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Chronic obstructive pulmonary disease (COPD) is characterized by lower alveolar oxygen content and hypoxia. Hypoxia itself is able to evoke a vascular reflex in a pulmonary vasoconstriction, the explanation of which is, in part, unknown. Pulmonary vasoconstriction leads to different degrees of pulmonary artery pressure (PAP) increase which statistically suggests that the higher the PAP, the poorer the survival rate. Many substances are involved in the vascular homeostasis. An important role is played by cyclooxygenase as well as lipoxygenase pathways metabolites, the antagonists of which have been extensively used in the treatment of pulmonary hypertension in subjects suffering from COPD. An even more important role is played by the endothelium. It is able to modify its metabolism towards the production of substances (e.g., endothelin, EDRF, etc.) which are able to negatively influence the vascular tone. Complete identification of such substances, when possible, would allow us to have a better understanding of the complexity of the mechanism which controls the pulmonary vascular district. In this direction we could hopefully look forward to the detection of specific new drugs able to improve the management of the disease by preventing it from worsening to that extent which statistically and drastically correlates with the worst prognosis.

The analysis of correlations between the time and speed parameters found out that in healthy subjects and patients with chronic nonspecific bronchitis (CNB) the blood flow in great hepatic vessels is provided by the amount of blood entering the aorta in the systole. When central hemodynamics is affected in the CNB exacerbation, this factor becomes essential also for the arterial inflow into middle-size and small branches of the hepatic artery. Persistent bronchial obstruction and labile pulmonary hypertension rise as a result of failure of adequate relations between systemic, pulmonary and hepatic hemodynamics. The condition of great arterial vessels of the liver gets dependent on lesser and greater circulation. The response of the middle-size and small branches of the hepatic artery in chronic obstructive bronchitis (functional class II) is independent of the vascular tone of the lesser and greater circulation. The conclusion is made that intrahepatic blood flow in patients with secondary pulmonary hypertension is regulated by vasoactive factors acting at the level of the organ (mainly kallikrein-kinin system and prostaglandins).

Altogether 96 normal women and 82 women with chronic nonobstructive bronchitis were examined during pregnancy using zonal rheography of the lungs. It was established that in pregnant women afflicted with chronic nonobstructive bronchitis, the regional ventilation and hemodynamics of the pulmonary circulation underwent rearrangement. It was discovered that in the second half of pregnancy there develop the signs of latent respiratory insufficiency manifesting themselves in an increase of the rheographic parameters of the ventilation perfusion relations. The regression equation is offered to calculate the proper values of the ventilation/blood flow ratio depending on the time of pregnancy.

Transbronchial regional electroplethysmography was employed to measure the blood flow and air content in 67 children aged 3-15 years. Of these, 44 children suffered from chronic bronchitis and 23 from bronchiectasis. Children with recurrent bronchitis examined during the inactive phase of the disease marked by clinicoendoscopic silence were used as controls. In children with chronic bronchitis who escaped bronchial deformity, the levels of the regional blood flow were similar to those seen in the controls. Meanwhile in diffuse deforming bronchitis the reduction of the blood flow was noted in the posterobasal segments on both sides. In local deformities and bronchiectasis the levels of the air content and blood flow were decreased in the affected area whereas in the adjacent part the blood flow was more intense as compared with the symmetrical part on the opposite side, which was likely to be connected with the irritative effect of the focus of lesion.

In the present era of direct monitoring of pressure in patients with chronic obstructive pulmonary disease (COPD), an appreciation of all factors that may influence the observed pulmonary vascular pressures is essential. Our study examines the impact of respiratory variations in intrathoracic pressure on the recorded pulmonary vascular pressures in 28 patients with COPD. Althouth pulmonary hypertension was present in only nine subjects at rest, all had an abnormal increase in the mean pulmonary arterial pressure during supine exercise. In 15 subjects, this abnormal response was, in part, related to an increase in pulmonary arterial wedge pressure to 15 mm Hg or more. The increase in pulmonary arterial wedge pressure was directly related to the amplitude of the peak-to-peak respiratory variation of such wedge pressure. This variation correlated with the specific airway resistance but was not related to the arterial oxygen pressure or pulmonary vascular resistance. These findings indicate the important influence of exaggerated respiratory effort on the measurement of pulmonary arterial wedge pressure and mean pulmonary arterial pressure in patients with chronic obstructive pulmonary disease.

Pulmonary wedge angiograms were compared with haemodynamic measurements at rest and during light exercise in 47 patients with chronic bronchopulmonary disease. The patients were divided into two groups on the basis of the angiograms. In group I (26 patients) less than 50% of the angiograms were abnormal, whilst in group II (21 patients) more than 50% of angiograms were abnormal. Pulmonary artery pressure and pulmonary vascular resistance were lower in group I than in group II and these differences became more marked during exercise. The pulmonary wedge pressure increased significantly on exercise in group II. Similarly, driving pressure in relation to cardiac output increased more from rest to exercise in group II than in group I. We conclude that wedge angiograms are one way to estimate the reduction in the pulmonary vascular bed.

We have investigated the dependance of observed pulmonary artery mean pressure (PAP) on body surface, age, PaO2, pH, PaCO2, hematocrit, and spirometric data (VC, FEV1/VC, RV/TLC) in 70 patients with chronic obstructive lung disease (COLD). After elimination of all variables that failed to correlate with PAP, multifactorial analysis showed that only two of nine independent variables, namely PaO2 and body surface, correlated significantly with PAP. According to our calculations, 28.9% of total PAP is predictable by PaO2, 1.5% by H+ concentration, 2.8% by RV/TLC, and 2.5% by body surface. Fully 64.2% of total variability was not accounted for by our regression analysis; thus the error of predicted PAP was so great (+/- 17 mm Hg for P = 0.05) as to invalidate the method. We also recalculated our subjects' PAP values by applying Enson's and Grassi's equations to our own lung function and biochemical data, and compared the predicted PAP values thus obtained with those measured directly in our subjects. Both equations proved imprecise and/or inaccurate in the individual case. From this we conclude that whereas available equations may be suitable for predicting the mean PAP value of a large population sample, the same equations cannot give a reliable prediction in individual cases.

Hypoxic pulmonary vasoconstriction is considered as one of the factors leading to pulmonary hypertension in patients with chronic bronchitis, but the magnitude and the variability of the pulmonary vascular response to hypoxia in these patients have not been well established. We investigated the pulmonary hemodynamic changes induced by breathing two hypoxic mixtures (FIO2 = 0.15 and 0.13) in 26 patients with chronic bronchitis with airway obstruction (FEV1/VC = 49 +/- 14 percent). Results show that there is a wide variability of the pulmonary vascular response to acute hypoxia in chronic bronchitis patients, but it is not possible to say whether such differences play a role in the natural history of the disease.

Thirty-three patients with infectious allergic bronchial asthma and chronic obstructive bronchitis and 47 normal subjects were examined with the aid of a complex of bloodless research methods for the pulmonary circulation and central hemodynamics under graded physical exercise of minor power. Investigation at rest did not disclose any hemodynamic disorders in the greater and pulmonary circulation. Application of bicycle ergometry to patients with chronic obstructive bronchitis and bronchial asthma in a stage of remission made it possible to reveal latent hemodynamic disorders of the pulmonary circulation that manifested by long-term elevation of the pressure in the pulmonary artery and pulmonary vascular resistance, restitution of the central hemodynamics according to the hyperkinetic type. The use of the generally accepted formulas for calculating the proper magnitudes of the ejection period and mechanical systole with the heart rate exceeding 90 per minute resulted in overdiagnosis of the overload of the right ventricle. The authors offer the regression equations for calculating these parameters during tachycardia.

In 22 chronic bronchitics with or without emphysema, the authors measured regional pulmonary perfusion in the supine position and calculated the ratios of radio-active tracer (131I-MAA) concentrations in the lung apices and bases (U/L ratio). This ratio was found to be normal in the right lung and tendentially high (though not to a statistically significant degree) in the left lung, this being probably due to the presence of an enlarged heart (13 patients showed evidence of right ventricle hypertrophy and/or overload). The correlation between the U/L ratio and functional impairment of respiration expressed spirometrically failed to reach statistical significance and the same was true of the correlation between the U/L ratio and mean pulmonary arterial pressure at rest.

Catheterization of the pulmonary artery and radiocirculography were used in 30 patients with chronic bronchitis (CB) in order to study changes in hemodynamics induced by intravenous injections of 5 and 10 mg verapamil or by 4-5 weeks of the treatment with finoptin and corinfar. Out of 47 studies, 22 (47%) showed a positive effect which was primarily recorded in patients (72%) suffering from apparent pulmonary hypertension (PH). The effect manifested itself in the form of a decrease in the total pulmonary resistance and/or in the mean pulmonary arterial pressure. In 13 cases (27%), the effect turned out negative. Meanwhile 12 cases (26%) demonstrated no effect at all. A beneficial effect was mostly recorded after administering 5 mg verapamil, whereas administration of 10 mg verapamil and prolonged use of finoptin and corinfar produced varied actions, with the negative effect being observed even more frequently as compared to the positive one. The pattern of the pulmonary hemodynamic response to a single intravenous injection of verapamil was also preserved in 60% of cases undergoing continuous treatment with finoptin and corinfar. Calcium antagonists can be used for the treatment of PH in patients suffering from CB. At the same time it is required that all the patients may be necessarily examined for hemodynamics.

Hemodynamic values obtained during right heart catheterization in about 35 patients with chronic bronchitis were compared with the same variables 3.3 years later (range, 2 to 5 years). In the group of 13 patients with mean pulmonary arterial pressure less than 20 mm Hg at the first catheterization, the average value was 15.8 mm Hg at rest and 25.2 mm Hg during moderate exercise at the first investigation, and 16.9 and 26.3 mm Hg, respectively at the second catherization; the changes were not significant. In the group of pulmonary hypertensive patients, the mean pulmonary arterial pressure was 27.0 mm Hg at rest and 44.1 mm Hg during moderate exercise at the first catheterization, and 26.8 and 38.9 mm Hg, respectively, at the second catheterization. Thus, even in this group, there was no deterioration in pulmonary hemodynamics, because there was no significant change in right or left filling pressure, or in cardiac output. There was, however, a marked decrease in systemic arterial pressure, which was significant in the group with pulmonary hypertension. This decrease in left ventricular afterload could be partly responsible for the stabilization of pulmonary hemodynamics, and it could be due to the peripheral vasodilating effect of hypoxia and hypercapnia.

In order to study the relations between maximal oxygen consumption during exercise (VO2max) and the pulmonary circulation when pulmonary artery pressure (PPA) and pulmonary vascular resistance (PVR) are normal or close to normal, we evaluated twenty-three patients with chronic bronchitis, in stable clinical condition. All these patients performed a progressive exercise test on a bicycle ergometer until exhaustion (VO2max); they were also subjected to right heart catheterization at rest and during light exercise at constant load. In these patients with moderate functional impairment, we observed on average a significant, although weak, correlation (r = -0.52, P less than 0.01) between pulmonary vascular resistance at rest and VO2max. When VO2max exceeded 2 1 min-1, PVR was below 210 dyn s cm-5. From the heart rate during maximal exercise we computed the oxygen pulse (O2Pmax). In eight patients O2Pmax was reduced (less than or equal to 11 ml) with maximal heart rate close to its predicted value; in seven of these subjects PVR was abnormal and Ppa at rest was at least 20 mmHg. Thus it seems that in chronic obstructive bronchitis mild disturbances in pulmonary circulation may be a contributory factor in the limitation of exercise performance, and a maximal exercise test may help to detect pulmonary hypertension in these patients.

The pressure/flow relationship in the pulmonary circulation has been studied in 43 patients with chronic bronchitis, at rest (R) and during exercise at two levels: 30 or 40 W (E1), and 60 or 80 W (E2), without interruption. For the entire group, pulmonary vascular resistance was 142 +/- 70 dyn X s X cm-5 at rest, 131 +/- 55 at the first exercise level and 118 +/- 60 at the second level. Individual changes were variable, however; a "linearity index" was computed as delta(PPA-PW)/delta Q from the first to the second exercise level divided by the same value from rest to the first exercise level. This index was below 0.75 in 27 patients (i.e. the pressure/flow slope was lower for the second exercise level and the pressure/flow curve was concave to the flow axis), it was above 1.25 in nine patients (i.e. the slope increased with exercise and the pressure/flow curve was convex to the flow axis), and the pressure/flow relationship was close to rectilinear in seven patients. Functional disturbances were mild in these subjects, and in the majority of them pulmonary vascular resistance did not increase with exercise.