Vein harvest ischemia: a peripheral vascular complication of coronary artery bypass grafting

Lower-extremity ischemia can lead to impaired healing of saphenous vein excision sites in patients with significant peripheral vascular disease (PVD). Five patients who required infrainguinal revascularization for wound necrosis of the harvest site after coronary artery bypass grafting are described. The male/female ratio was 2:3 with a mean age of 67 (range 45-87) years. The most commonly associated problems were insulin-dependent diabetes mellitus (80%) and congestive heart failure (60%). The saphenous vein was harvested from the thigh and leg in three patients and exclusively from the leg in the others. Manifestations of ischemia ranged from persistent ulceration to complete wound disruption threatening limb loss. Impaired healing was isolated to infragenicular wounds in all patients. Pedal pulses were not detected in any of the affected extremities. Determination of the ankle/brachial pressure indices (ABI) revealed values of < 0.5 in three affected limbs. Non-compressible vessels resulted in falsely raised ABI of > 1.0 in the remaining two limbs; however, Doppler waveform analysis in these patients demonstrated significant PVD. Aggressive wound care and antibiotic therapy were continued for mean of 9 weeks before operative intervention. Infrainguinal reconstruction included femoropopliteal (two), femorotibial (two) and popliteal-tibial bypass (one). Autologous arm and saphenous veins in addition to expanded polytetrafluoroethylene grafts were used effectively. Limb salvage and wound healing were achieved in 100% of the patients without untoward sequelae. It is concluded that unrecognized PVD in patients undergoing coronary artery bypass grafting can lead to significant morbidity. Patients at risk may be identified with a combination of history, physical examination and non-invasive testing.(ABSTRACT TRUNCATED AT 250 WORDS)     

The laminar organization of the afferent connections of the cortical column in field 17 in the cat

The laminar structure of the cortical column connections in area 17 of the cat was studied using the microiontophoretic injection of the horseradish peroxidase. Following the enzyme injection in one column at different depths below the cortical surface the identification of morphological types of labelled neurons and the estimation of their localization were performed. When enzyme has been delivered in the whole depth of the column pyramidal neurons labelled were found in upper (I/III) and lower (V/VI) layers (ratio II;I). When the depth of enzyme injection exceeded the cortex width the cells in layer IV were labelled as well. The ratio between the quantity of cells labelled in upper and lower layers was preserved. (II; I). After the enzyme injection in the upper part of the column labelled cells were found mainly in the upper layers. It is concluded that the neurons of the column of have extensive (up to 5 mm), predominantly horizontal afferent connections with the cells in upper and lower layers while the connections with neurons in layer IV are local and do not extend beyond 0.5 mm.     

Potential role of TGF-beta in diabetic nephropathy

Renal injury in diabetes mellitus is a major cause of morbidity and mortality. Several manifestations of diabetic nephropathy may be a consequence of altered production and/or response to cytokines or growth factors. Transforming growth factor-beta (TGF-beta) is one such factor because it promotes renal cell hypertrophy and regulates the production of extracellular matrix molecules. In addition, high ambient glucose increases TGF-beta1 mRNA and protein level in cultured proximal tubular cells and glomerular epithelial and mesangial cells. Neutralizing anti-TGF-beta antibodies or antisense TGF-beta1 oligodeoxynucleotides prevents the hypertrophic effects of high glucose and the stimulation of matrix synthesis in renal cells. Several reports have described overexpression of TGF-beta in the glomeruli and tubulointerstitium of experimental and human diabetes mellitus. We recently provided evidence that the kidney in diabetic patients displays net renal production of immunoreactive TGF-beta1, whereas there is net renal extraction in nondiabetic subjects. We also demonstrated that short-term treatment of streptozotocin-diabetic mice with neutralizing monoclonal antibody directed against TGF-beta significantly reduces kidney weight and glomerular hypertrophy, and attenuates the increase in extracellular matrix mRNA levels. The factors that mediate increased renal TGF-beta activity involve hyperglycemia per se and the intermediary action of other potent mediators such as angiotensin II, thromboxane, endothelins, and platelet-derived growth factor.     

Oligomerization is an intrinsic property of calsequestrin in normal and transformed skeletal muscle

In skeletal muscle fibers, the high-capacity medium-affinity Ca(2+)-binding protein calsequestrin functions as the major Ca(2+)-reservoir of the sarcoplasmic reticulum. To determine the oligomeric status of calsequestrin, immunoblotting of microsomal proteins following chemical crosslinking was performed. Diagonal non-reducing/reducing two-dimensional gel electrophoresis was employed to unequivocally differentiate between cross-linked species of 63 kDa calsequestrin and calsequestrin-like proteins of higher relative molecular mass. Since chronic low-frequency stimulation has a profound effect on the expression of many muscle-specific protein isoforms, we investigated normal and conditioned muscle fibers. Calsequestrin was found to exist in a wide range of high-molecular-mass clusters in normal and chronically stimulated skeletal muscle fibers. Hence, oligomerization is an intrinsic property of this important Ca(2+)-binding protein and does not appear to be influenced by the fast-to-slow transformation process. Although fiber-type specific differences exist in the physiology of the skeletal muscle Ca(2+)-regulatory system, oligomerization of calsequestrin seems to be essential for proper functioning.     

Questionability of the benefits of routine laparotomy as the surgical approach for pheochromocytomas and abdominal paragangliomas

BACKGROUND: Improvement of preoperative imaging of pheochromocytomas and abdominal paragangliomas may render routine laparotomy questionable as the surgical approach of choice for these lesions. METHODS: We studied the records of 100 patients with chromaffin tumors who underwent abdominal exploration. The disease was familial in 28 patients and was malignant in 19. Seventy-five patients had intraadrenal disease (bilateral in 13). Computed tomography (CT), metaiodobenzylguanidine (MIBG) scintigraphy, and magnetic resonance imaging (MRI) were performed since 1979, 1984, and 1987 in 97, 73, and 43 patients, respectively. False-positive and false-negative results were defined as any discrepancy between imaging results and surgical findings. RESULTS: Overall accuracy of preoperative localization was 85% with CT scan, 77% with MIBG scintigraphy, and 86% with MRI. In unilateral pheochromocytoma, accuracy was 94% with CT scan, 80% with MIBG scintigraphy, and 96% with MRI. When all three studies were performed (n = 38), overall accuracy was 97% and only one extraadrenal tumor in a patient with familial pheochromocytoma was overlooked. CONCLUSIONS: The outstanding accuracy of available imaging techniques questions the strategy of routine laparotomy for sporadic and seemingly benign pheochromocytomas, favoring more elective approaches such as the posterior approach or laparoscopy.     

Prevalence of serological markers of autoimmunity in hemodialysis patients with hepatitis C virus

Pulmonary arteriovenous malformation can occur in up to 25% of patients after a classic Glenn shunt. Although unproven, exclusion of hepatic venous blood from the lungs has been proposed as a possible cause. We present a patient born with anomalous hepatic venous drainage into the left atrium with an intact atrial septum in whom pulmonary arteriovenous malformation developed in childhood. This was reversed after diversion of the hepatic venous drainage to the right atrium, supporting exclusion of hepatic venous flow as the cause of pulmonary arteriovenous malformation. The association with the hepatopulmonary syndrome is discussed.