduction surgery.

BACKGROUND: Significant pulmonary hypertension during exercise has been observed in patients with severe chronic obstructive pulmonary disease. Although favorable effects on pulmonary function and dyspnea symptoms have been demonstrated, the influence of lung volume reduction surgery (LVRS) on the pulmonary hypertension during exercise is still a controversial subject. METHODS: A pulmonary function test and 6-minute walking test were performed before and 3, 6, 12 and 24 months after LVRS (n = 12). Pulmonary hemodynamics at rest and during exercise was studied 6 months after operation. Morphology was examined in pulmonary arteries with external diameters of 100 - 200 micro m in the resected lung, and the wall thickness (defined as intima plus media) and percentage wall thickness (percentage wall thickness of the external diameter) of the pulmonary artery were calculated. RESULTS: LVRS improved early-phase pulmonary function and 6-minute walking distance. Although the increase in pulmonary capillary wedge pressure during exercise was significantly ameliorated, exercise pulmonary hypertension did not change after LVRS. The percent wall thickness was highly correlated with Delta Ppa (difference between mean pulmonary artery pressure at rest and mean pulmonary artery pressure during exercise) not only before, but also 6 months after LVRS. CONCLUSION: LVRS has no significant influence on exercise-induced pulmonary hypertension in patients with severe emphysema. From a histological analysis of the pulmonary artery in the resected lung, remodeling the pulmonary artery that may exist in the remaining lung is possibly one of the important factors preventing postoperative improvement in exercise pulmonary hypertension in patients with chronic obstructive pulmonary disease.

Aged↗
PubMed1995

Long-term effects of prenatal indomethacin administration on the pulmonary circulation in rats.

Mechanical properties of the adult pulmonary vasculature are affected by perinatal experience of hypoxic pulmonary hypertension. In the present study, we followed the long-term effects of perinatal pulmonary hypertension induced by means other than hypoxia in rats. Daily injections of indomethacin (1 mg.kg-1 body weight (BW)) were given to the parturient rats. Their newborn pups had significantly increased number of muscularized peripheral pulmonary vessels. Pulmonary hypertension, however, did not persist to adulthood (mean pulmonary arterial pressure (Ppa) was 17.2 +/- 1.3 torr in the experimental group and 16.4 +/- 0.8 torr in controls). Pulmonary hypertension induced in adult rats by exposure to chronic hypoxia or by acute hypoxic challenges was similar in indomethacin-treated and control rats. Normoxic perfusion pressure/flow (P/Q) plots in isolated lungs were less steep in indomethacin-treated than in control rats. Acute hypoxia increased the slope of P/Q plots in indomethacin treated rats but not in controls. The described changes in the pulmonary vasculature induced by indomethacin are similar to those found previously in adult rats born in hypoxia. We conclude that perinatal pulmonary hypertension permanently modifies the pulmonary vasculature.

Animals↗
PubMed1994

The effect of inhaled nitric oxide on the pulmonary circulation of the neonatal pig.

To study the pulmonary vasodilator selectivity of low levels of inhaled nitric oxide (NO) in a model of neonatal pulmonary hypertension, we sequentially exposed anesthetized, spontaneously breathing neonatal pigs to each of four different inspired gas mixtures: room air, room air with 25 parts per million NO, hypoxia (14% O2 in N2), and hypoxia with 25 parts per million NO. The room air, room air with NO, hypoxia, and hypoxia with NO exposures were of 15-min duration. The following measurements were made: mean systemic arterial, mean pulmonary arterial, and wedge pressures; thermodilution cardiac output; esophageal pressure; tracheal flow; and arterial PO2, PCO2, pH, hemoglobin, and methemoglobin. Inhalation of NO decreased pulmonary arterial pressure in both room air and hypoxia conditions (mean pulmonary arterial pressure 16 +/- 1 torr room air, 13 +/- 1 torr room air with NO, p < 0.005; and mean pulmonary arterial pressure 21 +/- 2 torr hypoxia, 14 +/- 1 torr hypoxia with NO, p < 0.005). NO had no significant effect on systemic arterial pressure, cardiac output, dynamic lung compliance, pulmonary resistance, or the measured blood variables during either control or hypoxic conditions. The results indicate that inhaled NO was a selective pulmonary vasodilator that could effectively reverse acute hypoxic pulmonary vasoconstriction. The normoxic vasodilation produced by NO inhalation also indicates the existence of basal vasomotor tone in the anesthetized, spontaneously breathing neonatal pig. The short-term exposures used produced no detectable manifestations of toxic side effects.

Administration, Inhalation↗
PubMed1997

Effects of inhaled nitric oxide on postoperative pulmonary circulation in patients with congenital heart disease.

We studied 22 patients with residual pulmonary hypertension or symptoms of postoperative pulmonary hypertensive crisis. They received low-dose inhalation (10 ppm) of nitric oxide (NO), a selective pulmonary vasodilator, after total correction for congenital heart anomalies. Fifteen minutes of NO inhalation improved the pulmonary circulation and lessened the imbalance in the ventilation-perfusion ratio in both groups. Thus, NO inhalation is effective in the treatment of pulmonary hypertension and in the prevention of pulmonary hypertensive crises after total correction for congenital heart anomalies. All patients continued to receive NO therapeutically. The duration of such therapeutic NO inhalation was well correlated with postoperative Qp/Qs (p = 0.014) and Rp/Rs (p = 0.029).

Administration, Inhalation↗
PubMed1977

Study of the pulmonary circulation in a canine asthma model.

Measurements of respiratory mechanics, gas exchange, and pulmonary hemodynamics were made before and serially for 2 hours after inhalation challenge with Ascaris suum extract in dogs with natural sensitivity to this antigen. Nine of 14 dogs randomly exposed to an inspired oxygen fraction of 0.21 or 0.60 to 0.70, responded to the challenge with bronchospasm reflected by a transient decrease of mean specific respiratory system conductance to 50 per cent of baseline after 5 to 15 min. This was accompanied by a decrease in alveolar ventilation in all and acidosis in some animals. No changes were observed in transmural pulmonary arterial pressure, cardiac output, pulmonary vascular resistance, and pulmonary blood volume in all 9 dogs who responded with bronchospasm, whether or not arterial hypoxemia was allowed to develop. In contrast, a significant increase in pulmonary vascular resistance occurred in control dogs in whom comparable degrees of arterial hypoxemia were produced by 10 per cent oxygen breathing or mechanical bronchial obstruction by placing beads in lobar and segmental airways. No changes in any parameter measured occurred in the 5 dogs who did not develop bronchospasm after antigen challenge. The results indicated that moderately severe, antigen-induced bronchospasm in anesthetized dogs has no effect on the pulmonary circulation even when associated with arterial hypoxemia. Because nonuniformity of alveolar hypoxia allowing redistribution of blood flow is probably not responsible for this failure to develop increases in pulmonary vascular resistance in induced asthma, it is suggested that the elaboration of chemical mediators may have interfered with the hypoxic pulmonary vasoconstrictor response.

Acidosis↗
PubMed2001

Improved right heart function with a compliant inflow artificial lung in series with the pulmonary circulation.

BACKGROUND: We previously reported a 50% incidence of immediate right heart failure using a rigidly housed, noncompliant inflow artificial lung in series with the pulmonary circulation in a healthy ovine survival model. Three device modifications resulted: (1) an inflow cannula compliance chamber, (2) an inlet blood flow separator, and (3) modification of the artificial lung outlet geometry, all to reduce resistance and mimic the compliance of the pulmonary vascular bed. METHODS: In 7 sheep, arterial grafts were anastomosed end-to-side to the proximal and distal main pulmonary artery, with the paracorporeal artificial lung interposed. A pulmonary artery snare between anastomoses diverted full pulmonary blood flow through the artificial lung for up to 72 hours. RESULTS: Six of 7 sheep exhibited good cardiac function throughout the test period: mean central venous pressure was 6.8 mm Hg (range, 4 to 11 mm Hg), mean cardiac output, 4.17 +/- 0.12 L/min (range, 2.4 to 6.3 L/min); before and after device mean pulmonary arterial pressure, 21.8 and 18.5 mm Hg, and left atrial pressure, 10.8 mm Hg. CONCLUSIONS: This modified artificial lung prototype with an inflow compliance chamber, blood flow separator, and modified outlet geometry has greatly improved cardiac function and initial survival in our healthy ovine model.

Anastomosis, Surgical↗
PubMed1979

Effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation in man.

The effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation were investigated in 13 patients in whom systemic hypertension developed following coronary artery bypass surgery. Pulmonary vascular resistance was decreased by the inhibitor, from 128 +/¿ 19 to 92 +/- 20 dynes sec cm-5 (or by 30 +/- 7 per cent; P less than 0.005), and this resulted in a decrease in mean pulmonary artery pressure from 17 +/- 1 to 13 +/- 1 mm Hg (or by 23 +/- 3 per cent, P less than 0.005). Consequently, right ventricular work was decreased by the inhibitor by 30 per cent (P less than 0.01), despite an increase in cardiac output (increase in stroke volume) by 16 +/- 6 per cent (P less than 01). This increase occurred despite a 13 +/- 3 per cent decrease in right ventricular filling pressure. The changes in pulmonary vascular resistance correlated with the pretreatment plasma renin activity (r = 0.74, P less than 0.01), as did the decrease in mean pulmonary artery pressure (R = 0.82, P less than 0.001), but neither change was related to the decrease in left ventricular fillling pressure nor to changes in cardiac output or mean arterial pressure. These results indicate that blockade of the formation of angiotensin II by the converting enzyme inhibitor results in reductions in pulmonary vascular resistance and pulmonary artery pressure which are unrelated to alterations in left ventricular function. Thus, angiotensin inhibition may have therapeutic value in various clinical states characterized by pulmonary hypertension--especially if renin levels are high.

Adult↗
PubMed1993

[Study of pathophysiology of pulmonary circulation in polycythemia using scintigraphy].

In order to evaluate the pathophysiology of pulmonary circulation in polycythemia, Tl-201 myocardial scintigraphy and perfusion lung scintigraphy with 99m-Tc MAA were performed in 19 cases with polycythemia including polycythemia rubra vera and in 11 cases with secondary polycythemia due to pulmonary diseases. Tl-201 lung uptake, right ventricular visualization and pulmonary perfusion impairment were studied. In the 19 cases, Tl-201 lung uptake was observed in all cases and 54.5% of them showed moderate lung uptake. The grade of right ventricular visualization was moderate in one case and slight in 16 cases; right ventricular hypertrophy was shown in 89.5% of all cases by Tl-201 scintigraphy, only one of which showed right ventricular hypertrophy on electrocardiography. Abnormalities of lung perfusion consisted of scattered small areas of hypoperfusion in 36.8%, peripheral hypoperfusion in 78.9% and uneven distribution of pulmonary perfusion in 94.7%. The degree of hypoperfusion was slightly related to decrease in FEV1.0%, V25 and PaO2 and increase in circulating blood volume and peripheral red blood cell counts. Abnormalities of pulmonary function consisted of increased RV/TLC in 50.0%, increased CV/VC in 35.7% and decreased V25 in 36.8%. Arterial blood gases showed hypoxemia in 57.1%, the degree of which was slightly related to increase in RV/TLC and CV/VC and decrease in V25. Cases of secondary polycythemia due to pulmonary diseases showed more marked right ventricular visualization, pulmonary perfusion impairment and abnormalities of various kinds of pulmonary function than polycythemia rubra vera cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The role of nitric oxide, endothelin, and prostaglandins in the transition of the pulmonary circulation.

This review emphasizes the importance of three endothelial-derived products in regulating fetal and transitional pulmonary vascular tone. Although the pathophysiologic events that culminate in PPHN are poorly understood, it is likely that endothelial cell dysfunction, with an alteration in the normal "balance" of endothelial-derived mediators, is a contributing factor. In addition to the three vasoactive mediators described herein, several other neurohumoral agents influence fetal and transitional pulmonary vascular tone. In addition, structural changes in the pulmonary circulation, with abnormal proliferation of smooth muscle and extracellular matrix components, also contribute to failure of normal postnatal adaptation. Continued research is necessary to better define the complex interactions that result in the normal transition from the fetal to the postnatal state. Continued advances in the understanding of the normal transition will allow a more rational approach to management of the failed transition reflected in the disease state, PPHN.

Endothelins↗
PubMed1982

Evidence for a theory of physical fragmentation of megakaryocytes, implying that all platelets are produced in the pulmonary circulation.

The mathematical description of a fragmentation mechanism which leads to log normal volume distribution is applied to platelet production from megakaryocyte cytoplasm. Large cytoplasmic fragments and whole megakaryocytes are released from the bone marrow into the circulation. Physical fragmentation of the cytoplasm occurs in the pulmonary circulation producing the observed heterogeneity of platelet volume. Experimental evidence is used to provide quantitative verification that physical fragmentation is the process which produces all platelets. With this theory the currently accepted concept of the predesignation of the platelet population by the demarcation membrane system in megakaryocyte cytoplasm becomes redundant.

Animals↗
PubMed1995

[Acute effects of platelet activating factor on the pulmonary circulation in rats].

To investigate the acute effects of platelet activating factor (PAF) on pulmonary circulation and cardiovascular function in rats, twenty anesthetized Wistar rats were given 100-800 ng/kg PAF by bolus intrapulmonary artery infusion. Mean pulmonary artery pressure (mPAP), mean systemic artery pressure (mSAP) and cardiac output (CO) were measured before and after administration. The results showed that PAF infusion caused: a rise in mPAP from 2.11 +/- 0.20 kPa to 2.65 +/- 0.11 kPa (100 ng/kg, P > 0.05), from 2.32 +/- 0.25 kPa to 2.85 +/- 0.24 kPa (200 ng/kg, P < 0.05) and from 2.11 +/- 0.33 kPa to 3.01 +/- 0.45 kPa (400 ng/kg, P < 0.05)p; a down in mSAP from 16.0 +/- 2.11 kPa to 9.1 +/- 2.39 kPa (100 ng/kg, P < 0.05); from 16.3 +/- 1.38 kPa to 7.0 +/- 0.57 kPa (200 ng/kg, P < 0.05) and from 16.4 +/- 2.56 kPa to 6.3 +/- 0.89 kPa (400 ng/kg, P < 0.05); and a down in CO from 48.1 +/- 2.16 ml/min to 30.8 +/- 3.27 ml/min (100 ng/kg, P < 0.05), from 47.8 +/- 2.12 ml/min to 25.6 +/- 2.86 ml/min (200 ng/kg, P < 0.05) and from 48.3 +/- 2.24 ml/min to 20.0 +/- 2.39 ml/min (400 ng/kg, P < 0.05). These findings suggested that PAF play an important role in the pathophysiologic course of pulmonary hypertension.

Animals↗
PubMed1989

Fate of air emboli in the pulmonary circulation.

The lung serves an important nonrespiratory function by trapping and excreting venous air emboli. The site of trapping and the mechanism of excretion, however, are uncertain. To observe the behavior of bubbles in the pulmonary circulation, we injected venous air emboli into anesthetized dogs and videotaped their elimination from the pulmonary microcirculation by using in vivo microscopy. Small intravenous bubbles lodged exclusively in pulmonary arterioles and were eliminated from that site. To determine whether the gas was dissolving into nearby blood and then was carried to the capillaries for excretion, the rate of bubble radius change was measured during nonperfused conditions produced by balloon occlusion of lobar blood flow and compared with perfused conditions. Bubble volume decreased at the same rate during perfused and nonperfused conditions and thus was independent of regional blood flow. Molecular diffusion of gas directly across the arteriolar wall into alveolar spaces was the most likely mechanism of elimination because calculations based on the Fick equation for molecular diffusion predict an elimination rate nearly identical with those observed experimentally.

Animals↗