The patterns and costs of the Da Vinci robotic surgery system in a large academic institution.

The da Vinci ™Robotic System (dVRS) is the latest advancement in laparoscopic surgery allowing the surgeon more accurate and precise control of instrumentation with an added three-dimensional image. Technology comes with a price, $1.3 million.

Cyclosporine inhibits endotoxin-induced vasodilation of isolated rat resistance arterioles.

Background: An isolated arteriole fails to dilate in response to endotoxin unless a segment of aorta is included in the perfusion system. The unknown substance released by the aorta after exposure to endotoxin is dependent upon the NF-kappaB pathway and induces inducible nitric oxide synthase (iNOS) in the arteriole. The purpose of this study was to determine if cyclosporine A (CSA) that inhibits both NF-kappaB and iNOS would prevent the vasodilatory response to endotoxin.

Endotoxin releases a substance from the aorta that dilates an isolated arteriole by up-regulating INOS.

Background: Loss of vascular tone in resistance arterioles has been implicated as the cause of hypotension in septic shock. It is believed that the overproduction of nitric oxide (NO) by the inducible isoform of nitric oxide synthase (iNOS) results in the vasodilatation seen in septic shock. However, we have shown that endotoxin has no effect on vascular tone of an isolated resistance vessel unless the endotoxin flows over a segment of aorta or vena cava upstream in the superfusion line.

Endotoxin releases a precursor to vasodilation from large veins in an NF-kappaB-dependent manner.

Introduction: Our previous studies have shown that when a segment of rat aorta was placed upstream and in series to a rat cremasteric isolated arteriole, endotoxin (ET) exposure produced significant vasodilatation. Without the aorta, no loss of tone was noted, indicating that a precursor, as of yet unidentified, was washed downstream, thereby inducing vasodilation. Prior treatment of the donor of either the aorta or the arteriole with pyrrolidine dithiocarbamate (PDTC), a potent NF-kappaB inhibitor, prevented the loss of tone.

Pioglitazone prevents hypertension and reduces oxidative stress in diet-induced obesity.

The objective of this study was to determine the effect of pioglitazone on blood pressure (BP) and oxidative balance in obese, hypertensive, Sprague-Dawley rats and to identify some of the molecular mechanisms involved. After 12 weeks of a moderately high-fat diet, rats diverged into obesity-prone (OP) and obesity-resistant (OR) groups (n=6 per group). At the end of the diet, peroxisome proliferator activated receptor-gamma (PPARgamma) mRNA expression and activity in the renal cortex and medulla of OP rats were significantly lower compared with that in OR rats.

Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity.

High-salt diet is known to induce or aggravate hypertension in animal models of hypertension and in humans. When Sprague-Dawley rats (n = 60) are fed a moderately high-fat diet (32% kcal fat, 0.8% NaCl) for 10 wk, about one-half develop obesity [obesity prone (OP)] and mild hypertension, whereas the other half [obesity resistant (OR)] maintain body weight equivalent to a low-fat control (C) and are normotensive.

Adaptation of resistance arteries to increases in pressure.

During the development of hypertension, hypertrophy of smooth muscle cells and deposition of extracellular matrix thicken the walls of large arteries without reducing the size of the lumen. The small arteries and arterioles remodel inwardly through a eutrophic process of rearrangement of the same smooth muscle cells around a smaller lumen. Pressure, through an increase in circumferential wall stress, can account for both hypertrophy and inward, eutrophic remodeling.

PDTC and Mg132, inhibitors of NF-kappaB, block endotoxin induced vasodilation of isolated rat skeletal muscle arterioles.

NF-kappaB is a ubiquitous transcription factor that mediates the inflammatory response. Inhibition of NF-kappaB may be of potential therapeutic benefit in the treatment of septic shock. The antioxidant pyrrolidine dithiocarbamate (PDTC) has been shown in previous work to selectively inhibit NF-kappaB activation.

Src autophosphorylation is an early event in pressure-mediated signaling pathways in isolated resistance arteries.

Elevated blood pressure is associated with varying degrees of arterial growth and remodeling. The mechanisms by which mechanical stress is converted into cellular alteration have yet to be fully elucidated. Our laboratory has demonstrated that Src tyrosine kinases and the extracellular signal-regulated kinase subtype of the mitogen-activated protein kinase family mediate pressure-induced c-fos expression in rat mesenteric arteries.

Role of angiotensin II and free radicals in blood pressure regulation in a rat model of renal hypertension.

One-kidney, 1-clip rats (1K1C) or uninephrectomized controls were treated with either the superoxide dismutase mimetic tempol (0.5 mmol. kg(-1).

Interleukin-10 prevents loss of tone of rat skeletal muscle arterioles exposed to endotoxin.

Background: The anti-inflammatory cytokine interleukin-10 (IL-10) is known to inhibit the development of septic shock in animal models. This study was conducted to investigate the effect of IL-10 on the loss of vascular tone during exposure to endotoxin. Unlike numerous proinflammatory cytokines, the effects of IL-10 at the level of the microvasculature have not been previously studied.

Src tyrosine kinases and extracellular signal-regulated kinase 1/2 mitogen-activated protein kinases mediate pressure-induced c-fos expression in cannulated rat mesenteric small arteries.

Chronic hypertension is associated with remodeling of small arteries. There is evidence that the high pressure itself may cause these structural changes, but the responsible mechanisms are not clearly defined. Previously we showed that pressure-induced c-fos expression in intact cannulated rat mesenteric small arteries was inhibited by genistein, a general tyrosine kinase inhibitor.

Oxidative stress in a rat model of obesity-induced hypertension.

The mechanisms underlying the development of hypertension in obesity are not yet fully understood. We recently reported the development of hypertension in a rat model of diet-induced obesity. When Sprague-Dawley rats (n=60) are fed a moderately high fat diet (32 kcal% fat) for 10 to 16 weeks, approximately half of them develop obesity (obesity-prone [OP] group) and mild hypertension (158+/-3.

Isolated resistance artery preparation.

The blood vessels that contribute most to precapillary resistance are known as resistance arteries, consisting of arterioles and small arteries with diameters of less than 500 μm (1). These vessels regulate the vascular resistance, and thus the blood supply, through the adjustment of their lumen diameter, which is accomplished by modulation of the level of tone in the vascular smooth muscle cells. The smooth muscle and endothelial cells in the blood vessel wall are sensitive to a great diversity of stimuli including distending pressure, shear stress, neurohumoral factors, and metabolites.

Development of hypertension in a rat model of diet-induced obesity.

Although obesity is a risk factor for hypertension, the relationship between these 2 conditions is not well understood. Therefore, we examined some parameters of hypertension and cardiovascular disease in a dietary model of obesity. Male Sprague-Dawley rats were provided either a control diet (C) or a diet containing 32% kcal as fat (similar to a Western diet) for 1, 3, or 10 weeks.

Impaired arteriolar mechanotransduction in experimental diabetes mellitus.

Decreased arteriolar distensibility in diabetes may impair signal transduction mechanisms that are required for converting a pressure stimulus into smooth muscle contraction. These studies aimed to determine if pressure-induced increases in arteriolar intracellular Ca(2+) are altered in diabetes and whether diabetes is associated with alterations in composition of the extracellular matrix. Studies of mechanical properties used single, isolated, and cannulated cremaster arterioles from streptozotocin (60 mg/kg) diabetic rats and age-matched controls.

AT(1) receptor inhibition does not reduce arterial wall hypertrophy or PDGF-A expression in renal hypertension.

To separate the role of ANG II from pressure in hypertrophy of the vascular wall in one-kidney, one-clip (1K1C) hypertension, experimental and sham-operated rats were given the AT(1)-receptor antagonist losartan (20 mg x kg(-1) x day(-1)) or tap water for 14 days. Mean arterial pressure was elevated in both experimental groups compared with controls. Rats were anesthetized with pentobarbital sodium, and the thoracic aorta and carotid, small mesenteric, and external spermatic arteries were harvested and embedded in paraffin.

Teaching vascular adaptations to mechanical stress.

Blood vessels change their number and structure in attempt to meet tissue demands for blood flow while simultaneously controlling mechanical stresses. A great deal of information is emerging in this field, especially concerning the role of the endothelium and signaling pathways for mechanotransduction. While not delving too deeply into the rapidly changing details, the students can be introduced to this exciting field by describing the structural changes that take place and outlining the major theories that are being investigated.

Genistein inhibits pressure-induced expression of c-fos in isolated mesenteric arteries.

We have previously demonstrated that elevating intraluminal pressure from 90 to 140 mm Hg in isolated mesenteric arteries increases the expression of proto-oncogenes. These proto-oncogenes encode nuclear transcription factors that regulate the expression of target genes during various stages of the cell cycle. Thus, pressure-induced proto-oncogene expression may represent a mechanism by which pressure can induce growth and/or proliferation of vascular smooth muscle.

PDGF-A expression correlates with blood pressure and remodeling in 1K1C hypertensive rat arteries.

We previously demonstrated remodeling of large and small arteries in angiotensin II-treated rats, paralleled by an increased expression of platelet-derived growth factor (PDGF)-A chain mRNA in large arteries. Both remodeling and PDGF-A expression were associated with elevation of blood pressure rather than a direct effect of angiotensin II. To further delineate the role of PDGF-A and elevated blood pressure, we assessed the level of PDGF-A and -B mRNA and protein in the wall of large as well as small arteries in the one-kidney, one-clip (1K1C) hypertensive rat, a non-renin-dependent model of hypertension.

Medial and endothelial platelet-derived growth factor A chain expression is regulated by in vivo exposure to elevated flow.

Previous work from this laboratory demonstrated that in vivo exposure to elevated arterial flow stimulates endothelial and smooth muscle cell hyperplasia concomitant with lumen enlargement, medial wall hypertrophy, and increases in medial extracellular connective tissue in rat mesenteric small arteries. In an effort to elucidate the role of growth factors in mediating this arterial remodeling response, in situ hybridization was performed on control and high flow arterial sections using 35S-labeled riboprobes for PDGF-A, PDGF-B, basic FGF, and TGFbeta1 mRNA. Results demonstrate that after exposure to elevated arterial flow for 24 h, expression of PDGF-A mRNA in the media was significantly elevated over basal levels (+215%, p < 0.

Pressure mediates angiotensin II-induced arterial hypertrophy and PDGF-A expression.

Angiotensin II (Ang II) may induce arterial hypertrophy either directly or through an increase in arterial pressure. To separate these 2 mechanisms, rats were implanted with osmopumps delivering either Ang II (100 ng x kg-1 x min-1) or saline. 5-Bromo-2'-deoxyuridine (BrdU) was delivered to both groups by osmopump (2.

Flow-induced arterial remodeling in rat mesenteric vasculature.

This study was designed to characterize in vivo arterial remodeling of male Wistar rat small mesenteric arteries exposed to varying levels of elevated blood flow in the presence of normal arterial pressure. Through a series of arterial ligations, respective ileal artery and second-order branch blood flows acutely increased approximately 36 and approximately 170% over basal levels. Their respective diameters increased 12 and 38% and their wall area increased 58 and 120% in a time-dependent fashion between 1 and 7 days postlitigation compared with same-animal control vessels.