Thoracic Artery Research Articles

Valve Replacement After T-Grafting: “Beating Heart Surgery”

Patent internal thoracic and radial artery T-graft will adequately perfuse the heart during reoperation. Five of 1,023 patients with prior T-grafting had aortic (3) or mitral valve redo operations in which the heart was allowed to beat (after an initial dose of cardioplegia) during the operation without clamping the patent T-graft. Rapid resumption of cardiac function after one dose of cardioplegia and no intraoperative or postoperative evidence of myocardial infarction indicated adequacy of perfusion without apparent myocardial injury. This approach avoids injury to the T-graft from dissection and clamping, saves time, and simplifies the operation.

Congenital arteriovenous fistula between an intercostal artery and the left brachiocephalic vein

Congenital arteriovenous fistulas between the thoracic arteries and the systemic veins are rare, and in clinical terms may mimic patency of the arterial duct. We present a neonate with a large arteriovenous fistula between the left sixth intercostal artery and the left brachiocephalic vein, to the best of our knowledge a unique site of drainage. To our knowledge, ours is also the earliest presentation and treatment of a thoracic arteriovenous fistula.

Collateral function is impaired in aged F344 × BN rats with aortic pathology

Introduction: This study was performed to determine if hindlimb collateral function is impaired in a rat model which develops age-related vascular pathology similar to that observed in humans. Methods: Rats aged 6 (n = 6) and 24 (n = 6) months were studied. Under pentobarbital anesthesia, iliac artery blood flow was measured before and during occlusion of the femoral artery. The thoracic aorta, abdominal aorta, iliac arteries, and femoral arteries were harvested after perfusion fixation with paraformaldehyde and subsequently plastic embedded, sectioned, and stained. Results: Prior to occlusion, iliac flows were 3.0 ± 0.01 mL/min and 3.5 ± 0.02 mL/min respectively in 6 and 24 month old rats. After occlusion in the young rats, flow dropped initially by 0.8 ± 0.01 mL/min and then recovered by 0.7 ± 0.02 mL/min, essentially reaching pre-occlusion values. In 24 month old animals, flow decreased initially by 0.9 ± 0.01 mL/min but only recovered 0.4 ± 0.01 mL/min (p < 0.05). Intimal thickening was apparent only in the thoracic aorta of 24 month old animals. Conclusions: The increase in iliac artery blood flow after femoral artery occlusion reflects dilation of collateral vessels. The reduced compensation in older animals suggests that flow-dependent collateral dilation is reduced. This is consistent with studies which have demonstrated a progressive increase in endothelial dysfunction with aging. These observations together with the aortic pathology are consistent with the hypothesis that vascular aging not only promotes large vessel pathology, but also suppresses the capacity for compensation such as collateral dilation.

Percutaneous Closure of Complex Fistula Between the Internal Mammary Artery and a Lobar Branch of a Pulmonary Artery

A through review of the literature identified only 20 reported cases of fistula involving the internal mammary (internal thoracic) artery and a lobar branch of a pulmonary artery. Surgical closure was frequently done to avoid complications associated with this anomaly. We report the first patient in whom percutaneous treatment was accomplished with a combined technique involving an Amplatzer Duct Occluder device and coils.

Vitamin C Deficiency Exerts Paradoxical Cardiovascular Effects in Osteogenic Disorder Shionogi (ODS) Rats

Vitamin C is considered to be a very efficient water-soluble antioxidant, for which several new cardiovascular properties were recently described. The aim of this study was to determine in vivo the effects of a severe depletion of vitamin C on cardiac and vascular variables and reperfusion arrhythmias. For this purpose, we used a mutant strain of Wistar rats, osteogenic disorder Shionogi (ODS). After 15 d of consuming a vitamin C-deficient diet, ODS rats had a 90% decrease in plasma and tissue levels of ascorbate compared with ODS vitamin C-supplemented rats and normal Wistar rats. However, plasma antioxidant capacity, proteins, alpha-tocopherol, urate, catecholamines, lipids, and nitrate were not influenced by the vitamin C deficiency in ODS rats. Moreover, there was no difference between ODS vitamin C-deficient and -supplemented rats in heart rate and arterial pressure. After 5 min of an in vivo regional myocardial ischemia, various severe arrhythmias were observed, but their intensities were not modified by vitamin C in vitamin C-deficient ODS rats. The vascular reactivity, measured in vitro on thoracic arteries, was not altered by ascorbate deficiency in ODS rats. These unexpected results suggest that unidentified compensatory mechanisms play a role in maintaining normal cardiac function and vascular reactivity in vitamin C-deficient rats.

Hypotrophy of conduit artery walls of the offspring of nitric oxide-defective rats

The objective of the present study was to investigate the structure of the arterial walls of the offspring stemming from nitric oxide (NO)-defective hypertensive parents. The parents were treated with NG-nitro-L-arginine methyl ester (40 mg kg-1 day-1) for 5 weeks. Blood pressure was measured noninvasively in six 30-day-old rats and nine age-matched controls. The cardiovascular system was perfused with glutaraldehyde at 120 mmHg. The thoracic aorta and carotid artery were processed for electron microscopy, and geometry was determined by light microscopy. Endothelial cells, smooth muscle cells (SMC) and extracellular matrix (ECM) were determined by the point counting method in electron micrographs of the carotid artery. The blood pressure of experimental offspring was 150.0 +/- 2.3 vs 104.6 +/- 2.1 mmHg (P < 0.01) for the controls and their heart/body weight ratio of 3.9 +/- 0.1 vs 4.4 +/- 0.2 (P < 0.05) for the controls indicated cardiac hypotrophy. The wall thickness (tunica intima and media) of the thoracic aorta and carotid artery of experimental offspring was decreased to 78.9% (P < 0.01) and 83.8% (P < 0.01), respectively, compared to controls, as confirmed by a respective cross-sectional area of 85.3% (P < 0.01) and 84.1% (P < 0.01). The wall thickness/inner diameter ratio was reduced to 75% (P < 0.01) in the thoracic artery and to 81.5% (P < 0.01) in the carotid artery. No change in endothelial cell volume density or ECM was observed in the tunica intima of the carotid artery, and SMC volume density was lower in the tunica media (37.6 +/- 0.9 vs 44.7 +/- 1.1% for controls, P < 0.01), indicating compromised SMC development. Interference with arginine metabolism, a decrease in NO, and other factors are possible mechanisms underlying the structural alterations of the cardiovascular system of offspring from NO-defective hypertensive rats.

Familial aortic aneurysm in Leonberg dogs

A thoracic aortic aneurysm was diagnosed in a 6-month-old male Leonberg dog by use of radiography, transthoracic and transesophageal echocardiography, and magnetic resonance imaging. The aneurysm was associated with a twisted ascending aorta and dilatation of several other thoracic arteries (pulmonary trunk, brachiocephalic trunk, and left subclavian artery). Histologic examination of the aorta revealed cystic medial necrosis, with disruption of the elastic network, collagen fibers, and the muscle glycoprotein fibrillin-1. The dam and sire of the dog and 8 littermates were examined by use of transthoracic echocardiography. The sire and 1 male littermate also had an aneurysm of the ascending aorta. To the authors' knowledge, this is the first report of familial aortic aneurysm in dogs.

Age-related changes in contractions of chicken aorta and ischiadic artery

The characteristics of the contraction of vascular smooth muscle were examined in thoracic aorta and ischiadic artery of chickens aged 3, 6, 10 and 18 weeks. High K+ solution induced a sustained contraction in smooth muscle preparations of aorta and ischiadic artery in vitro. The contraction of the ischiadic artery became greater with age, whereas the contraction of the aortic preparation did not. In the ischiadic artery, the magnitude of the contraction divided by the weight of the muscle preparation was constant at all ages studied. However, those in the aortic preparation decreased with age. These results suggest that the changes in the contractile responses of vascular smooth muscle owing to the age of chickens vary widely according to the preparations of blood vessels, and that the functional smooth muscle cells in the thoracic aorta of chicken do not increase with age.

Vascular proliferation and transforming growth factor-β expression in pre- and early stage of diabetes mellitus in Otsuka Long-Evans Tokushima fatty rats

The roles of transforming growth factor (TGF)-β1 in vascular proliferation, atherosclerosis, and plaque still remain controversial. TGF-β1 has been previously reported to inhibit the proliferation and migration of vascular smooth muscle cells and endothelial cells, in vitro. On the other hand, administration or transgenic overexpression of TGF-β1 enhances extracellular matrix synthesis and cellular hyperplasia of the intima and media in the normal artery and injured artery in vivo. We evaluated the correlation of arterial proliferation with plasma levels of TGF-β1 and TGF-β receptor type II, respectively, in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new strain of spontaneous non-insulin-dependant diabetes mellitus (NIDDM) models. OLETF rats ( n=30) were divided into three groups aged 5, 15, and 30 weeks. Long-Evans Tokushima Otsuka (LETO) rats ( n=30) were used as age-matched non-diabetic controls. Plasma TGF-β1 and insulin were determined by enzyme-linked immunosorbent assay. Immunoreactive TGF-β receptor type II antigen was detected by immunohistochemistry on the thoracic artery. Arterial media area was measured microscopically. Oral glucose tolerance test was performed to examine the stage of diabetes mellitus. The thoracic aorta wall section area increased significantly from the age of 15 weeks in OLETF rats, versus LETO rats. In both OLETF and LETO rats, plasma TGF-β1 increased significantly from the age of 15 weeks. In OLETF rats, plasma TGF-β1 increased significantly over that in LETO rats ( P<0.001). Furthermore, TGF-β receptor type II was detected on aortic wall as strong signals in OLETF rats, but only weakly in LETO rats. OLETF rats showed hyperinsulinemia and insulin resistance from the age of 15 weeks. With oral glucose tolerance test, from the age of 15 weeks, the high glucose level in OLETF rats was prolonged to 2 h after loading, and the insulin levels at both fasting and after loading were significantly higher than those of LETO rats ( P<0.001). There are significant linear relations between plasma TGF-β1 antigen and aorta wall section area, and plasma TGF-β1 antigen and fasting insulin level ( P<0.001, respectively). We found that plasma TGF-β1 and vascular TGF-β type II receptors existed to a greater extent in pre- and early stages of diabetes mellitus (DM) in OLETF rats compared with LETO rats. The greater extent of each in OLETF rats was associated with hyperinsulinemia and/or vascular thickening.

Accumulation of calcium and phosphorus accompanied by increase of magnesium and decrease of sulfur in human arteries.

To elucidate the accumulation of elements in the arteries with aging, the authors investigated age-related changes of elements in human arteries, such as the thoracic aorta, femoral, basilar, coronary, radial, and common iliac arteries by inductively coupled plasma-atomic emission spectrometry. The subjects consisted of 17 men and 9 women, ranging in age from 55 to 92 yr in the cases of the five arteries, except for the common iliac arteries, in which the subjects consisted of 16 men and 8 women, ranging in age from 65 to 93 yr. It was found that there were significantly direct correlations between calcium and phosphorus contents and between calcium and magnesium contents in all of the six arteries: thoracic aorta, femoral, basilar, coronary, radial, and common iliac arteries. Significantly direct correlations were also found between phosphorus and magnesium contents in the five arteries, except for the basilar artery. In contrast, significantly inverse correlations were found between calcium and sulfur contents and between phosphorus and sulfur contents in the four arteries, except for the coronary and radial arteries. These revealed that the accumulation of calcium and phosphorus in the arteries was accompanied by an increase of magnesium in the arteries and by a decrease of sulfur in the arteries.

Selective accumulations of aluminum in five human arteries.

The aim of the present study was to determine variability of aluminum (Al) accumulation in human arteries and to observe the relationship between Al and five other elements (Ca, Fe, Mg, P, and Si) in the arteries. The Al contents in the thoracic aorta, basilar, coronary, femoral, and radial arteries of 26 human subjects were estimated by an inductively coupled plasma-atomic emission spectrometer and compared quantitatively to five elements. Al was detected in 88% of the cases in both the femoral and radial arteries, 73% in the coronary artery, 58% in the aorta, and 31% in the basilar artery. The average Al content was highest in the femoral artery (48.3 +/- 15.0 microg/g dry weight) and lowest in the basilar artery (8.1 +/- 3.6 microg/g). The Al had positive correlations with P, Ca, or Mg in both the aorta and femoral artery, and with Ca or P in the basilar artery. In the coronary artery, a correlation was found between Al and Si. No relationships were found between Al and each of the five elements in the radial artery. From these results, Al varied widely among the five arteries and accumulated more in the femoral and radial arteries but less in the basilar artery. These accumulations of Al were positively correlated with Ca or P in several arteries, but not sufficiently to explain the accumulation of Al. Further investigations are required to understand the mechanism of the variability of Al accumulation in the arteries.

Chronic hypoxia, pregnancy, and endothelium-mediated relaxation in guinea pig uterine and thoracic arteries.

Vasodilation that occurs during normal pregnancy is associated with enhanced relaxation and decreased contractile response to agonists, which are in part due to increased stimulated and basal nitric oxide (NO). In preeclampsia and/or pregnancies carried at high altitude (HA), this normal vascular adjustment is reversed or diminished. We previously reported that HA exposure did not inhibit the pregnancy-associated decrease in contractile response to agonist or basal NO in guinea pig uterine arteries (UA). We therefore sought to determine whether altitude interfered with effects of pregnancy on endothelium-dependent relaxation through a reduction in stimulated NO. We examined the relaxation response to ACh in UA and bradykinin in thoracic arteries (TA) and effects of NO inhibition with 200 microM N(G)-nitro-L-arginine (L-NNA) in arterial rings isolated from nonpregnant and pregnant guinea pigs exposed throughout gestation to low altitude (LA, 1,600 m, n = 26) or HA (3,962 m, n = 22). In pregnant UA, relaxation to ACh was enhanced (P < 0.05) at both altitudes and NO inhibition diminished, but did not reverse, ACh relaxation. The effect of L-NNA on the relaxation response to ACh was less in HA than in LA animals (P = 0.0021). In nonpregnant UA, relaxation to ACh was similar in LA and HA animals. L-NNA reversed the relaxation response to ACh at HA but not at LA. In TA, relaxation to bradykinin was unaltered by pregnancy or altitude and was completely reversed by NO inhibition. These data suggest that effects of NO inhibition are diminished in UA during pregnancy at HA. Additional studies are needed to confirm whether these effects are mediated through inhibition of stimulated NO. HA exposure did not inhibit relaxation to ACh, perhaps because of stimulation of other vasodilators.

Expression of renal and vascular angiotensin II receptor subtypes in children.

Angiotensin II (Ang II) AT1 receptors modulate most of the known physiological functions of Ang II in the kidney and cardiovascular structures. In contrast, the physiological role of AT2 receptors, which are abundantly expressed in fetal tissues, is not clearly defined. The changes that occur in the expression and distribution of AT2 receptors in the kidney and arteries during the first 2 years of life have not been studied. We have localized and characterized the expression of Ang II receptor subtypes, AT1 and AT2, in the kidney, interlobular arteries, thoracic aorta, and middle cerebral artery, in children during their first 2 years of life, using quantitative autoradiography. Renal glomeruli and middle cerebral arteries expressed exclusively AT1 receptors. In contrast, more than 80% of the Ang II receptors expressed in thoracic aorta and interlobular arteries belonged to the AT2 subtype. These findings demonstrate that the expression of Ang II receptor subtypes in different vascular structures in young children varies according to the tissue.

CHRONIC NITRIC OXIDE INHIBITION AGGRAVATES HYPERTENSION IN ERYTHROPOIETIN-TREATED RENAL FAILURE RATS

Alterations in nitric oxide (NO) and endothelin-1 (ET-1) production have recently been reported in erythropoietin (r-HuEPO)-induced hypertension in renal failure rats. The present study was designed to evaluate the effect of NO synthase inhibition with the L-arginine analog NG-nitro-L-arginine methyl ester (L-NAME) on blood pressure (BP) and ET-1 production in control and in uremic rats treated or not treated with r-HuEPO. Renal failure was induced by a two-stage 5/6 nephrectomy. Control and uremic rats were studied separately and subdivided into four groups: vehicle, r-HuEPO, L-NAME + vehicle and L-NAME + r-HuEPO. L-NAME (100 mg/kg/day), r-HuEPO (100 U/kg, subcutaneously, three times per week), the vehicle or both were administered during 4 weeks in control rats and during 2 weeks in uremic rats. Systolic BP was recorded before and after the onset of treatment at weeks 2 and 4 in control rats and at weeks 1 and 2 in uremic rats. Hematocrit, serum creatinine, plasma, blood vessel (thoracic aorta and mesenteric artery bed) and renal cortex immunoreactive (ir) ET-1 concentrations were measured at the end of the protocol. L-NAME enhanced BP in control and uremic rats and the increase was significantly higher in uremic rats under r-HuEPO therapy (222 ± 7 mmHg vs 198 ± 6 mmHg, p<0.05). L-NAME induced an increase in thoracic aorta ir-ET-1 concentrations in control and uremic rats. In contrast, ir-ET-1 concentrations were unchanged in the mesenteric arterial bed and the renal cortex of control and uremic animals. R-HuEPO increased thoracic aorta ir-ET-1 contents in L-NAME treated control and uremic rats. These results underline the important role of NO release in opposing the action of vasopressors on blood vessel tone which appears more important in uremic rats treated with r-HuEPO. L-NAME treatment increased large vessel, but not small resistance artery ir-ET-1 concentrations, suggesting differential regulation of ET-1 production in different vascular beds under chronic NO synthase inhibition.

A new flap model in the rat: the pectoral skin flap.

The purpose of this study was to describe a new axial-pattern experimental flap model in the rat. Wistar rats weighing 200 to 250 g were used in the experiment. In 15 rats, the superficial anatomy of the ventral thoracic region was studied by anatomic dissection, dye injection, and microangiography, using 5 rats in each group. The anatomic studies revealed that the ventral thoracic skin derives its principal blood supply from the long thoracic artery--a branch of the common thoracic artery. Based on these anatomic studies, the pectoral skin flap model, pedicled on the long thoracic vessels, was created in the rat. The flap is bounded medially by the midsternal line, laterally by the anterior axillary line, and superiorly and inferiorly by transverse lines passing at the level of the suprasternal notch and the xyphoid process respectively. In 5 animals, bilateral flaps (N = 10) were raised and replaced in situ. In 15 animals, oversized flaps were created by extending the flap for both a greater width (N = 10) and length (N = 10). Although all the flaps limited to the cutaneous territory as described were found to survive totally, oversized flaps underwent partial necrosis distally. The authors conclude that the pectoral flap is a simple and reliable skin flap model for future biological and pharmacological study because it is very easy to raise, has a consistent vascular pedicle, and has well-defined borders with consistent landmarks.

Novel Alternative Splice Variants of cGMP-binding cGMP-specific Phosphodiesterase

After our recent findings that the amino-terminal portion of rat cGMP-binding, cGMP-specific phosphodiesterase (cGB-PDE) differs from those of bovine and human cGB-PDEs, we found two forms of canine cGB-PDE cDNAs (CFPDE5A1 and CFPDE5A2) in canine lung. Each contained a distinct amino-terminal sequence, CFPDE5A1, possessing an amino-terminal portion with sequence similar to those of bovine and human, and CFPDE5A2, having one similar to that of rat. Other portions coding for the cGMP binding domains and the catalytic domain were conserved. Both CFPDE5A1 and CFPDE5A2 transcripts were detected in the cerebellum, hippocampus, retina, lung, heart, spleen, and thoracic artery. CFPDE5A1 transcripts were particularly abundant in the pylorus, whereas CFPDE5A2 transcripts were quite low in this tissue. CFPDE5A1 and CFPDE5A2 expressed in COS-7 cells had cGMP Km values of 2.68 and 1.97 microM, respectively, and both were inhibited by a low concentration of a cGB-PDE inhibitor, Zaprinast. Both CFPDE5A1 and CFPDE5A2 bound cGMP to their allosteric cGMP binding domains, and this cGMP binding was stimulated by 3-isobutyl-1-methylxanthine. Thus, two types of alternative splice variants of canine cGB-PDE have been identified and shown to have similar biological properties in vitro.

The Response of Blood Flow Between the Internal Thoracic and Ileocecal Arteries to Inotropic Agents in a Canine Model

The Response of Blood Flow Between the Internal Thoracic and Ileocecal Arteries to Inotropic Agents in a Canine Model

Anterior Abdominal Wall Necrosis Following Bypass for Aortoiliac Occlusive Disease

An uncommon complication of ipsilateral anterior abdominal wall ischemic necrosis ("trash abdominal wall"), following microembolic occlusion of a unilateral patent internal iliac artery and collaterals during aortobifemoral bypass for aortoiliac disease, is presented. Recognition of the presence or lack of a collateral system from lateral thoracic and intercostal arteries to branches of the superficial epigastric on preoperative angiogram and its role in the perfusion of the anterior abdominal wall is stressed. Preserving both or at least one internal iliac artery and avoiding microembolism from endarterectomy will minimize the risk for this complication.

Abnormal origin of internal thoracic and vertebral arteries

Abnormal origin of internal thoracic and vertebral arteries

Peripheral Vascular Alterations During Experimental Heart Failure in the Rat

Structural changes of the peripheral vascular component as seen during hypertension and atherosclerosis have been suggested during heart failure but have never been reported. Therefore, we studied possible structural alterations in the peripheral vasculature in an experimental model of heart failure, induced by ligation of the left coronary artery in rats. Large conduit and resistance-type arteries were excised at 1, 3, 5, and 12 weeks after myocardial infarct induction (MI) or sham surgery. Vessel dimensions (medial cross-sectional area [CSA], internal and external diameters, and media-to-lumen ratios) as well as medial collagen and elastin volume fractions were measured by computerized morphometry. The hydroxyproline assay was used to determine collagen and elastin content biochemically. In separate groups of animals, peripheral tissue flows were measured by using radioactive microspheres 5 and 12 weeks after MI. To evaluate the effects of the degree of heart failure, the animals of the 12-week group (n = 10) were subdivided into groups of moderate (< 45% infarct size) and large (> 45% infarct size) infarction. At all time points, body weights of sham-operated and MI rats were comparable. Lung weights of infarcted animals were increased proportionally to infarct size. No major changes in vessel dimensions were seen at the earlier time points. Twelve weeks after coronary artery ligation, significantly smaller CSAs were observed in several large conduit arteries such as the thoracic aorta, carotid artery, and superior mesenteric artery. These changes coincided with reductions in both internal and external diameters. In contrast, internal and external diameters of mesenteric and pulmonary resistance arteries were increased after 12 weeks of coronary artery ligation.(ABSTRACT TRUNCATED AT 250 WORDS)