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[Behavior of pressure and flow parameters of pulmonary circulation in bronchologic studies in general anesthesia using 2 injectable anesthetics].

Flow- and pressure-parameters of the pulmonary circulation were measured in the course of bronchologic investigations under general anaesthesia using as narcotics in group I (n = 14) Hexobarbital, in group II (n = 10) Propanidid (Sombrevin). The increase of mean pulmonary artery and mean PCW-pressure in group II is significantly higher than in group I. This seems to be caused by a more reduced myocardial function due to Sombrevin. Heart rate and pulmonary vascular resistance increase in both groups uniformly. The pO2 is markedly reduced up to 4 hours after the investigation accompanied by an increase of pCO2.

Adult↗

Pregnancy in cardiac patients: possible influence of volume overload by pregnancy on pulmonary circulation.

To evaluate the influence of volume overload by pregnancy on heart diseases, the relations between cardiac status before pregnancy and clinical courses during pregnancy were studied, especially from the viewpoint of pulmonary circulation. In 206 pregnant cardiac patients whose prepregnancy laboratory data were known, the deterioration (appearance or advance of heart failure) during pregnancy was prospectively related to: pulmonary congestion (p less than 0.05), enlarged left atrium (p less than 0.05), atrial fibrillation (p less than 0.01) and right ventricular hypertrophy (p less than 0.005) in mitral stenosis; cardiomegaly (p less than 0.05) and atrial fibrillation (p less than 0.005) in mitral regurgitation; cardiomegaly (p less than 0.005) in congenital heart diseases; and to previous congestive heart failure (p less than 0.005) in total cases. All of the cases with systolic pulmonary artery pressure higher than 50 mmHg deteriorated during pregnancy. Some cases with no deteriorating laboratory findings showed dyspnea suddenly at the end of pregnancy. In 1033 cardiac patients who had experienced pregnancy, deterioration during pregnancy was seen more frequently in cases with mitral valvular diseases that in those with aortic valvular diseases. No deterioration was seen in pulmonary stenosis patients. Abnormal status of pulmonary circulation may be one of the important determining factors of deterioration by pregnancy in cardiac patients. The criteria for permitting pregnancy in cardiac patients are proposed.

Adult↗

[Assessment of the state of pulmonary circulation in infants of the 1st year of life with complete transposition of great vessels and ventricular septal defects].

The condition of pulmonary circulation in children of the first year of life with complete transposition of the great vessels (CTGV) and interventricular septal defect (IVSD) was evaluated by comparing the complex of hemodynamic and angiometric values obtained in catheterization of the heart cavities and angiocardiography. All patients were divided into two hemodynamic groups according to the blood flow in the lungs: group 1 - with the ratio of pulmonary to systemic circulation (PC/SC) greater than 1; group 2 - with the PC/SC ratio less than 1. In group 1 patients the ratio of effective pulmonary circulation (EC) to PC is always less than the ratio of EC to SC both in normal and in increased total pulmonary resistance (TPR); in group 2 patients, in contrast, EC/PC greater than EC/SC when TPR is above 10 mu/m2. The evaluation of the degree of pulmonary hypertension in infants with CTGV and IVSD should therefore be based not only on the absolute values of PC, EC, and TPR but also on such differential-diagnostic signs as the PC/SC, EC/SC, and EC/PC ratios.

Age Factors↗

[Hemodynamics of pulmonary circulation in patients with hypertension complicated by chronic ischemic heart disease].

Pulmonary circulation hemodynamics were studied in 175 patients with essential hypertension (EH), coronary disease (CD), atherosclerotic and post-infarction cardiosclerosis and combinations thereof. Pulmonary hemodynamic disorders were found both in cases of EH and CD, being more pronounced in EH patients. When the two diseases are combined, changes reflecting the state of pulmonary hemodynamics are more marked than those occurring in patients with EH or CD alone. When combined, EH and CD mutually aggravate each other's clinical course and symptomatology.

Chronic Disease↗

[Role of endothelin-B receptors in the pulmonary circulation].

Endothelin-1 (ET-1) is a potent vasoactive peptide and is thought to play an important role in the regulation of vascular tone. ET-1 can both constrict blood vessels, via endothelin-A (ET-A) receptors in vascular smooth muscle cells, and dilate then via endothelin-B (ET-B) receptors in endothelial cells in the systemic circulation. To determine the role of ET-B receptors in the pulmonary circulation, we examined the hemodynamic effects of a selective ET-B receptor agonist (IRL 1620) in rats. In rat lungs perfused with a salt solution, IRL 1620 caused pulmonary vasoconstriction in a dose-dependent manner. In lungs perfused with a hypoxic half-blood solution (10% O2), doses of IRL 1620 less than 10 nM caused pulmonary vasodilation, but higher doses caused pulmonary vasoconstriction. IRL 1620 caused transient vasodilation of the systemic circulation at every dose used (0.1, 1, and 5 nmol/kg) in anesthetized rats. In contrast, the effects of IRL 1620 on the pulmonary circulation varied with the dose. Small doses (0.1 or 1 nmol/kg) caused pulmonary vasodilation, but a higher dose (5 nmol/kg) caused pulmonary vasoconstriction. These results show tachyphylaxis in the pulmonary vasodilator response to IRL 1620, but not in the systemic vasodilator response. The present data show the dual action (vasoconstriction and vasodilation) of ET-B receptors.

Animals↗

Characterization and distribution of endothelin receptors in the pulmonary circulation: investigation of isolated, perfused, and ventilated rabbit lungs.

The aim of the study was to investigate the distribution of 2 subtypes of endothelin-receptors, mediating the effects of endothelin-1 (ET-1) in the pulmonary circulation. Until now, it is still unclear, whether ET(A) receptors or ET(B) receptors or even both are localized in pulmonary vessels. The experiments were performed on 72 isolated and ventilated rabbit lungs that were perfused with a cell- and plasma-free buffer solution. The arterial pressure and the lung weight gain were continuously registered. Intermittently perfusate samples were taken for determination of thromboxane A2 (TXA2) and prostacyclin (PGI2). The injection of ET-1 (10(-8) M, n = 6) resulted in a biphasic increase in pulmonary arterial pressure (PAP) that was accompanied by the generation of TXA2 and PGI2. Pretreatment with the ET(A)-receptor antagonist LU135252 (10(-6) M, n = 6) suppressed the pressure response after ET-1 application (P < 0.01 at 120 min) and reduced the generation of TXA2 (P < 0.05 at 120 min) and PGI2 (P < 0.05 at 120 min). Pretreatment with the cyclooxygenase inhibitor diclofenac (10 microg/mL; n = 6) also reduced the PAP increase after ET-1 injection. In contrast to this, the pulmonary vascular pressure reaction after ET-1 application was elevated, when ET(B)-receptor antagonist BQ788 (10(-6) M; n = 6) was given. Furthermore, the PGI2 to TXA2 ratio was shifted from 2.3 to 0.9, reflecting a predominance of vasoconstrictive TXA2. The simultaneous application of LU135252 and BQ788 significantly reduced the PAP increase after ET-1 application, but no beneficial effects were observed compared with the application of LU135252 solely. The injection of the ET(B)-receptor agonist sarafotoxin S6c (S6c; 10(-8) M, n = 6) also induced an increase in PAP that was not attenuated by pretreatment with the ET(B)-receptor antagonist BQ788 (10(-6) M, n = 6). LU135252 (n = 6) as well as the application of LU135252 in combination with BQ788 (n = 6) failed to suppress the pressure response after S6c, whereas the cyclooxygenase inhibitor diclofenac (10 microg/mL, n = 6) alone and in combination with LU135252 and BQ788 (n = 6) was able to prevent the PAP increase after S6c injection (P < 0.001). The results demonstrate that the ET-1-induced increase in pulmonary vascular resistance is mainly mediated via ET(A) receptors, whereas ET(B) receptors seem to mediate vasodilation, which was shown by an imbalance of TXA2 and PGI2 generation. On the other hand, the ET(B)-receptor agonist S6c induced vasoconstriction, which was only attenuated by the cyclooxygenase inhibitor diclofenac. From the current results we conclude that, apart from vasoconstrictor ET(A) receptors, at least 2 ET(B)-receptor subtypes are expressed in the pulmonary circulation, one mediating vasoconstriction, which was not blocked by BQ788, and one mediating vasodilation, which was influenced by BQ788.

Animals↗

Effect of intravenous terbutaline on arterial blood gas tensions, ventilation, and pulmonary circulation in patients with chronic bronchitis and cor pulmonale.

Terbutaline sulphate was given intravenously to 10 patients with pulmonary vascular disease secondary to chronic hypoxia. The resting cardiac index increased after terbutaline in all the patients between 5 and 74% above the control level. The greatest change was seen in patients who had received the largest total dose. The rise in cardiac index was associated with a fall in pulmonary vascular resistance although mean pulmonary artery pressure remained unaltered. There was a significant increase in the venous admixture but this did not adversely affect the arterial oxygen tension. The peak expiratory flow rate did not change significantly but there was an increase in ventilation from a mean value of 4.36 1/min/m2 to 4.67 1/min/m2. The results show that terbutaline has little adverse effect on the pulmonary circulation or gas exchange in patients with irreversible airways disease who are in a stable state.

Aged↗

Pulmonary circulation and systemic circulation: similar problems, different solutions.

Both the systemic and the pulmonary circulations respond to local hypoxia in the appropriate manner, the former by vasodilating, thereby providing more oxygen, and the latter by constricting and rerouting blood flow to areas where more O2 is available. In either case, changes in local conductance affect total conductance, and through that variable, the perfusing pressure; as a result, the effects of local vasomotion should be reduced. In the systemic circulation, arterial pressure can be prevented from falling by two important mechanisms: vasoconstriction of other vascular beds, and an increase in cardiac output. There are no similar means for protecting pulmonary arterial pressure against a rise when vessels in hypoxic areas contract; the only defense is provided by passive expansion of the vascular bed. Thus, in the lung regional circulatory readjustments conflict with the need to maintain a reasonably low pulmonary arterial pressure and local regulation (and maintenance of arterial oxygenation) may be subordinate to prevention of pulmonary hypertension.

Animals↗

[Bloodless evaluation of the degree of disorders of pulmonary circulation in patients with acquired heart defects].

A multistage treadmill test was conducted by the authors' program in 75 patients with mitral and aortic valvular disease and in 25 healthy individuals with noninvasive evaluation of the anaerobic threshold (AT) and the pumping function of the heart according to the dynamics of the oxygen debt. During the treadmill test in patients with pulmonary hypertension and arterio-capillary type of stasis in pulmonary circulation the AT occurred before the pumping function of the heart became decompensated. The diagnostic sensitivity of the AT outstripping appearance to marked types of pulmonary circulation stasis was 48% and to pulmonary hypertension - 80%. It was found that the AT occurring in the treadmill test before disorders of heart pumping function is an unfavourable prognostic criterion for late-term (8-12 months) results of isolated mitral valve prosthetics.

Adolescent↗

The structure of the pulmonary circulation in tetralogy of Fallot with pulmonary atresia. A quantitative cineangiographic study.

UNLABELLED: Cineangiograms of 172 patients with tetralogy of Fallot and pulmonary atresia were qualitatively and quantitatively analyzed retrospectively. FINDINGS: Twenty-eight (16%) patients had congenital absence of the central and unbranched hilar portions of the left or right pulmonary artery or both, and thus had congenitally nonconfluent pulmonary arteries. Five additional patients (3%) with originally confluent pulmonary arteries had nonconfluent ones because of an end-to-end surgical shunt, as did seven others (4%) because of thrombosis of one pulmonary artery. Among the 132 patients with confluent right and left pulmonary arteries, 70 (53% of 132) had incomplete arborization (distribution) of one or both, as did 23 (82% of 28) of those with congenitally nonconfluent pulmonary arteries (P for difference = 0.005). Ten (36% of 28) of the latter group had fewer than 10 pulmonary vascular segments (normal is 20) in continuity with central pulmonary arteries, compared with four (3%) of the former group. The proximal left and right pulmonary arteries were small but variable in size in all groups (median value 1.05 McGoon ratio), but were largest in the patients with confluent pulmonary arteries. Seventy-nine (60% of 132) patients with confluent left and right pulmonary arteries had large aortopulmonary collateral arteries, as did 100% of those with congenitally nonconfluent pulmonary arteries (P less than 0.001). The number of large aortopulmonary collateral arteries correlated inversely with the completeness of arborization of the left and right pulmonary arteries (P less than 0.0001). Inferences: Most patients with tetralogy and pulmonary atresia have gross morphologic abnormalities in the pulmonary vasculature and differ quantitatively in this regard from those with tetralogy and pulmonary stenosis. The prevalences of the various types of these abnormalities are considerably interrelated.

Adolescent↗

Pulmonary circulation time: comparison of mean, median, peak, and onset (appearance) values using indocyanine green and first-transit radionuclide techniques.

To assess the difference between a variety of mathematical methods for assessing pulmonary transit time, we evaluated 11 acutely anesthetized and instrumented mongrel dogs at a control stage and then during infusions of isoproterenol or phenylephrine, or after the induction of ischemia. Green-dye optical density curves were obtained to evaluate a variety of pulmonary circulation times. Mean transit time, median time, peak time, and onset time all correlated well (r greater than or equal to 0.93), with the mean time being the longest, followed by the median time (4% less than the mean time, p less than 0.05), peak time (15% less than the mean time p less than 0.01), and onset or appearance time (49% less than the mean time, p less than 0.001). In the 34 available data points the mean time averaged 4.67 +/- 1.7 seconds, the median time averaged 4.47 +/- 1.74 seconds, the peak time averaged 3.98 +/- 1.7 seconds, and the onset time averaged 2.27 +/- 1.43 seconds. Similar results were obtained from the first-pass radionuclide angiograms from 17 adult male subjects. We conclude that median, peak, and onset times are reasonable though predictably shorter approximates of mean pulmonary transit time. They may be utilized during interventions (particularly when alternative counting methods are planned, as with radionuclide or possibly digital angiographic techniques) as guides to changes in the pulmonary circulation.

Animals↗