Showing papers on "Pulmonary artery published in 1982"

The renin-angiotensin-aldosterone system, antidiuretic hormone and sympathetic nerve activity in an experimental model of congestive heart failure in the dog

Abstract: 1. Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240-280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal. 2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a factor of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid. 3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values. 4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs. 5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems may be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone may cause hyponatraemia by water retention, representing a state of 'dilutional hypo-osmolality'.

Thrombosis as a complication of pulmonary-artery catheterization via the internal jugular vein: prospective evaluation by phlebography.

Abstract: SINCE its introduction in 1970,1 the flow-directed balloon-tipped (Swan–Ganz) catheter has gained clinical acceptance and increased usage for continuous monitoring of the hemodynamic status of severely ill patients. Among the complications occasionally reported with the use of this device, deep-vein thrombosis has been rare. Swan et al.1 have described a case in which a thrombus developed in the superior vena cava and enveloped the shaft of the catheter. In 1974, Foote et al.2 described nine patients in whom the catheter was implicated as the cause of pulmonary ischemic lesions; in two patients, these pulmonary lesions were probably due to emboli . . .

Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

Abstract: Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 microM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 +/- 0.09 ml/min per g (mean +/- SEM) during control conditions to 1.69 +/- 0.27 ml/min per g during moderate pulmonary artery occlusion (P less than 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-to-subepicardial blood flow ratio fell from 1.36 +/- 0.14 to 0.77 +/- 0.06 (P less than 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 +/- 0.18 (P less than 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 +/- 0.10 to 2.25 +/- 0.30; P less than 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted.

Myocardial infarction before age 36: Risk factor and arteriographic analysis

Abstract: One-hundred twenty consecutive patients who were 35 years of age or younger underwent coronary arteriography after clinical myocardial infarction. Ninety-two percent were men. Four distinct subgroups were identified: Ninety-four patients (78 percent) had significant coronary artery disease (greater than 50 percent diameter narrowing of at least one major coronary artery), 20 (17 percent) had normal coronary arteries, 5 (4 percent) had major coronary arterial anomalies and 1 patient had coronary arteritis. Of the patients with obstructive coronary disease, risk factors were smoking in 89 percent, positive family history of coronary artery disease in 48 percent, hypertension in 21 percent and a history of lipid abnormality in 20 percent. Risk factors were distinctly less frequent in the groups without coronary atherosclerosis. In the group with coronary artery disease, the prevalence rate of one, two and three vessel disease was 32, 26 and 42 percent, respectively. Coronary arterial anomalies included anomalous origin of the left coronary artery from the pulmonary artery (three patients) and single right and single left coronary artery (one patient each). It is concluded that myocardial infarction before age 36 is a disease of men who smoke and who often have a family history of premature coronary artery disease. Twenty-two percent of patients will have normal coronary arteries, coronary arterial anomalies or coronary vasculitis. Coronary arteriography should be considered for patients who sustain a myocardial infarction before age 36 for purposes of diagnosis, management and prognosis.

Pulse wave reflection: can it explain the differences between systemic and pulmonary pressure and flow waves? A study in dogs.

Abstract: We have studied the effect of changes in pulse wave reflection on the configurations of pressure and flow in systemic and pulmonary circulation. Electromagnetic flow transducers, atrial catheters, and pacing leads were implanted in 10 dogs. In four animals, the flow transducer was placed on the pulmonary artery, in another four on the ascending aorta, and in two additional dogs on both vessels. One week later, ascending aortic and/or pulmonary artery flow and pressure (catheter tip manometer) were measured under general anesthesia (Nembutal, 30 mg/kg, iv). When the pulmonary circulation was studied (six dogs), measurements were made before and during serotonin infusion (0.5-0.75 mg/min). When the systemic circulation was studied (six dogs), measurements were made before and during nitroprusside infusion (50-200 micrograms/min). To quantify the arterial load, we calculated pulmonary and systemic input impedances. To estimate the amount of reflection, we used a reflection index which we defined as the amplitude ratio of reflected and forward wave. Nitroprusside decreased total peripheral resistance, increased total arterial compliance, and decreased the reflection index; similarity between aortic pressure and flow wave shapes increased, and they looked more like their pulmonary counterparts. Serotonin increased pulmonary vascular resistance, decreased pulmonary arterial compliance, and increased the reflection index. Resemblance of pressure and flow waves decreased. The differences in wave shapes can thus be explained by the amount of reflection: the less reflection the more pressure and flow resemble each other.

Bilateral coronary artery--pulmonary artery fistulas. Report of five cases and review of the literature.

Abstract: Bilateral coronary artery-pulmonary artery fistulas fistulas that originate from both coronary arteries are an uncommon subgroup of coronary fistulas and may have a distinct embryologic origin. We present five original cases and review the nine previously reported cases of this anomaly.

Right and left ventricular oxygen metabolism in open-chest dogs.

Abstract: A comparison of blood flow and myocardial O2 consumption (MVO2) in the right and left ventricles was made in 21 open-chest dogs. Simultaneous measurements were made of left anterior descending (LAD) and right coronary arterial blood flow and of O2 saturation in the coronary sinus and in from one to four anterior cardiac veins. Blood flow was greater in the LAD than in the right coronary artery, 87 +/- 5 vs. 46 +/- 3 ml.min-1.100 g-1. Similarly, the O2 saturation was 51 +/- 3% in the anterior cardiac veins and 40 +/- 1% in the coronary sinus. In a subset of seven dogs, the O2 saturation in blood from anterior cardiac veins varied substantially from vein to vein. The mean MVO2 was greater for the left than for the right ventricle, 8.6 +/- 1.4 vs. 4.0 +/- 0.3 ml O2.min-1,100 g-1. Increases in LAD flow with no increase in O2 extraction accounted for enhanced MVO2 of the left ventricle due to pacing, isoproterenol, or methoxamine. In contrast, pacing, isoproterenol, or constriction of the pulmonary artery increased MVO2 of the right ventricle by both augmented O2 extraction and a rise in right coronary blood flow. We conclude that right coronary arterial blood flow is lower per 100 g tissue and is less dependent on MVO2 than is LAD blood flow. The heterogeneity of O2 saturation in anterior cardiac veins suggests that regional differences in MVO2 may exist.

Suprasternal cross-sectional echocardiography in assessment of patient ducts arteriosus.

Abstract: Ninety-four patients with patent ductus arteriosus, whose ages ranged from 28 weeks gestation to 8 years, were assessed by suprasternal cross-sectional echocardiography. A further group of 37 cases without a patent ductus arteriosus were assessed by the same technique. The appearances of the ductus via this approach varied according to the ventriculoarterial connections. Reliable assessment of patency was possibly in 87 cases. In seven cases where the ductal lumen was less than 2 mm in size, a false negative diagnosis was made. In the 37 patients without a patent ductus arteriosus, no false positive diagnoses were made. Suprasternal cross-sectional echocardiography enables a reliable assessment of ductal patency, provided the lumen falls within the range of lateral resolution of the equipment being used.

Treatment of hypertension with ketanserin, a new selective 5-HT2 receptor antagonist.

Abstract: The new selective 5-HT2 receptor blocking agent ketanserin was given in a dose of 10 mg intravenously to 12 patients with essential hypertension. It caused a distinct fall in supine systemic arterial, right atrial, pulmonary artery, and pulmonary capillary "wedge" pressures. Cardiac output, renal blood flow, and glomerular filtration rate showed no persistent changes. Thus 5-HT2 receptor blockade caused dilatation of both resistance and capacitance vessels and of the renal vascular bed. Heart rate and plasma concentrations of renin and noradrenaline rose after ketanserin. These data suggest that 5-HT may have a role in maintaining high blood pressure.

Can central venous blood replace mixed venous blood samples

Abstract: To estimate the value of central venous blood as representative of real changes in pulmonary shunt (Qsp/Qt), mixed venous oxygen saturation and arteriovenous oxygen content difference [C(a-v)O2] during active phases of adult intensive care therapy, 86 blood samples were withdrawn from 42 patients as quadruple simultaneous collections from systemic artery, pulmonary artery (PA), superior caval vein (CV) and right atrium (RA). We found a significant positive correlation of the measured variables and especially of the subsequent changes of these variables in individual patients between PA blood samples and both CV and RA blood samples (p less than 0.001). We, therefore, conclude that a central venous catheter can replace the PA catheter to collect blood representative of mixed venous blood samples for the above purposes. However, the exact numerical value of mixed venous blood samples can only be measured from blood collected from the PA itself.

Crotalaria-induced pulmonary hypertension. Uptake of 3H-thymidine by the cells of the pulmonary circulation and alveolar walls.

Abstract: Feeding with Crotalaria spectabilis seeds induces structural changes in the pulmonary arterial circulation characteristic of pulmonary hypertension: increased medial and adventitial thickness, the appearance of muscle in smaller arteries than normal, and reduction in the number of peripheral arteries. By autoradiographic techniques, after injection of 3H-thymidine into rats fed Crotalaria for 3, 7, 14, 21, 28, or 35 days, the contribution of hyperplasia to these changes has been assessed at two levels of the pulmonary artery--the hilum and the periphery. In the hilar pulmonary artery, a biphasic increase in labeling index (LI) is seen in each cell type. After 3 days of feeding, the medial smooth muscle cells show a slight but significant increase (1.5 times the control value), and, after 7 days, so do the adventitial fibroblasts (3 x) and the endothelial cells (EC) (2 x). After 14 days LI for all three cell types is again at control values, but after 21 days (wall thickness is no increased) each cell type shows at least a fivefold increase; by 35 days all are again near control levels. In the intra-acinar region, by 14 days, "newly" muscularized arteries are identified and increase in number and proportion up to 35 days; 3H-thymidine uptake is not evident in this cell type until 35 days have passed. The ECs of these arteries, however, show a striking increase in LI after 14 days as do those of the alveolar capillaries. The ECs of the intra-acinar veins show a biphasic response being increased after 7, 28, and 35 days. The present study has shown that Crotalaria ingestion induces hyperplasia and hypertrophy of pulmonary arterial cells at pre- and intra-acinar levels. The early increase in LI probably represents a response to the original cell injury, the later changes, a response to continuing damage or, in part, adaptation to the pulmonary hypertension now present.

Vasodilators and Prostaglandin Inhibitors in Primary Pulmonary Hypertension

Abstract: Ten women with primary pulmonary hypertension had resting hemodynamic measurements taken before and after the nonparenteral administration of various vasodilators and prostaglandin inhibitors. Only sublingual isoproterenol, alone or combined with sublingual isosorbide dinitrate, effected a substantial (greater than 20%) drop in pulmonary vascular resistance; this decrease was accompanied by little change in pulmonary artery pressure. Isosorbide dinitrate was the only drug that elicited any reduction in pulmonary artery pressure; pulmonary vascular resistance decreased modestly. The oral administration of diazoxide, hydralazine, phentolamine, and tolazoline elicited little change in pulmonary artery pressure or resistance. Except for tolazoline, all these agents significantly decreased systemic blood pressure and resistance. Prostaglandin inhibition by indomethacin (acute and chronic dosing) increased pulmonary and systemic vascular resistances and reduced cardiac output. Aspirin combined with dipyridamole elicited no changes. The vasodilators and prostaglandin inhibitors studied evoked little improvement in resting pulmonary hemodynamic abnormalities in primary pulmonary hypertension.

Concealed left atrial membrane: pitfalls in the diagnosis of cor triatriatum and supravalve mitral ring

Abstract: Cor triatriatum and supravalve mitral ring are forms of congenital left ventricular inflow obstruction produced by membranes within the left atrium. Typically, these defects occur as isolated anomalies with manifestations of pulmonary venous obstruction. Four children are presented whose left atrial membrane was associated with other significant cardiac defects, including, in one patient each, simple coarctation of the aorta, sinus venosus atrial septal defect, tricuspid atresia and complex coarctation of the aorta syndrome. The patient with the latter defect had undergone previous pulmonary arterial banding. None of these patients demonstrated significant pulmonary venous obstruction at cardiac catheterization. All patients had a normal value for either pulmonary arterial diastolic or pulmonary arterial wedge pressure. Three mechanisms explained the lack of pulmonary venous obstruction: (1) a large cross-sectional area of membrane openings, (2) an atrial septal defect that was confined to the pulmonary venous chamber and decompressed it by allowing blood to escape into the right atrium, and (3) decreased pulmonary blood flow. The diagnosis was facilitated by two dimensional echocardiography. Accurate diagnosis of left atrial membrane in the setting of other cardiac defects is of practical significance because pulmonary venous obstruction may occur after surgery for the associated defects.

Absent pulmonary artery. A hint to its embryogenesis.

Abstract: Cardiac catheterization was performed in nine patients with unilateral absence of a pulmonary artery. Aortography revealed a diverticulum of the innominate artery in five of six patients in whom the aortic arch and absent pulmonary artery were on opposite sides. It is suggested that the diverticulum indicates fetal systemic blood supply to the affected lung through the distal part of the sixth aortic arch, which--consisting of ductal tissue--obliterated after birth, leaving the diverticulum where the ductus joins the innominate artery.

Pharmacological responses of human and porcine lung parenchyma, bronchus and pulmonary artery.

Abstract: 1 Responses of preparations of human and porcine isolated bronchus and pulmonary artery to carbachol (CCh), methacholine, histamine, 5-hydroxytryptamine (5-HT), (-)-noradrenaline (NA), (-)adrenaline (Adr) and (+/-)-isoprenaline (Iso) were compared with responses to the same agonists in isolated lung parenchyma strips. 2 All preparations from both human and porcine lung contracted in response to histamine and all, except preparations of porcine pulmonary artery, contracted in response to CCh. Human and porcine pulmonary artery and parenchyma strip contracted in response to NA while bronchial preparations invariably relaxed. Iso caused relaxation of human and porcine bronchus and parenchyma strip. Although 5-HT was completely inactive in tissues isolated from pig lung, this amine was a powerful spasmogen in human pulmonary artery, relaxed human bronchus and caused variable responses in human parenchyma. 3 Results indicate that the pharmacological characteristics of human and porcine parenchyma strips may be explained in terms of responses of vascular or airways smooth muscle.

Two dimensional echocardiographic assessment of communications between ascending aorta and pulmonary trunk or individual pulmonary arteries.

Abstract: The value of two dimensional echocardiography in identifying communications between the ascending aorta and pulmonary trunk or individual pulmonary arteries was assessed in 24 children, all of whom had either angiocardiographic and surgical or angiocardiographic confirmation alone. Fourteen cases had truncus arteriosus, four aortopulmonary window, four anomalous origin of the left pulmonary artery from the ascending aorta, and two anomalous origin of the right pulmonary artery from the ascending aorta. It was possible to identify reliably each individual abnormality with a combination of suprasternal, precordial, and subcostal cuts. Problems only arose in differentiating truncus arteriosus from pulmonary atresia and ventricular septal defect when the main pulmonary artery and infundibular region of the right ventricle were extremely hypoplastic.

Haemodynamic and hormonal effects of captopril in primary pulmonary hypertension.

Abstract: The treatment of primary pulmonary hypertension is unsatisfactory. Since, in animals, experimental pulmonary vasoconstriction may be mediated in part by angiotensin II, we treated five primary pulmonary hypertensive patients with captopril for four days. To ensure accuracy of haemodynamic and hormone data, the patients were studied under conditions of constant body posture, regulated dietary sodium and potassium intake, and unchanged diuretic therapy. Captopril reduced mean pulmonary arterial pressure in parallel with plasma angiotensin II levels. Right ventricular ejection fraction recordings increased considerably in three of four patients. Systemic arterial pressure fell, but there was no change in right atrial pressure, cardiac output, or heart rate. The decline in plasma (and urine) aldosterone levels presumably contributed to the positive cumulative potassium balance and the rise in plasma potassium (mean 0.7 mmol/1). These encouraging results suggest that converting enzyme inhibitors warrant a formal trial with prolonged follow up in the treatment of primary pulmonary hypertension.

Captopril as treatment for patients with pulmonary hypertension. Problem of variability in assessing chronic drug treatment.

Abstract: We gave captopril, an angiotensin converting-enzyme inhibitor, to four patients with unexplained pulmonary hypertension to see if it would lower pulmonary arterial pressure or pulmonary vascular resistance. The patients were studied at rest and during supine bicycle exercise, before and after 48 hours of captopril treatment (up to 450 mg/day). During the treatment, each patient was monitored, with systemic and pulmonary pressures measured hourly, and cardiac output every two to four hours. We found no significant effect of captopril, either at rest or with exercise, on the cardiac output, pulmonary artery pressure, or pulmonary vascular resistance, measured at the end of 48 hours treatment. We noted, however, that during the 48 hour period, all patients showed pronounced swings in their pulmonary and systemic artery pressures and cardiac outputs that had no relation to the administration of captopril or time of day. We conclude that captopril appears to be ineffective in causing a sustained reduction in the pulmonary artery pressure or pulmonary vascular resistance in patients with primary pulmonary hypertension. It appears, however, that these patients experience spontaneous variability in their pulmonary resistance from hour to hour which needs to be further studied before a reliable assessment of long-term drug treatment can be made.

Evidence for pulmonary CO2 chemosensitivity: effects on ventilation.

Abstract: To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (VE), we separated the systemic and pulmonary circulations and controlled partial pressure of CO2 (PCO2) independently in each circuit under hyperoxic conditions and measured VE. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall; and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l . kg-1 . min-1. Systemic PCO2 (PSCO2) was held constant at three different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between approximately 7 and 85 Torr. With PSCO2 at 43.5 +/- 0.4 Torr, VE increased 2.67 +/- 0.61 l . min-1 as PpCO2 was varied between these limits. With PSCO2 at 63.8 +/- 2.5 Torr, VE increased 3.95 +/- 0.73 l . min-1 over these same limits of PpCO2. With PSCO2 below 25--30 Torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on VE was abolished by vagotomy. These results suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of VE.

Supravalvular pulmonary stenosis after anatomic correction of transposition of the great arteries: causes and prevention.

Abstract: Twenty-two patients who underwent anatomic correction of transposition of the great arteries at the arterial level at the age of 8 weeks to 14 years were reinvestigated 1-4.6 years (mean 2.0 years) after operation. A Dacron tube was used to bridge the gap between the proximal pulmonary route and the distal pulmonary artery in four patients and a tube made of homologous dura mater (2.5 cm in diameter) was used in 18. The nonvalved conduit was placed on the right side of the ascending aorta in nine patients and on the left side in 13. Supravalvular pulmonary stenosis with a gradient of 45-95 mm Hg was found in three patients, all of whom had had the conduit placed on the right side. There was normal growth of the pulmonary artery proximal and distal to the stenotic area. Operation for the relief of the stenosis with insertion of a pericardial patch across the stenosed area was performed in two patients. We conclude that supravalvular pulmonary stenosis after anatomic correction of transposition of the great arteries occurs only when the new pulmonary artery is placed on the right side of the ascending aorta and that the use of a large tube of dura mater appears to allow for rapid growth in early life.

Pulmonary vascular and alveolar development in tetralogy of Fallot: a recommendation for early correction.

Abstract: Using quantitative morphometric techniques, we analysed pulmonary arterial and alveolar development in the lungs of seven children aged 1.2-12 years who died during or soon after repair of tetralogy of Fallot. One child had a residual ventricular septal defect and survived for five months. One other child had had a previous Waterston-Cooley anastomosis (Waterston shunt). Postmortem lung volume in relation to body surface area was generally below normal for age, the alveoli were small, and the total alveolar number was below normal in five of the seven cases. Microscopically, airway and alveolar structure appeared normal. The preacinar arteries were larger and the intra-acinar arteries were smaller than normal for age. The preacinar elastic pulmonary arteries appeared to contain less elastin and in both preacinar and intra-acinar muscular arteries the media was thinner than normal, although muscle was normally distributed along the arterial pathway. Eccentric areas of intimal fibrosis were small and uncommon. The bronchial arteries were generally more prominent than usual both macroscopically and microscopically, but no abnormal bronchopulmonary connections were present. After corrective surgery a residual ventricular septal defect and pulmonary hypertension were associated with arterial medial hypertrophy, and this change was also found in the right lung of a normotensive patient who had had a Waterston shunt. This group probably represents the most favourable clinical picture of tetralogy in patients who usually survive but, even so, pulmonary arterial and alveolar development was abnormal. The structural findings are discussed in relation to the functional outcome in patients with tetralogy who have survived. Repair of the abnormality during the first two to three years of life is recommended.

Pulmonary artery catheterisation. An assessment of risks and benefits in 220 surgical patients.

Abstract: The benefits and risks of pulmonary artery catheterisation were assessed in 220 patients having cardiac or vascular surgery. Prior to induction of anaesthesia 20% of patients had pulmonary artery wedge pressure measurements which indicated the need for blood volume support, vasodilator therapy or modification of the anaesthetic induction technique. Of those patients for cardiac surgery, 38% had important changes before cardiopulmonary bypass requiring blood volume support or vasodilator therapy. These changes were not reflected by similar changes in the central venous pressure. The risks of the technique were minimal. Minor complications occurred in 25% of patients (transient arrhythmias) and more serious complications occurred in 3.6% of patients. There was no mortality or long-term sequelae. We conclude that the benefits of pulmonary artery catheterisation outweigh its risks in patients having major cardiac and vascular surgery.

Identification of Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease from Routine Chest Radiographs1–2

Abstract: The mean pulmonary artery pressure (PAP) was measured in 34 patients with moderate to severe chronic obstructive pulmonary disease (FEV1, 1,010 ± 460 ml) and was correlated with the following 4 ind...