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PubMed1977

Development of the pulmonary circulation in ventricular septal defect: a quantitative structural study.

The application of quantitative morphometric techniques to evaluation of the lungs of nine children who died with a ventricular septal defect between the ages of 3 months and 4 years showed that the presence of pulmonary hypertension interferes with the growth and development of the pulmonary circulation. In all cases the preacinar arteries were of normal size and not dilated, and arterial size and number within the acinus were reduced and similar to those seen in the normal child at birth. Arterial and venous muscularity was increased as judged by an increase in wall thickness and by the presence of muscle in smaller and more peripheral arteries than is normal. Elevation of resistance was associated with failure of the intraacinar pulmonary circulation to develop normally rather than to obliterative pulmonary vascular disease. In view of the rapidity with which impairment of growth and elevation of resistance can develop, closure of a large defect is recommended before age 2 years.

Child↗
PubMed1975

[Contractility of the right ventricle and pulmonary circulation pressure in young sportsmen].

The paper presents some data on the structure of the systole of the right ventricle obtained by means of kinetocardiography in 280 sportsmen, aged 12-14 years, with different functional states of their organisms (non-trained, poorly and well-trained, with chronic overstraining of the heart), as well as some data on the level of the systolic pressure in the pulmonary circulation system (by the Buzstin method) at rest and during the restorative period after exercises (test of the Leningrad Institute of Physical Culture, bycycle tests). The more the organism is trained, the more distinct the stages ofthe syndrome of regulated myocardial hypodynamia were found to be, a moderate hyperfunctionof the heart is noted during physical exercises that is accompanied by slight elevations of the pressure in the pulmonary system. In cases of chronic cardiac overstraining myocardial hypodynamia, stage I--II, was found, pressure elevation in the pulmonary circulation system -- in 21.4% of the examined persons at rest, its sharp elevation after exercises (up to 78.6 mm Hg) and prolongation of the restorative period. The obtained data demonstrate the perfection of the function of the right ventricle and of the pulmonary circulation under systematic training in the adolescents, and their deterioration in cases of chronic overstraining of the heart.

Adolescent↗
PubMed2002

Dynamic time-resolved contrast-enhanced two-dimensional MR projection angiography of the pulmonary circulation: standard technique and clinical applications.

OBJECTIVE: Time-resolved pulmonary two-dimensional MR projection angiography is a fast acquisition technique that allows the generation of dynamic projection angiograms by a method similar to that used to generate digital subtraction angiograms. MR images are obtained after subtracting the mask defined at the beginning of the sequence from later images, thus generating time-resolved continuous projection angiograms that depict the passage of a bolus through the pulmonary circulation. This article describes the application of this novel technique in three patients with pathologic conditions not previously described with this modality and two control subjects. CONCLUSION: The analysis of the findings on dynamic time-resolved contrast-enhanced two-dimensional MR projection angiography shows that this technique is useful not only in revealing morphologic changes associated with pulmonary disorders but also in following the passage of the bolus through the cardiopulmonary circulation. The latter capability allows qualitative detection of normal or abnormal pathways and thus is potentially of value in the assessment of several pulmonary disorders.

Adolescent↗
PubMed1975

Effect of pulmonary circulation on coronary flow and ventricular performance of isolated heart.

Left ventricular performance and coronary flow in isolated dog hearts were observed for to discuss whether lungs have any nonrespiratory function. The results of our experiments showed the fact that pulmonary circulation seemed to have some metabolic functions to prevent the increase in coronary flow and the decline in ventricular performance. And it was also suggested that isolated lungs removed a factor responsible for coronary vasodilation and the decline of ventricular performance. But it could not be fully negrected that the pulmonary circulation added a factor which prevents the increase in coronary flow.

Animals↗
PubMed1991

Plasma endothelin concentrations in patients with pulmonary hypertension associated with congenital heart defects. Evidence for increased production of endothelin in pulmonary circulation.

BACKGROUND: To elucidate the pathophysiological significance of endothelin in pulmonary hypertension associated with congenital heart defects, we measured plasma endothelin-like immunoreactivity (ET-LI) concentrations by using radioimmunoassay in 18 patients with pulmonary hypertension (PH group; age, 6 months to 12 years) in comparison with 27 patients without pulmonary hypertension (non-PH group; age, 6 months to 12 years). METHODS AND RESULTS: Blood samples were obtained from the vena cava, right atrium, right ventricle, left or right pulmonary artery, and pulmonary vein or the pulmonary arterial wedge position (pulmonary venous blood) during cardiac catheterization. Plasma ET-LI concentrations in the PH group were significantly higher than those in the non-PH group at all sampling sites. In the PH group, plasma ET-LI concentration showed a significant increase between the right ventricle and pulmonary artery and between the pulmonary artery and pulmonary vein. The increment of plasma ET-LI concentrations from the right ventricle to the pulmonary vein was significantly larger in the PH group than in the non-PH group and was significantly correlated with pulmonary artery pressure. CONCLUSIONS: Plasma ET-LI concentrations were elevated in patients with pulmonary hypertension; the elevation was due to the increased production of ET-LI in pulmonary circulation, indicating the possible involvement of endothelin in the pathophysiology of pulmonary hypertension.

Blood Pressure↗
PubMed1989

The effect of closing the ductus arteriosus on the pulmonary circulation of the fetal sheep.

In the mammalian fetus the ductus arteriosus allows right ventricular output to be shunted away from the lungs to the systemic circulation. This study was performed to determine how closing the ductus arteriosus of the fetal sheep would affect the pulmonary circulation. Under halothane anaesthesia 6 near-term fetal sheep were delivered with the umbilical circulation intact. Catheters were placed in the right atrium, the pulmonary artery, and the aorta. Pulmonary blood flow was measured by injecting radioactive microspheres into the right atrium while a reference sample was withdrawn from the pulmonary artery. Closing the ductus arteriosus increased pulmonary arterial pressure by 22% from 51 +/- 3 to 62 +/- 3 mmHg and increased pulmonary blood flow disproportionately by 198% from 232 +/- 74 to 692 +/- 80 ml/min per 100g. Thus, pulmonary vascular resistance decreased by 75% from 0.451 +/- 0.65 to 0.095 +/- 0.010 mmHg 100g min/ml. These findings extend the observation that pressure and flow in the pulmonary circulation of the air-breathing lung do not have a linear relationship passing through the origin to include a striking example in the fluid-filled lung of the intact fetus. They also raise questions about the nature of the elevated vascular resistance in the fetal lung.

Animals↗
PubMed1995

Adenosine-induced vasodilation: receptor characterization in pulmonary circulation.

Adenosine mediates vascular smooth muscle relaxation in the pulmonary circulation. The A2 receptor has been suggested to mediate adenosine-induced vasodilation (AIV). In this study, the effect(s) of selective adenosine agonist and antagonist on the hypoxic pressor response (HPR) was assessed in the isolated blood-perfused rat lung. Adenosine (0.075-7.5 mM) infusion (0.125 ml/min) into the pulmonary artery dose dependently attenuated the HPR. AIV was mimicked by 10 microM 5'-(N-ethylcarboxamido)adenosine (NECA), a nonselective adenosine agonist. Adenosine- and NECA-induced vasodilation were attenuated by 67 microM 8-(p-sulfophenyl)theophylline. In contrast, NECA-induced vasodilation was not attenuated by the A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (1 microM). At 10 microM, a minimal vasodilatory effect was seen with the nonselective adenosine agonists CV-1808 and N6-(2-phenylisopropyl)adenosine (R-PIA) compared with NECA. The highly selective A2a agonist 2-[p-(2-carboxyethyl)phenyl amino]-5'-N-ethyl carboxamido adenosine (CGS-21680C, 10 microM) and A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA, 10 microM) had no vasodilatory effect. Neither the K+ channel blockers tetraethylammonium chloride (10 mM) and glibenclamide (100 microM) nor the NO synthase inhibitor N omega-nitro-L-arginine methyl ester attenuated NECA-induced vasodilation. These findings suggest that AIV is mediated via the A2b receptor and that AIV occurs via an NO-independent mechanism.

Adenosine↗
PubMed1975

Effects of the 15-methyl analogs of prostaglandins E2 and F2alpha on the pulmonary circulation in the intact dog.

The effects of the 15-methul analogs of prostaglandins E2 (PGE2) and F2alpha (PGF2alpha) on the pulmonary circulation were studied in the intact dog under conditions of controlled blood flow. Infusions of either analog into the lobar artery increased lobar arterial pressure by more than 100 per cent. The rise in lobar arterial pressure was accompanied by a rise in lobar venous pressure and in pressure gradient from lobar artery to small vein but no change in pressure in the left atrium. The methyl analogs were about 10 times more potent than PGE2 and PGF2alpha in elevating pulmonary vascular resistance in the dog. The effects of the analogs on the pulmonary vascular bed were similar in experiments in which the lung was perfused with dextran or with blood. Both analogs contracted isolated helical segments of canine intrapulmonary artery and vein in a dose-related manner. In other experiments the effects of passive increases in venous pressure produced by distension of a balloon catheter in the lobar vein were contrasted with the action of the analogs on the pulmonary vascular bed. Balloon distension increased pressure in the lobar artery and small vein but had no effect on pressure in the left atrium. However, in contrast to the increase in gradient with the analogs, balloon distension decreased the pressure gradient from lobar artery to small vein. Results of the present study indicate that the prostaglandin analogs increase pulmonary vascular resistance by actively contricting pulmonary veins and vessels upstream to small veins, presumed to be small arteries. It is concluded that the analogs are potent pressor substances in the pulmonary circulation.

Animals↗
PubMed1987

Comparison of the alpha adrenoceptor activity of dopamine, ibopamine and epinine in the pulmonary circulation of the dog.

The ability of dopamine, ibopamine and epinine to elicit alpha adrenoceptor-mediated vasoconstriction was studied in the in situ, autoperfused pulmonary circulation of the open-chest anesthetized dog. Animals were pretreated with propranolol to eliminate beta adrenoceptor-mediated relaxation of the pulmonary vasculature. Heparinized blood was withdrawn from the left femoral artery and transferred via a peristaltic pump to the pulmonary arterial branch supplying the left diaphragmatic lobe of the lung. The flow rate of the pump was adjusted so that mean pulmonary perfusion pressure in the lobe was equal to resting diastolic pulmonary artery pressure (10 +/- 1 mm Hg). Under conditions of constant left atrial pressure and pulmonary blood flow, intralobar administration of dopamine, ibopamine and epinine elicited dose-dependent increases in perfusion pressure of the lobe, reflecting increases in pulmonary vascular resistance. Prazosin (100 micrograms/kg i.v.), a selective alpha-1 adrenoceptor antagonist, inhibited the pulmonary vasopressor responses to dopamine, ibopamine and epinine. Rauwolscine (100 micrograms/kg i.v.), a selective alpha-2 adrenoceptor antagonist, inhibited pulmonary pressor responses to dopamine and epinine without altering significantly the pulmonary vasoconstrictor response to ibopamine. These data indicate that dopamine and epinine stimulate both postjunctional vascular alpha-1 and alpha-2 adrenoceptors to elicit pulmonary vasoconstriction in the dog, whereas ibopamine, when injected directly into the pulmonary circulation, stimulates primarily postjunctional vascular alpha-1 adrenoceptors. However, when ibopamine was administered intraduodenally, both prazosin and rauwolscine were found to inhibit the resulting pulmonary vasopressor response. This finding is consistent with the hypothesis that ibopamine is converted to its active metabolite epinine, which stimulates both pulmonary vascular alpha-1 and alpha-2 adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Effects of acute incremental volume overload on cardiac chamber size, function, and the pulmonary circulation: analysis by digital intravenous angiography.

To assess the effects of acute incremental volume overload on cardiac size, function, and the pulmonary circulation, we studied six anesthetized dogs using intravenous digital angiography. Aortocaval (AC) fistulas were placed in four dogs, and fistulas in both a carotid and iliac artery were placed in two dogs. Data were obtained at four points: (1) control stage; (2) partial shunt (PS, where either AC partially open or iliac fistula was open and carotid fistula was closed); (3) full shunt (FS, AC shunt open or both iliac and carotid shunts open); and (4) control stage 2. Little change in heart rate (HR) or arterial pressure occurred. With FS, both mean pulmonary artery and wedge pressures increased (p less than 0.05); however, systemic and pulmonary vascular resistances declined. Cardiac output rose (1.54 +/- 0.42 L/min at control) to 2.44 +/- 0.84 L/min at PC (P less than 0.05 vs control) and to 3.13 +/- 0.89 L/min at full shunt (p less than 0.01 vs control). Both left (0.40 +/- 0.09 to 0.55 +/- 0.10 to 0.66 +/- 0.10, p less than 0.05 and p less than 0.01 vs control, respectively) and right (0.34 +/- 0.10 to 0.40 +/- 0.10 to 0.51 +/- 0.09, the latter p less than 0.01 vs control) ventricular ejection fractions rose, as did left (30.7 +/- 13 ml to 35.1 +/- 13 ml to 37.8 +/- 13 ml, the latter p less than 0.05 vs control) and right (37.4 +/- 6.1 ml to 44.2 +/- 16.6 ml to 51.4 +/- 17 ml, the latter p less than 0.01 vs control) ventricular end-diastolic volumes. Atrial volume (determined at ventricular end-systole) also increased (9.4 +/- 3.6 ml to 11 +/- 3.5 ml to 12.9 +/- 4.3 ml, the latter p less than 0.05 vs control). These increases in cardiac function and size occurred in association with a shortening of pulmonary transit time (5.4 +/- 0.8 to 3.5 +/- 0.7 seconds to 2.9 +/- 0.5 seconds, the latter two p less than 0.05 and p less than 0.01 vs control, respectively), with no significant change in pulmonary blood volume. We conclude that acute volume overload produces cardiac chamber dilatation, along with increases in systolic function. Both pulmonary and systemic vascular resistance declined, and the transit time in the pulmonary circulation shortened. Digital intravenous ventriculography is a useful technique for the analysis of the central circulation during acute hemodynamic manipulations.

Angiography↗
PubMed1984

Effects of dopamine on the pulmonary circulation of the dog.

The effects of dopamine infusion (10 and 20 micrograms kg-1 min-1) on pulmonary arterial pressure (PAP) and pulmonary arterial resistance (PAR) were studied. Experiments were carried out on 60 anesthetized dogs using two different models: model A, with mechanical perfusion of pulmonary circulation and constant left ventricular output, and model B, with physiologic pulmonary perfusion and non-fixed ventricular output. When pulmonary blood flow was constant, dopamine did not change PAP or PAR at either dose. When cardiac output (CO) was allowed to increase, PAP increased with dopamine at both doses, whereas PAR did not change with 20 micrograms kg-1 min-1 dopamine and was reduced by the 10 micrograms kg-1 min-1 dose. We conclude that the increase in PAP could not be explained solely by the rise in CO, but was probably related to an inhibitory effect of dopamine on pulmonary vascular accommodation and to increases in CO, especially when the drug was utilized at higher doses.

Animals↗
PubMed1982

[Morphometric characteristics of the blood vessels of the pulmonary circulation in the lung following unilateral pneumonectomy].

In 29 mongrel dogs with the body mass of 20-27 kg a left-sided pulmonectomy was performed. The right lung was examined 1, 3, 7, 15 days and 1, 2, 4, 6 months after the operation. Postmortem injection of its circulatory bed with roentgen-opaque dyes was performed, then total cleared preparations and histotopograms were made. Morphometrical analysis of branches running off the pulmonary arteries of the muscular type was carried out in the reconstructed vessels. The animals' hearts were subjected to certain macro-morphometrical methods of investigation. A complex analysis of the macro-microscopic and morphometrical investigation of the pulmonary circulation vessels revealed a definite tendency in the dynamics of the vascular changes. In large branches of the pulmonary artery belonging to the muscular-elastic and elastic types, a predominant dilatatory reaction was noted in the whole course of the experiment, while for the branches of the muscular type morphological signs of spasm were specific during the first 3 days after the operation. Only after 7-60 days dilatation in the branches of the muscular type was observed with a subsequent normalization of their tonus. In tributaries of the pulmonary veins and capillaries, the dilatatory reactions were revealed to predominate. An increased loading on the right cardiac parts could be considered as a mechanism ensuring a maximal effective functioning of the pulmonary circulation after a unilateral pulmonectomy.

Animals↗
PubMed1991

Behavior of the pulmonary circulation at rest and during exercise in miliary tuberculosis.

We studied the hemodynamic behavior of the pulmonary circulation at rest and during exercise in six patients with MTB. As a group, in contrast to advanced fibrocaseous tuberculosis, these patients exhibited normal pulmonary hemodynamics at rest and during exercise. Only minor abnormalities in pulmonary vascular resistance at exercise (increased PAd-PWP gradient) were noted in two of the patients. The increase in Rp during exercise does not appear to be related to acute hypoxic vasoconstruction but rather to functional changes (compliance or recruitment or both) of the pulmonary microvasculature. In the genesis of these functional changes, chronic alveolar hypoxia and the inflammatory-fibrotic process might be interacting.

Adult↗
PubMed2002

Transient increase in endothelin-1 levels in the pulmonary circulation during exercise while breathing of oxygen in patients with chronic obstructive pulmonary disease.

OBJECTIVE: The effects of endothelin-1 (ET-1) on pulmonary vascular tone depend on the complex interplay of ET-1-induced vasoconstriction and vasodilation due to the secondary generation of endothelium-derived vasorelaxants. Therefore, it is likely that the response to ET-1 varies, depending on whether it is applied to the luminal or adventitial side of pulmonary vessels. Therefore, this study was designed to determine the change in luminal ET-1 levels during exercise in patients with chronic obstructive pulmonary disease (COPD). METHODS: All subjects performed a constant-load exercise test for 5 minutes on the ergometer with right heart catheterization while breathing room air or oxygen. ET-1 levels at rest, just after exercise, and 1 hour after exercise were measured in the pulmonary capillary wedge region. PATIENTS: Thirty-six patients with COPD. RESULTS: While breathing room air, ET-1 levels did not significantly differ between at rest, just after exercise and 1 hour after exercise [at rest; 4.15 (0.43) pg/ml, just after exercise; 4.15 (0.44) pg/ml, 1 hour after exercise; 4.13 (0.42) pg/ml]. In contrast, while breathing oxygen, ET-1 levels were significantly higher just after exercise [4.41 (0.43) pg/ml] than at rest [3.90 (0.37) pg/ml, p=0.0116] and 1 hour after exercise [3.93 (0.38) pg/ml, p=0.0246]. The change in ET-1 levels between before and just after exercise (delta ET-1) was negatively correlated with change in mPAP (delta mPAP) (r=-0.638, p=0.0001). However, delta ET-1 was not significantly correlated with any FEV1 (% predicted), DLCO, PaO2, or baseline pulmonary hemodynamics. CONCLUSION: The impairment of ET-1 release into the luminal side was observed in patients with COPD during exercise while breathing room air. However, oxygen supplementation reversed the capacity of ET-1 release, and delta ET-1 with exercise was negatively correlated with delta mPAP.

Aged↗