Experimental evaluation of atriopulmonary anastomosis in the presence of high pulmonary resistance.

We studied pulmonary resistance as a surgical criterion for atriopulmonary shunt. We created a model of experimental pulmonary hypertension by establishing a systemic-pulmonary shunt in 11 dogs. Two to 3 months after the shunt operation, total pulmonary resistance was calculated before (7.24 +/- 1.54 U . m2) and after (3.50 +/- 1.54 U . m2) ligation of the shunt. An atriopulmonary anastomosis technique was then performed and the hemodynamic status of the dogs during the first 2 postoperative hours was evaluated. Pathologic study of the lungs disclosed no arterial lesions. From our experimental work, we conclude that the surgical criterion for establishing the indication for this operation should be pulmonary resistance, which is conditioned by the state of the intrapulmonary vessels. We propose a procedure for determining real pulmonary resistance in the course of preoperative catheterization.

A new surgical technique for orthoterminal correction: experimental development.

A new technique is presented for surgical correction of tricuspid atresia, univentricular heart, pulmonary atresia with intact ventricular septum and hypoplastic ventricle, and hypoplastic left heart syndrome. The procedure consists of an angled right atriotomy, creation of an interatrial septal defect and a right neoatrium that is anastomosed to the pulmonary artery, and creation of a left neoatrium communicating with the left atrium through the interatrial septal defect. The technique was evaluated in 28 mongrel dogs. In 15 of these experimental procedures, the objective was to acquire skill in performing the technique. In the remaining 13, the procedure was executed with cardiopulmonary bypass. Hemodynamic studies were made at 30, 60, 120, and 180 minutes after operation. The results and advantages of the procedure are discussed. We consider it feasible for clinical application.

Does focal destruction of the thoracic aorta wall by Staphylococcus aureus lead to the development of infected aneurysms? An experimental study.

OBJECTIVE: The infrequency of infected aneurysms suggests that either infection of segments of the aortic wall is uncommon, or that infections do not always lead top infected aneurysm formation. The purpose of the study was to determine whether focal Staphylococcus aureus infection of aortic wall segments leads consistently to the development of infected aneurysms and to evaluate the segments in which infection did not lead to the infected aneurysm formation. METHODS: Twenty pigs were inoculated with 0.1 ml of a Staphylococcus aureus inoculum in three segments of the thoracic aorta wall (study group). In another 10 pigs, 0.1 ml of saline solution was injected in three segments of the thoracic aorta wall (control group). STUDY GROUP: histological abnormalities and bacterial culture of the inoculation sites were evaluated at 10 days (n = 5 pigs), 30 days (n = 5 pigs), and 90 days (n = 10 pigs). CONTROL GROUP: histological abnormalities were evaluated at 10 days (n = 5 pigs) and 90 days (n = 5 pigs). STUDY GROUP: infected aneurysms developed in only two animals killed at 30 days. At 90 days, destruction of the elastic tissue, scar tissue and neointima formation were found in all the aortic segments studied. CONTROL GROUP: no significant changes were found in any of the segments evaluated. CONCLUSION: In our experimental model, acute local infection by S. aureus caused the development of infected aortic aneurysm in only 10% of the animals. In the remaining 90%, healing of the site of infection followed resolution of the infection.

Does a critical hemodynamic situation develop from right ventriculotomy and free wall infarct or from small changes in dysfunctional right ventricle afterload?

An experimental model for right ventricle free wall infarct associated with double ventriculotomy and tricuspid insufficiency was created to evaluate whether right ventricle failure can cause profound refractory heart failure or whether modifications in right ventricular afterload are more influential in this regard. In our model, the left ventricle, interventricular septum and right atrial wall were maintained intact and pulmonary banding made it possible to modify right ventricular afterload during the experiment. The results of our study showed that pure right ventricular failure does affect the hemodynamic state negatively, but it is not itself, a cause of death in dogs. A slight increase in the dysfunctional right ventricular afterload produced a profound deterioration in the hemodynamic state that required pulmonary artery debanding within no more than 10 minutes.

Effect of magnesium sulfate administration on subendocardial and subepicardial perfusion.

The objective of this study was to determine the effect of systemic MgSO4 infusion on subendocardial and subepicardial perfusion. Seventeen spontaneously breathing piglets were examined. Myocardial perfusion was measured using radiolabeled microspheres at baseline, 30 and 60 min after either MgSO4 (80 mg/kg) or saline infusion. Blood pressure, heart rate, and cardiac output were also measured at these time intervals. Comparison of the magnesium-induced changes in systemic blood pressure and on subendocardial and subepicardial perfusion at 30 and 60 min with values obtained with saline solution at 30 and 60 min, yielded no statistically significant difference (Tables 1-3). The ratio of subendocardial/subepicardial blood flow and subendocardial and subepicardial coronary vascular resistance at 30 and 60 min revealed no statistically significant differences between the magnesium and the control group (Table 3). There were no statistically significant difference in cardiac output and heart rate during any of the measured periods (Table 2). Our results suggest that the administration of MgSO4 does not alter the ratio of subendocardial/subepicardial blood flow and the ratio of subendocardial/subepicardial coronary vascular resistance.

[Experimental evaluation of the role of the coronary sinus pressure in the regulation of coronary return volume via the coronary sinus. Surgical considerations in atrio-pulmonary diversion procedures]. / Valoración experimental del papel de la presión en seno coronario en la regulación del volumen de retorno vía seno coronario. Consideraciones quirúrgicas en las técnicas de derivación atriopulmonar.

In order to find out the validity of the vascular waterfall mechanism in coronary venous circulation, the role of coronary sinus pressure in the regulation of coronary return volume via the coronary sinus is studied in healthy animals. An experimental model of pressure regulation in the coronary sinus was prepared, and aortic pressure, EKG and the cardiac output (measured by thermodilution) were recorded. The return volume via the coronary sinus was measured at coronary sinus pressure of 10 or less, 15, 20, and 25 mmHg or more, for a total of 36 determinations. Increased coronary sinus pressure did not produce significant changes in aortic pressure, heart rate, cardiac index or coronary return volume via coronary sinus. When coronary sinus pressure was 25 mmHg or more, there was a significant decline in the average of coronary return volume via coronary sinus. Nevertheless, stepwise variant regression showed that the coronary sinus pressure per se does not condition the volume of coronary return via the coronary sinus. Our results suggest that in the healthy animals, the vascular waterfall mechanism in coronary venous circulation is not valid. Our results suggest that in the correction of congenital cardiac malformations using atriopulmonary anastomosis procedures, employing techniques that ensure coronary sinus drainage into the left atrium, in order to avoid the hemodynamic repercussions attributable to the vascular waterfall mechanism, is not justified.

[Effect of cAMP on the function of endothelial cells and fibromuscular proliferation after the injury of the carotid and coronary arteries in a porcine model]. / Efecto del AMPc sobre la función de las células endoteliales y la proliferación fibromuscular tras la lesión de las arterias carótida y coronaria en un modelo porcino.

INTRODUCTION AND OBJECTIVE: Reendothelization of damaged blood vessels protects against the vascular injury response. We evaluated in vivo whether a systemic increase in cAMP accelerates reendothelization and attenuates intimal hyperplasia in injured swine carotid and coronary arteries. METHODS: Both carotid arteries of 10 swines were subjected to balloon injury. Five animals had been treated with 2 ml (10 mg) of Forskolin, an activator of the adenylate cyclase, and another 5 with 2 ml of saline solution. These animals were sacrificed at day 8, and carotid artery reendothelization was evaluated. The descendent coronary (DC) artery of another 19 pigs was injured by atherotome. Nine animals had been treated with 2 ml of Forskolin, and another 10 with 2 ml of saline solution. These animals were sacrificed at day 28, with myointimal proliferation and arterial geometric remodelation being evaluated. Likewise, in these animals intracellular cAMP levels were measured at baseline and 28 and 60 minutes after saline solution or Forskolin administration and 90 min after arterial injury. RESULTS: Eight days after balloon injury, carotid artery reendothelization was greater in the Forskolin-treated group compared with the control group (p = 0.02), and the number of CD31 positive cells was statistically increased in the treated group (38 +/- 11 cells) versus controls (11 +/- 9 cells). Although the degree of vascular injury caused by atherotome was similar in all of the arteries in the control group, restenosis was only observed in 40% of these animals. Correlation analysis demonstrated that intracellular cAMP may condition arterial geometric remodeling and the diameter of the lumen after vascular injury. CONCLUSION: Our results suggest that cAMP may promote reendothelization and attenuate fibromuscular proliferation.

Intracellular (polymorphonuclear) magnesium content in patients with bronchial asthma between attacks.

Previous studies have demonstrated the role of polymorphonuclears in asthma, the importance of increases in intracellular concentrations of ionized calcium in the release of chemical mediators, the role of magnesium as natural calcium channel blocker, and the importance of magnesium deficiency in plasma histamine concentration and in tissue prostanoid concentration. The objective of our study was to measure the polymorphonuclear magnesium content in patients with asthma in the interval between attacks. We measured the polymorphonuclear magnesium content, and serum and erythrocyte sodium, calcium, and magnesium concentrations in 21 healthy volunteers and 50 patients with different types of asthma. In our patients, the polymorphonuclear magnesium content was lower than in the control group (P < 0.001), while magnesium levels in erythrocytes and serum and the levels of other ions in erythrocytes and serum were normal. This is the first report to document low polymorphonuclear magnesium content in patients with bronchial asthma. The reduction of polymorphonuclear magnesium content may have an important role in the pathogenesis of asthma.

Effect of atherosclerosis on thermo-mechanical properties of arterial wall and its repercussion on plaque instability.

Data from the literature report febrile reactions prior to myocardial infarction in patients with normal coronary arteries and that coronary syndromes seem to be triggered by bacterial and viral infections, being fever the common symptom. The thermo-mechanical behavior of thoracic aortas of New Zealand White rabbits with different degrees of atherosclerosis was measured by means of pressure-diameter tests at different temperatures. Specific measurements of the thermal dilatation coefficient of atheroma plaques were performed by means of tensile tests. Results show a different thermo-mechanical behavior, the dilatation coefficient of atheroma plaque being at least twice that of the arterial wall. Temperature-induced mechanical stress at the plaque-vessel interface could be enough to promote plaque rupture. Therefore, increases of corporal temperature, either local or systemic, can play a role in increasing the risk of acute coronary syndromes and deserve a more comprehensive study.