Quantitative Prediction of the Location of Carotid Bifurcation and Neurovascular Structures in the Carotid Region: A Cross-Sectional Cadaveric Study.

INTRODUCTION: The carotid region is encountered in vascular and neurological surgery and carries a potential for vascular and cranial nerve trauma. The carotid bifurcation is an especially important landmark and difficult to predict based on currently established landmarks. This study is a detailed analysis of the carotid region and proposes a novel methodology to predict the height of the bifurcation. MATERIALS AND METHODS: Superficial and deep dissections were performed on the anterior triangle of the neck to expose the carotid region in twenty-one formalin-fixed donor cadavers. Musculoskeletal and neurovascular structures were assessed in relation to the carotid bifurcation and the medial border of the clavicle (MBC). RESULTS: The carotid bifurcation occurred, on average, 11.4 mm higher on the left (p < 0.001; 95% CI: 9.28, 13.54). The superior thyroid artery (p < 0.001), facial vein (p < 0.001), and cranial nerve XII (p < 0.001) were all more distal on the left side when measured from the MBC while the angle of the mandible and stylohyoid muscle remained symmetric. Left- and right-sided vascular structures were symmetric when measured from the carotid bifurcation. CONCLUSIONS: Neurovascular structures within the carotid region are likely to be anatomically superior on the left side while vessels are likely to remain symmetric in relation to the carotid bifurcation. When measured from the MBC, the bifurcation height can be predicted by multiplying the distance between the MBC and mastoid process by 0.65 (right side) or 0.74 (left side). This novel methodological estimation may be easily learned and directly implemented in clinical practice.

Balloon angioplasty to facilitate autogenous arteriovenous access maturation: a new paradigm for upgrading small-caliber veins, improved function, and surveillance.

Balloon angioplasty maturation is emerging as an important method to increase utilization and improve function of autogenous arteriovenous hemodialysis accesses (AVFs). Through the sequential dilation of small veins, large-diameter AVFs can be created with the inherent benefits of easier cannulation, greater overall surface area, improved patency, and fewer complications. A usable AVF can be created in a shorter amount of time, decreasing the need for dialysis catheters. In addition, selective angioplasty of the AVF inflow and outflow can facilitate improved flow rates and increase access longevity. Our approach, including primary balloon angioplasty during AVF creation, sequential balloon angioplasty maturation, and surveillance fistulagrams will be presented.

Reversing established sepsis with antagonists of endogenous high-mobility group box 1.

Despite significant advances in intensive care therapy and antibiotics, severe sepsis accounts for 9% of all deaths in the United States annually. The pathological sequelae of sepsis are characterized by a systemic inflammatory response, but experimental therapeutics that target specific early inflammatory mediators [tumor necrosis factor (TNF) and IL-1beta] have not proven efficacious in the clinic. We recently identified high mobility group box 1 (HMGB1) as a late mediator of endotoxin-induced lethality that exhibits significantly delayed kinetics relative to TNF and IL-1beta. Here, we report that serum HMGB1 levels are increased significantly in a standardized model of murine sepsis, beginning 18 h after surgical induction of peritonitis. Specific inhibition of HMGB1 activity [with either anti-HMGB1 antibody (600 microg per mouse) or the DNA-binding A box (600 microg per mouse)] beginning as late as 24 h after surgical induction of peritonitis significantly increased survival (nonimmune IgG-treated controls = 28% vs. anti-HMGB1 antibody group = 72%, P < 0.03; GST control protein = 28% vs. A box = 68%, P < 0.03). Animals treated with either HMGB1 antagonist were protected against the development of organ injury, as evidenced by improved levels of serum creatinine and blood urea nitrogen. These observations demonstrate that specific inhibition of endogenous HMGB1 therapeutically reverses lethality of established sepsis indicating that HMGB1 inhibitors can be administered in a clinically relevant time frame.

Cholinergic antiinflammatory pathway inhibition of tumor necrosis factor during ischemia reperfusion.

OBJECTIVE: Ischemia-reperfusion injury is a pathologic event characterized by tissue damage. It is mediated by tumor necrosis factor (TNF) and other cytokines that activate complement and proteases and stimulate fibrinolysis, degranulation of white blood cells, and free radical production. We recently reported that vagus nerve stimulation (VNS) suppresses endotoxin-induced cytokine synthesis through alpha bungarotoxin-sensitive cholinergic receptors. VNS protects against endotoxin-induced shock by inhibiting hepatic and cardiac synthesis of TNF. Here, the effects of VNS on suppression of ischemia-reperfusion injury and cytokine release were studied in a rat model of aortic occlusion. METHODS: Adult male Lewis rats were subjected to laparotomy and suprarenal aortic clamping for 15 minutes followed by reperfusion. Blood pressure, heart rate, and respiratory rate were recorded every 3 minutes for 90 minutes. Exposed cervical vagus nerves in the experimental group were stimulated for 5 minutes before and after aortic occlusion, with constant voltage (1 V, 2 ms, 5 Hz); sham-operated animals received no stimulation. TNF levels in serum and organs were measured with enzyme-linked immunosorbent assay ELISA (BioSource International, Camarillo, Calif). Data analysis was performed with the Student t test. RESULTS: Control animals had shock develop (mean, 59% decrease in blood pressure) whereas blood pressure in the stimulated animals did not decrease (control versus stimulated animals, P <.05). VNS significantly inhibited TNF levels in serum (7 +/- 1 ng/mL versus 45 +/- 6 ng/mL; P =.0008), heart (21 +/- 11 ng/g protein versus 85 +/- 15 ng/g protein; P =.01), and liver (16 +/- 2 ng/g protein versus 42 +/- 12 ng/g protein; P =.02). CONCLUSION: VNS significantly attenuates TNF synthesis and shock during reperfusion injury in a standard model of aortic occlusion. Clinical evaluation of VNS for this condition may be warranted.

Pharmacological stimulation of the cholinergic antiinflammatory pathway.

Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis. Termed the "cholinergic antiinflammatory pathway," inhibition of TNF synthesis is dependent on nicotinic alpha-bungarotoxin-sensitive acetylcholine receptors on macrophages. Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation. Here, we studied the effects of pharmacological and electrical stimulation of the intact vagus nerve in adult male Lewis rats subjected to endotoxin-induced shock to determine whether intact vagus nerve signaling is required for the antiinflammatory action of CNI-1493. CNI-1493 administered via the intracerebroventricular route was 100,000-fold more effective in suppressing endotoxin-induced TNF release and shock as compared with intravenous dosing. Surgical or chemical vagotomy rendered animals sensitive to TNF release and shock, despite treatment with CNI-1493, indicating that an intact cholinergic antiinflammatory pathway is required for antiinflammatory efficacy in vivo. Electrical stimulation of either the right or left intact vagus nerve conferred significant protection against endotoxin-induced shock, and specifically attenuated serum and myocardial TNF, but not pulmonary TNF synthesis, as compared with sham-operated animals. Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock.