Bronchial artery perfusion scintigraphy to assess bronchial artery blood flow after lung transplantation.
The bronchial arterial system is inevitably interrupted in transplanted lungs when removing the organs from the donor, but it can be reestablished by direct bronchial artery revascularization (BAR) during implantation. The purpose of this study was to visualize and quantify the distribution of bronchial artery perfusion after en bloc double lung transplantation with BAR, by injecting radiolabeled macroaggregated albumin directly into the bronchial artery system. METHODS: BAR was performed using the internal mammary artery as conduit. Patients were imaged 1 mo (n = 13) or 2 y (n = 9) after en bloc double lung transplantation with BAR. Immediately after bronchial arteriography, 100 MBq macroaggregated albumin (45,000 particles) were injected through the arteriographic catheter. Gamma camera studies were then acquired in the anterior position. At the end of imaging, with the patient remaining in exactly the same position, 81mKr-ventilation scintigraphy or conventional intravenous pulmonary perfusion scintigraphy or both were performed. Images were evaluated by visual analysis, and a semiquantitative assessment of the bronchial arterial supply to the peripheral parts of the lungs was obtained with conventional pulmonary scintigraphy. RESULTS: The bronchial artery scintigraphic images showed that the major part of the bronchial arterial flow supplied central thoracic structures, but bronchial artery perfusion could also be demonstrated in the peripheral parts of the lungs when compared with conventional pulmonary scintigraphy. There were no differences between scintigrams obtained from patients studied 1 mo and 2 y post-transplantation. CONCLUSION: Total distribution of bronchial artery supply to the human lung has been visualized in lung transplant patients. This study demonstrates that this nutritive flow reaches even the most peripheral parts of the lungs and is present 1 mo as well as 2 y after lung transplantation. The results suggest that bronchial artery revascularization may be of significance for the long-term status of the lung transplant. (+info)
Endothelium-dependent hyperpolarization in resting and depolarized mammary and coronary arteries of guinea-pigs.
1. The membrane potential responses in guinea-pig coronary and mammary arteries attributable to endothelium-derived nitric oxide (NO), prostaglandin (PG) and hyperpolarizing factor (EDHF), and to exogenous NO and the prostacyclin analogue, iloprost, were compared at rest and when depolarized with the thromboxane analogue, U46619. 2. In the coronary artery, stimulation of the endothelium with acetylcholine (ACh) evoked hyperpolarization attributable to NO and a PG with similar pD2s at rest and in the presence of U46619. However, in depolarized tissues, the pD2 of the response attributed to EDHF required a 10 fold lower concentration of ACh compared with at rest. 3. In the mammary artery, lower concentrations of ACh were required to evoke NO- and EDHF-dependent hyperpolarizations in depolarized mammary artery compared with at rest, while PG-dependent hyperpolarization did not occur until the concentration of ACh was increased some 10 fold both at rest and in U46619. 4. The smooth muscle of the coronary artery of guinea-pigs was some 4 fold more sensitive to exogenous NO and iloprost than was the mammary artery. 5. In conclusion, the membrane potential response in arteries at rest, that is, in the absence of constrictor, may be extrapolated to events in the presence of constrictor when NO and PG are under study. However, the sensitivity to ACh and the magnitude of the hyperpolarization attributed to EDHF obtained in tissues at rest may underestimate these parameters in depolarized tissues. (+info)
Endothelin-1 is induced by cytokines in human vascular smooth muscle cells: evidence for intracellular endothelin-converting enzyme.
Endothelin-1 (ET-1) is the predominant endothelin isopeptide generated by the vascular wall and therefore appears to be the most important peptide involved in regulation of cardiovascular events. Many pathologic conditions are associated with elevations of ET-1 in the blood vessel wall. Because these conditions are often cytokine driven, we examined the effects of a mixture of cytokines on ET-1 production in human vascular smooth muscle cells (VSMCs) derived from internal mammary artery and saphenous vein (SV). Incubation of IMA and SV VSMCs with tumor necrosis factor-alpha (10 ng/ml) and interferon-gamma (1000 U/ml) in combination for up to 48 h markedly elevated the expression of mRNA for prepro-ET-1 and the release of ET-1 into the culture medium. This cytokine-stimulated release of ET-1 was inhibited by a series of dual endothelin-converting enzyme (ECE)/neutral endopeptidase inhibitors, phosphoramidon, CGS 26303, and CGS 26393, with an accompanying increase in big ET-1 release but with no effect on expression of mRNA for prepro-ET-1. These same compounds were 10 times more potent at inhibiting the conversion of exogenously applied big ET-1 to ET-1. ECE-1b/c mRNA is present in SV VSMCs, however no ECE-1a is present in these cells. Thus VSMCs most probably contain, like endothelial cells, an intracellular ECE responsible for the endogenous synthesis of ET-1. Under the influence of pro-inflammatory mediators the vascular smooth muscle can therefore become an important site of ET-1 production, as has already been established for the dilator mediators nitric oxide, prostaglandin I2, and prostaglandin E2. (+info)
Minimally invasive coronary surgery in women.
OBJECTIVE: To evaluate the minimally invasive surgery in coronary artery bypass grafting and the feasibility for revascularization of triple vessel coronary artery disease. METHODS: Nine female patients, aged 49.1 to 81.6 years (mean 64.3), were operated on for triple vessel disease through minimally invasive surgical techniques. The surgeries were performed through limited left parasternal incision under femorofemoral extracorporeal circulation. The myocardium was protected by antegrade infusion of cold blood cardioplegic solution while the aorta was cross-clamped. Under direct vision, the left saphenous vein grafts were connected sequentially to the diagonal branch, obtuse marginal branch and posterior descending branch, and the left internal thoracic arterial graft was anastomosed to the left anterior descending artery in each patient. RESULTS: The number of distal anastomoses was 3 to 4 with a mean of 3.7. The aortic crossclamp time was 52 to 130 minutes (82 +/- 25 minutes). The duration of extracorporeal circulation was 78 to 151 minutes (115 +/- 29 minutes). The postoperative course was uneventful in all patients. The postoperative length of stay was 4 to 12 days (7.2 +/- 2.0 days). Follow-up (4.2 to 8.7 months, mean 6.4) was complete in all patients and there were no late deaths or angina. Coronary angiography of 2 patients showed patent grafts. All patients were satisfied with the good cosmetic healing of the incision. CONCLUSION: Our experience demonstrates that minimally invasive surgery in coronary artery bypass grafting is technically feasible and may be an alternative approach in surgical revascularization of triple vessel coronary artery disease, especially in female patients. (+info)
Five-year outcome in patients with isolated proximal left anterior descending coronary artery stenosis treated by angioplasty or left internal mammary artery grafting. A prospective trial.
BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass surgery (CABG) improve the clinical status of patients with isolated proximal left anterior descending coronary artery stenosis. At 2 years, only additional revascularization was more frequently required after PTCA. METHODS AND RESULTS: We monitored 134 patients randomized to PTCA (n=68) or CABG (n=66) for +info)
Differential expression of connexin43 and desmin defines two subpopulations of medial smooth muscle cells in the human internal mammary artery.
Upregulation of connexin43-gap junctions is associated with transition of contractile vascular smooth muscle cells (SMCs) to the synthetic state. To determine whether phenotypically distinct subpopulations of medial SMCs differentially express connexin43, we investigated the human distal internal mammary artery, a structurally heterogeneous vessel with features ranging from elastic to elastomuscular to muscular. Immunoconfocal microscopy combined with quantitative analysis and complemented by in situ hybridization showed that SMCs in the elastic medial regions expressed high levels of connexin43 but low levels of desmin, whereas those of muscular medial regions expressed low levels of connexin43 but high levels of desmin. Ultrastructurally, SMCs of both regions were of the contractile phenotype, but the former cells were irregular in shape with relatively prominent synthetic organelles whereas the latter were spindle shaped with fewer synthetic organelles. Vimentin, smooth muscle alpha-actin, calponin, h-caldesmon, and myosin heavy chains (SM1 and SM2) were equally highly expressed by most cells in both subpopulations. The connexin43/desmin expression pattern of SMCs in regions of intimal thickening resembled those of elastic medial regions. These findings refine the view suggested from previous studies that high levels of connexin43 expression are associated with SMCs of a less contractile/more synthetic phenotype. In the internal mammary artery, the 2 subpopulations of SMCs with markedly different connexin43 expression levels both represent a differentiated contractile phenotype, but the subpopulation showing high levels of connexin43-gap junctions is characterized by low levels of desmin and structural features that reflect a more synthetic tendency. (+info)
Effects of coronary artery bypass grafting using internal mammary arteries for diabetic patients.
OBJECTIVES: In our institute, internal mammary arteries (IMAs) have been preferred for coronary artery bypass grafting (CABG) in diabetic patients. The purpose of this study was to evaluate the influence of diabetes and IMA grafting on survival after CABG. BACKGROUND: The influence of diabetes on the results of CABG is not well documented, and there is controversy about whether the use of IMAs conveys greater survival benefits to diabetic patients. METHODS: A total of 420 consecutive patients who underwent CABG from April 1990 to July 1998 were reviewed; 211 of these patients had diabetes mellitus at the time of surgery. Internal mammary artery grafts have been used with increasing frequency, and bilateral IMAs have been used when possible since 1993. Internal mammary artery grafts were used in 164 nondiabetic patients (78%) and in 155 diabetic patients (73%). Seventy-eight nondiabetic patients and 74 diabetic patients received bilateral IMA grafts. RESULTS: The postoperative mortality was 2.4% in the nondiabetic and 2.8% in the diabetic group. With regard to postoperative complications, diabetic patients had a significantly higher rate of chest wound infection (p < 0.05), irrespective of whether IMAs were used or not. The use of bilateral IMAs did not increase the risk of chest wound infection in nondiabetic or diabetic patients. Overall survival curve, cardiac death-free curve and cardiac event-free curve were not affected adversely by diabetes, and in diabetic patients, CABG with saphenous veins alone conveyed significantly (p < 0.01) less long-term benefit than did CABG with at least one IMA graft. CONCLUSIONS: It was suggested that IMA grafts should be preferred in diabetic patients. (+info)
Angiotensin-(1-7) is a modulator of the human renin-angiotensin system.
The renin-angiotensin system is important for cardiovascular homeostasis. Currently, therapies for different cardiovascular diseases are based on inhibition of angiotensin-converting enzyme (ACE) or angiotensin II receptor blockade. Inhibition of ACE blocks metabolism of angiotensin-(1-7) to angiotensin-(1-5) and can lead to elevation of angiotensin-(1-7) levels in plasma and tissue. In animal models, angiotensin-(1-7) itself causes or enhances vasodilation and inhibits vascular contractions to angiotensin II. The function of angiotensin-(1-5) is unknown. We investigated whether angiotensin-(1-7) and angiotensin-(1-5) inhibit ACE or antagonize angiotensin-induced vasoconstrictions in humans. ACE activity in plasma and atrial tissue was inhibited by angiotensin-(1-7) up to 100%, with an IC(50) of 3.0 and 4.0 micromol/L, respectively. In human internal mammary arteries, contractions induced by angiotensin I and II and the non-ACE-specific substrate [Pro(11),D-Ala(12)]-angiotensin I were antagonized by angiotensin-(1-7) (10(-5) mol/L) in a noncompetitive way, with a 60% inhibition of the maximal response to angiotensin II. Contractions to ACE-specific substrate [Pro(10)]-angiotensin I were also inhibited, an effect only partly accounted for by antagonism of angiotensin II. Angiotensin-(1-5) inhibited plasma ACE activity with a potency equal to that of angiotensin I but had no effect on arterial contractions. In conclusion, angiotensin-(1-7) blocks angiotensin II-induced vasoconstriction and inhibits ACE in human cardiovascular tissues. Angiotensin-(1-5) only inhibits ACE. These results show that angiotensin-(1-7) may be an important modulator of the human renin-angiotensin system. (+info)