Diastolic function: the influence of pneumoperitoneum and Trendelenburg positioning during laparoscopic hysterectomy.

BACKGROUND AND OBJECTIVE: Several reports concerning the haemodynamic changes during gynaecologic laparoscopy have been published so far, and the effects of head-down tilt and pneumoperitoneum have not been clearly separated. However, its main effect seems to be an increase in systemic vascular resistance. We investigated how the augmented afterload can affect diastolic function. METHODS: : Our study involved 20 healthy women, classified as having ASA status I: 10 undergoing laparoscopic hysterectomy and 10 undergoing conventional open hysterectomy. Measurements were made in awake patients and after induction of anaesthesia and then repeated after carbon dioxide insufflation and head-down positioning and at the end of surgery. Diastolic function was primarily studied by transthoracic echocardiography. RESULTS: We observed that pneumoperitoneum caused a significant reduction in stroke volume, cardiac output and left ventricular end-diastolic volume; the diastolic filling times showed a progressive reduction in the E-velocity (the velocity of early mitral inflow, corresponding to the ventricular passive filling phase, measured by pulsed-wave Doppler), a prolonged deceleration time and an augmented isovolumetric relaxation time. After head-down tilting, stroke volume, cardiac output and left ventricular end-diastolic volume increased in both laparoscopic hysterectomy and conventional open hysterectomy groups. CONCLUSION: We have found that pneumoperitoneum has important effects on left ventricular volumes, causing a drop in left ventricular end-diastolic volume; it also affects diastolic function with a delay in deceleration time and isovolumetric relaxation time without any effects on intracavitary pressures.

Tumor necrosis factor-alpha antagonism improves vasodilation during hyperinsulinemia in metabolic syndrome.

OBJECTIVE: Obesity is associated with chronic inflammation due to overproduction of proinflammatory cytokines, including tumor necrosis factor (TNF)-alpha. We assessed the effects of TNF-alpha neutralization by infliximab on vascular reactivity during hyperinsulinemia in obesity-related metabolic syndrome. RESEARCH DESIGN AND METHODS: Vascular responses to intra-arterial infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) were assessed in patients with metabolic syndrome, before and after administration of infliximab. RESULTS: Patients had blunted vasodilator responses to ACh and SNP during hyperinsulinemia compared with control subjects; a potentiation of the responsiveness to both ACh and SNP, however, was observed in patients following infliximab. The antioxidant vitamin C improved the vasodilator response to ACh in patients with metabolic syndrome, but its effect was not further enhanced by concurrent administration of infliximab. CONCLUSIONS: TNF-alpha neutralization ameliorates vascular reactivity in metabolic syndrome during hyperinsulinemia, likely in relation to decreased oxidative stress, thereby suggesting an involvement of inflammatory cytokines in vascular dysfunction of these patients.

Intravascular tumor necrosis factor alpha blockade reverses endothelial dysfunction in rheumatoid arthritis.

BACKGROUND: Patients with rheumatoid arthritis (RA) have endothelial dysfunction, which may predispose them to the risk of premature atherosclerosis. This study investigated the involvement of tumor necrosis factor (TNF) alpha in the pathophysiologic characteristics of this abnormality by use of the TNF-alpha-neutralizing antibody infliximab. METHODS: Endothelium-dependent and -independent vasodilator responses to intra-arterial infusion of increasing doses of acetylcholine and sodium nitroprusside, respectively, were assessed by strain-gauge plethysmography in patients (n = 10) with early RA during saline solution infusion and after intra-arterial infusion of infliximab (200 microg/min). RESULTS: Circulating markers of systemic inflammation (C-reactive protein and interleukin 6) were higher in patients than in control subjects (n = 10, both P < .05), whereas plasma levels of TNF-alpha and soluble TNF receptor types 1 and 2 were similar in both groups (all P > .05). During saline solution infusion, the vasodilator response to acetylcholine was blunted in patients with RA compared with control subjects (14.2 +/- 9.2 mL . min-(1). dL-(1) versus 23.7 +/- 9.2 mL . min-(1). dL-(1) at the highest dose, P = .004) whereas vasodilation to sodium nitroprusside was not different between groups (P = .10). In patients with RA infliximab did not modify circulating C-reactive protein levels (P = .29, versus saline solution) but did potentiate the vasodilator response to acetylcholine (21.0 +/- 11.1 mL . min-(1). dL-(1); P = .004, versus saline solution). The response to sodium nitroprusside, in contrast, was not modified by infliximab (P = .28 versus saline solution). CONCLUSIONS: Intravascular administration of anti-TNF-alpha antibody ameliorates endothelial function in patients with RA but does not concurrently affect systemic inflammatory changes. Our findings suggest that enhanced TNF-alpha generation within the vessel wall, rather than systemic mechanisms, plays a role in the pathobiologic features of endothelial dysfunction in RA.