Adaptive mechanisms of arterial and venous coronary bypass grafts to an increase in flow demand.
OBJECTIVE: To compare the mechanisms by which arterial and venous grafts increase their flow during pacing induced tachycardia, early and later after coronary bypass surgery. DESIGN: 43 grafts (13 epigastric artery, 15 mammary artery, 15 saphenous vein) evaluated early (9 (3) days (mean (SD)) after bypass surgery were compared with 41 other grafts (15 epigastric, 11 mammary, 15 saphenous vein) evaluated later after surgery (mean 23 months, range 6 to 168 months) by quantitative angiography and intravascular Doppler velocity analysis during atrial pacing. Controls were 17 normal coronary arteries. RESULTS: Baseline graft flow tended to be lower later after surgery than early (41 (16) v 45 (21) ml/min, NS). Blood flow increased during pacing by 30 (16)% early after surgery, less than later after surgery (+46 (18)%, p < 0.001) and less than in normal coronary arteries (+54 (27)%, p < 0.001 v early grafts; NS v late grafts). There was no difference between venous and arterial grafts. No significant vasodilatation was observed during pacing early after surgery in arterial and venous grafts. Later after surgery, significant vasodilatation was observed only in arterial grafts (mammary and epigastric grafts), from 2.41 (0.37) to 2.53 (0. 41) mm (+5.1% v basal, p < 0.001). Early after surgery and in venous grafts later after surgery, the increase in flow was entirely due to an increase in velocity. In later arterial grafts, the relative contribution of the increase in velocity to the increase in flow during pacing was lower in arterial grafts (70 (22)%) than in venous grafts (102 (11)%, p < 0.001) and similar to normal coronary arteries (68 (28)%). CONCLUSIONS: Early and later after surgery, arterial grafts and venous grafts both increase their flow similarly during pacing. Early arterial grafts and venous grafts increase their flow only through an increase in velocity. Later after surgery, arterial grafts act as more physiological conduits and increase their flow in the same way as normal coronary arteries, through an increase in velocity and calibre mediated by the endothelium. (+info)
Rat allotransplantation of epigastric microsurgical flaps: a study of rejection and the immunosuppressive effect of cyclosporin A.
The rejection of allotransplantation of epigastric microsurgical flaps and the effect of immunosuppression have been studied in 58 rats. Three sets of experiments were planned: (1) Wistar Furth isogenic donors and receptors (control set); (2) Brown Norway donors and Wistar Furth receptors (rejection set); and (3) Brown Norway donors and Wistar Furth immunosuppressed receptors (cyclosporin A set). Cyclosporin A (10 mg/kg/d) treated rats had a transplantation survival rate of up to 30 days: 83.3% among isogenic animals and 60% among allogeneic. There was 100% rejection by the 9th day after the transplantation in allogeneic non-immunosuppressed rats. Biopsies embedded with historesin were taken from the flap and normal contralateral skin (used as control) on the 3rd, 7th, 15th, and 30th days after the surgery. A quantitative study of infiltrating lymphocytes in the flaps, with and without cyclosporin A, was done by evaluating the local inflammatory infiltrate. A significant increase in the number of lymphocytes among the rejection and immunosuppressed groups was seen, as compared to the isogenic set. Local lymphocytosis in allogeneic non-immunosuppressed transplantations reached its highest level on the 3rd day after surgery, before gross findings of rejection, which could only be seen by naked eye on the 5th or 6th day. Therefore, we conclude that cyclosporin A is effective in preserving allogenic transplantation in rats. Biopsies of transplanted areas may contribute to earlier diagnosis of the need for immunosuppressive therapy. (+info)
Diadenosine polyphosphates cause contraction and relaxation in isolated rat resistance arteries.
The effects of diadenosine polyphosphates (APnA; n = 3-6) and adenine nucleotides on contractile reactivity of isolated rat mesenteric resistance arteries (MrA) and superior epigastric arteries (SEA), which display a dense and sparse autonomic innervation, respectively, were evaluated. All agonists examined, except adenosine and AMP, induced contractions. The rank order of potency was similar in both arteries: alpha,beta-methylene ATP (alpha,beta-meATP) > AP5A > AP6A > AP4A > ATP > ADP > AP3A. Contractions were stable during several minutes in SEA but highly transient in MrA. They were reduced after exposure to 10 microM alpha,beta-meATP and by 10 microM of the P2X antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid. During phenylephrine (10 microM)-induced contractions, the agonists induced a further contraction in SEA. In MrA, however, further contraction was followed by marked relaxation. The rank order of relaxing potency was comparable to that of the contractile potency of agonists. Also, the relaxing effects of APnA were blunted by 10 microM pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and after exposure to alpha,beta-meATP. In vitro and in vivo sympathectomy with 6-hydroxydopamine and removal of the endothelium did not modify the effects of APnA in MrA. Thus, the contractile effects of APnA in resistance arteries 1) are due to a P2X purinoceptor-mediated stimulation of the smooth muscle; 2) depend on the length of the phosphate chain; and 3) are followed by endothelium-independent relaxing effects in MrA but not SEA, which may involve receptors that are similar to those mediating contraction. The regional heterogeneity of APnA effects cannot be attributed to a direct neurogenic influence. (+info)
Heterogenous vascular effects of AP5A in different rat resistance arteries are due to heterogenous distribution of P2X and P2Y(1) purinoceptors.
In the accompanying article, we showed that AP5A displayed heterogenous vasoactive effects in rat resistance arteries. It induced a stable vasoconstriction in the superior epigastric artery (SEA) and a transient vasoconstriction in the mesenteric resistance artery (MrA). In the phenylephrine-precontracted MrA AP5A induced a marked vasorelaxation. In this study the noncompetitive inhibition of the AP5A-induced vasoconstriction with pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid was found to be significantly stronger in MrA than in SEA. The nonselective P2 purinoceptor antagonist suramin inhibited AP5A-induced vasoconstriction in MrA only. The vasoconstriction by the P2X purinoceptor agonist alpha,beta-methylene ATP was inhibited by with pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and suramin similarly to that induced by AP5A. Thus, the AP5A-induced vasoconstriction is due to P2X receptor activation, but two different P2X receptors seem to be operational in the two different vessels. The AP5A-induced vasorelaxation of phenylephrine-precontracted MrA was inhibited by the P2Y(1) receptor antagonist ADP3'5'. The vasorelaxation induced by ADPbetaS (P2Y(1) agonist) also was inhibited by ADP3'5'. These findings suggest that AP5A-induced vasorelaxation of MrA is caused by P2Y(1) receptor activation. The P1 (A(2)) receptor antagonist 3, 7-dimethyl-1-propargylxanthine only slightly inhibited AP5A-induced vasorelaxation at high concentrations. Adenosine and the A(2) receptor agonist CGS21680 failed to produce significant vasorelaxation. Therefore, vasorelaxation in MrA does not involve A(2) purinoceptor activation. AP5A-induced vasorelaxation was not inhibited by Ca(2+)- or ATP-dependent K(+) channel blockade with clotrimazole, apamin, or glibenclamide. These data indicate that vasoconstriction in MrA and SEA by AP5A is due to different P2X receptors, and vasorelaxation in precontracted MrA is due to P2Y(1) receptor activation. (+info)
Coronary artery bypass with only in situ bilateral internal thoracic arteries and right gastroepiploic artery.
BACKGROUND: With the rapid advance of catheter intervention, the direction taken by surgeons is not only to make conventional CABG less invasive but also to pursue better long-term results by using more arterial conduits. METHODS AND RESULTS: Between July 1989 and April 2000, 239 patients (218 men, 21 women) with a mean age of 59.7 (range 39 to 79) years underwent CABG with exclusive use of both internal thoracic arteries (ITAs) and the right gastroepiploic artery (RGEA). ITA grafts were harvested by using the skeletonization technique. Most patients (96%) had either triple-vessel or left main disease. Fifty percent of the patients were diabetic, and 16 were being treated with insulin. The left ventricular ejection fraction was +info)
Benefit of bilateral over single internal mammary artery grafts for multiple coronary artery bypass grafting.
BACKGROUND: The aim of this study was to evaluate the performance of bilateral internal mammary artery (BIMA) grafts in isolated CABG. METHODS AND RESULTS: Beginning in April 1985, elective primary multiple CABG for multivessel disease was performed in 1131 patients. The early and late results of 688 patients who received single internal mammary artery (SIMA) grafts and 443 patients who received BIMA grafts were compared (median follow-up, 6.15 years). Hospital mortality was not significantly different in the SIMA (0.9%) and BIMA (0.9%) groups. Graft patency was 97.3% in the BIMA group and 94.3% in the SIMA group (P<0.0001). The 7-year repeated CABG-free rate was significantly higher in the BIMA group (P=0.026). The 7-year new myocardial infarction-free rate in all patients tended to be higher in the BIMA group (P=0.06). The hazard ratio for all death or repeated CABG in patients with ejection fractions >0.4 and age <71 years was lower in the BIMA group (P=0.0499). CONCLUSIONS: Our data suggest that the use of BIMA grafts in patients with in situ coronary artery anastomoses achieves a significantly higher repeated CABG-free rate in all patients compared with the use of SIMA. (+info)
Medial artery calcification in ESRD patients is associated with deposition of bone matrix proteins.
BACKGROUND: In non-ESRD patients, recent studies have demonstrated that the process of vascular calcification resembles developmental osteogenesis. Patients with ESRD are known to have excessive vascular calcification, but this has previously been attributed to the non-cell-mediated process of metastatic calcification. METHODS: To determine if the calcification observed in patients with ESRD is related to a cell-mediated process, we removed a piece of inferior epigastric artery at the time of renal transplant. Calcium content of the entire vessel was quantified with spiral computed tomography (CT). The vessel was then examined histologically for calcification and the presence of bone matrix proteins by immunohistochemistry, and medial and intimal thickness quantified by histomorphometry. These findings were correlated with demographic, clinical and laboratory values. RESULTS: The proximal inferior epigastric artery was obtained from 41 patients undergoing renal transplantation, but two were inadequate for histologic examination. Twenty-seven of the remaining vessels had no evidence of calcification by MacNeal's or Alizarin red pH 4.2 staining, five vessels had mild/moderate calcification, and seven had severe calcification, all in the medial layer. Calcification assessed histologically was closely correlated with calcification score as assessed by spiral CT, normalized for vessel weight (P=0.027). Positive immunostaining for the bone matrix proteins osteopontin, type I collagen, bone sialoprotein, and alkaline phosphatase was strongly correlated with calcification (all P < or = 0.001), as was a history of coronary artery disease (P < 0.001), and diabetes (P=0.034). The calcification score by spiral CT correlated with these same factors and the serum phosphorus and calcium x phosphorus product (P=0.032 and 0.037). The location of immunostaining for the bone proteins was strongly associated with the presence of calcification. However, positive immunostaining also was observed in association with disorganization of the vascular smooth muscle cells in the medial layer due to deposition of a matrix-like substance, prior to overt calcification. CONCLUSIONS: In patients with ESRD undergoing renal transplantation, vascular calcification of the medial layer of the inferior epigastric artery is common (44%), can be detected by spiral CT, and is associated with deposition of bone matrix proteins. This implies an active cell-mediated process, raising hope that directed intervention can arrest this process. (+info)
A prospective evaluation of hypogastric artery embolization in endovascular aortoiliac aneurysm repair.
PURPOSE: Hypogastric artery embolization (HAE) is often performed in endovascular aortoiliac aneurysm repair to prevent potential endoleak, and this can be associated with pelvic ischemic sequelae. This prospective study was performed to evaluate the clinical outcome of HAE in patients who underwent endovascular aortoiliac aneurysm repair. METHODS: During a 15-month period, 12 patients who underwent either unilateral or bilateral HAE for endovascular aortoiliac aneurysm repair were prospectively evaluated. All patients underwent preoperative and postoperative penile pressure measurement and pulse-volume recording evaluation. Angiographic features relating to pelvic collaterals and clinical outcomes relating to pelvic ischemia were evaluated. RESULTS: Unilateral HAE was performed in eight patients (67%), and bilateral HAE was performed in four patients (33%). Mean reductions in penile brachial index (PBI) after unilateral and bilateral HAE were 13 +/- 6% (not significant) and 39 +/- 14% (P <.05), respectively. Erectile dysfunction occurred in three patients for unilateral HAE (38%) and in two patients for bilateral HAE (50%), with an overall PBI reduction of 36 +/- 12% (P <.01). No significant change in thigh brachial or ankle brachial index occurred after HAE. Hip and buttock claudication occurred in four patients for unilateral HAE (50%) and in two patients for bilateral HAE (50%), with an overall PBI reduction of 18 +/- 9% (P <.05). Other associated pelvic ischemic complications after bilateral HAE included one scrotal skin sloughing (25%) that occurred 3 days after aortic endografting and one sacral decubitus (25%) that occurred 4 months after aortic endografting. With analysis of angiographic collateral patterns, diseased profunda femoral artery (PFA; >50% stenosis) was noted in four patients, all in whom post-HAE pelvic ischemic symptoms developed (P <.05). In contrast, only four of the remaining eight patients with normal or mild PFA disease had pelvic ischemic sequelae after HAE. CONCLUSION: Erectile dysfunction after HAE correlates with significant reduction in PBI. Severe pelvic ischemic symptoms are more likely to occur after bilateral HAE, which should be avoided if possible. Moreover, patients with diseased PFA are at risk of development of pelvic ischemia after HAE. Our data suggest a potential role of concomitant profundapalsty at the time of aortic endografting to improve pelvic collateral flow and reduce pelvic ischemia in this subset of patients with HAE. (+info)