Extreme, progressive isovolemic hemodilution with 5% human albumin, PentaLyte, or Hextend does not cause hepatic ischemia or histologic injury in rabbits.
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BACKGROUND: Physicians and their patients are greatly concerned about perioperative blood administration. Although isovolemic hemodilution is utilized to decrease the incidence of transfusion, it is unclear at what degree of hemodilution hepatoenteric ischemia and injury occurs. The authors hypothesized that hepatic ischemia, systemic ischemia, and tissue injury would occur during hemodilution in rabbits, and that the severity of ischemia and injury may be dependent on the fluid administered. METHODS: Rabbits anesthetized with isoflurane were assigned randomly to a sham-operated group (n = 8) or groups that underwent four isovolemic hemodilutions (25% of the blood volume removed at hourly intervals), with blood replaced with one of three solutions: balanced electrolyte solutions containing 6% pentastarch (n = 8), 6% hetastarch (n = 9), or 5% human albumin in normal saline (n = 8). Arterial ketone body ratio and plasma lactate, respectively, served as measures of hepatic and systemic ischemia. Gastric, duodenal, and hepatic histologic injury was assessed post mortem. RESULTS: Hemodilution from a baseline hematocrit of about 33% to about 8% (third hemodilution) with all three colloids did not result in a significant increase in plasma lactate concentration or decrease in arterial ketone body ratio. At a hematocrit of about 5% (fourth hemodilution), the hetastarch group had a significantly (P < 0.05) greater plasma lactate concentration than the sham-operated and 5% human albumin groups. There were no significant differences in arterial ketone body ratio or histologic injury between the groups. CONCLUSIONS: Isovolemic hemodilution (approximately 5% hematocrit) with albumin, pentastarch, or hetastarch solutions does not result in significant hepatic ischemia or injury assessed by histology. (+info)
Nitric oxide and hemoglobin interactions in the vasculature.
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As an endothelium-derived relaxing factor, nitric oxide (NO) maintains blood flow and O2 transport to tissues. Under normal conditions a delicate balance exists in the vascular system between endothelium-derived NO, an antioxidant, and the pro-oxidant elements of the vascular system, O-2, and peroxynitrite (a by-product of the reaction of NO and superoxide); in addition there is a balance between neurogenic tonic contraction and NO-mediated relaxation. The former balance can be disrupted in favor of peroxynitrite and hydrogen peroxide under the conditions of ischemia/reperfusion. This review suggests that NO may be beneficial, not only in terms of its new potential in improving O2 transport without accompanying significant increase in tissue blood flow, but also in its ability to suppress the prooxidative reagents of the vascular systems. These include NO-mediated inhibition of transendothelial migration by leukocyte and the antioxidative effects of NO with regard to ischemia/reperfusion; the relevance of these hypotheses to systemic administration of NO donors is discussed. (+info)
Interferon-alpha may exacerbate cryoblobulinemia-related ischemic manifestations: an adverse effect potentially related to its anti-angiogenic activity.
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The discovery of the strong association between hepatitis C virus (HCV) infection and the development of mixed cryoglobulinemia has motivated active testing of antiviral-directed alternative therapies. Several trials have demonstrated that classic cryoglobulinemia-associated manifestations improve with interferon-alpha (IFNalpha) treatment. Herein we report on 3 HCV-infected patients with severe cryoglobulinemia-related ischemic manifestations who were closely followed up during IFNalpha therapy. Clinical evaluations with special attention to ischemic lesions, liver function tests, and cryocrit determinations were serially performed. In addition to prednisone and immunosuppressive agents, the patients received IFNalpha at 3 x 10(6) units, 3 times per week for 2 months, 3 months, and 4 months, respectively. In all 3 patients, systemic features improved, liver function results returned to normal, and cryocrit values decreased. However, ischemic lesions became less vascularized and ischemia progressed, leading to transmetatarsal and subcondylar amputation, respectively, in 2 of the patients and fingertip necrosis and ulcer enlargement in the third. Skin biopsies performed before IFNalpha therapy and after 2 months of IFNalpha therapy in the third patient showed a significant decrease in subepidermal microvessels. When IFNalpha was discontinued, the lesions finally healed. Cryoglobulinemia-related ischemic lesions may worsen during IFNalpha treatment, presumably through a decrease in inflammation-induced angiogenesis. The anti-angiogenic activity of IFNalpha may delay the appropriate healing of ischemic lesions. (+info)
Endothelial cell dysfunction and arterial wall hypertrophy are associated with disturbed carbohydrate metabolism in patients at risk for cardiovascular disease.
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To investigate the effects of fasting and postprandial glucose on endothelial cell function and intima-media thickness, we studied 60 men with cardiovascular risk factors. Postischemic, endothelium-dependent vasodilatation was measured after 3 minutes of ischemia at the radial artery with high-resolution echo tracking. Common carotid artery intima-media thickness was measured by B-mode ultrasound. Glucose tolerance was determined by a 75-g oral glucose load. Fasting glucose levels were inversely correlated with postischemic, endothelium-dependent vasodilatation (r=-0.24, P<0.05) and directly correlated with intima-media thickness (r=0.26, P<0.05). However, postischemic, endothelium-dependent vasodilatation and intima-media thickness were not correlated. All subjects with normal postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness, whereas some subjects with impaired postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness. Multiple regression analysis revealed a profound influence of age on intima-media thickness to the exclusion of all other variables. The same age-adjusted analysis for postischemic, endothelium-dependent vasodilatation accepted fasting glucose, followed by 2-hour postprandial glucose, as variables, but no others. Subjects with fasting glucose values >100 mg/dL showed reduced postischemic, endothelium-dependent vasodilatation (59 versus 120 microm, P<0.05) and a higher intima-media thickness (right: 0.76 versus 0.62 mm, P<0.05; left: 0.78 versus 0.63 mm, P<0. 05) compared with those with fasting glucose values <100 mg/dL. Subjects with 2-hour postprandial glucose values >125 mg/dL had no reduced postischemic, endothelium-dependent vasodilatation compared with subjects with a 2-hour postprandial glucose <125 mg/dL; however, their intima-media thickness (right: 0.66 versus 0.62 mm; left: 0. 68 versus 0.62 mm; P<0.05 for both) was greater. Thus, high fasting rather than postprandial glucose values are associated with both postischemic, endothelium-dependent vasodilatation and increased intima-media thickness. Postischemic endothelium-dependent vasodilatation may precede increased intima-media thickness. (+info)
Oedema in the lower limb of patients with chronic critical limb ischaemia (CLI).
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OBJECTIVE: approximately 70% of patients with chronic critical limb ischaemia (CLI) show clinical signs of oedema in the distal leg and foot. The primary aim of the present investigation was to quantify this oedema. In addition we investigated whether oedema formation could be due to deep venous thrombosis (DVT). METHODS: fifteen patients with unilateral CLI and oedema were studied, four males and 11 females, with a mean age of 77+/-10.3 years. Water displacement volumetry (WDV) was used to measure limb volume. Colour duplex ultrasound (CDU) and venous occlusion plethysmography (VOP) were applied to exclude functionally significant DVT. Blood chemistry was analysed to screen for some causative factors of generalised oedema formation. RESULTS: the mean volume of the limbs with CLI was 9% greater than the contralateral limbs (1279+/-325 ml vs. 1179+/-298 ml). None of the patients had functionally significant DVT. The mean plasma albumin concentration was reduced at 28.5+/-6.6 g/l. CONCLUSION: a significantly reduced plasma albumin concentration cannot be regarded as a causative factor, since the oedema is unilateral. The aetiology of oedema formation is probably multifactorial, and further investigations are under progress to elucidate relevant pathogenetic factors. (+info)
Preoperative prediction of graft patency for infrapopliteal arterial bypass using pulse-generated runoff.
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OBJECTIVE: to assess: (i) pulse-generated runoff (PGR) as a tool for preoperative prediction of graft patency; (ii) the effect of PGR use on graft patency. DESIGN: retrospective analysis of continuous patient data. MATERIALS: all patients undergoing bypass to the infrapopliteal vessels in the Oxford Regional Vascular Unit between 1989 and 1993. METHODS: preoperative assessment using ankle-brachial indices, intra-arterial digital subtraction angiography and PGR. Six-monthly and then yearly clinical and duplex sonography follow-up to assess graft patency. Univariate analysis of graft patency to assess discriminatory ability of PGR for graft patency. RESULTS: a biphasic signal in the artery of insertion was associated with significantly better graft patency rate at 1 month and at maximum follow-up than was a monophasic signal. A monophasic signal was associated with a 12-month patency of 25% and a mortality of 37.7%. Use of PGR did not affect graft patency significantly. CONCLUSION: PGR is a useful, non-invasive, means of preoperative patient assessment to determine the potential for maintained graft patency. (+info)
Influence of diabetes on revascularisation procedures of the aorta and lower limb arteries: early results.
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OBJECT: to evaluate the influence of diabetes mellitus on the therapeutic indications and the one-month results in patients with occlusive disease of the aorta and/or lower limbs arteries. MATERIAL: a retrospective study of fully computerised data of 1003 patients (753 men, 250 women) admitted consecutively to our vascular surgery unit over a 5-year period (1992-1996). Of the total, 169 were diabetics (group I) and 834 were non-diabetics (group II). Sixty-two per cent of patients in group I vs. 40% in group II presented with critical ischaemia or trophic changes (p<0.001). RESULTS: 15.4% of patients in group I vs. 4.1% in group II had primary amputation because of irreversible ischaemia or because arterial reconstruction was impossible. Of those who underwent revascularisation, 80% were infrainguinal in group I vs. 50% in group II. Forty-five per cent of patients in group I and 37% in group II had a percutaneous transluminal angioplasty (PTA) and approximately 3% in both groups had a combination of the two techniques. At one month, patients alive without major amputation numbered 64.4% in group I vs. 93.6% in group II, patients alive with major amputation numbered 26.6% in group I vs. 5.5% in group II, and mortality rates were 8.9% in group I vs. 0.8% in group II (P<0.001). CONCLUSIONS: the 5-times higher amputation and 10-times higher mortality rates for diabetics compared to non-diabetics call for better collaborative management of diabetics between general practitioners, vascular surgeons, diabetologists and cardiologists. PTA with a 90% initial success rate is indicated for short lesions even in the presence of limited gangrene. (+info)
Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney.
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The humoral mucosal immune response of the kidney involves the transport of secretory IgA (S-IgA) through renal epithelial cells by the polymeric immunoglobulin receptor (pIgR). The pIgR is cleaved and released as free secretory component (FSC) or attached to IgA (S-IgA). We examined the effects of an ischemic model of acute renal failure (ARF) on the expression of pIgR and the secretion of FSC and S-IgA in the urine. Kidney pIgR mRNA levels decreased in ischemic animals by 55% at 4 h and by 85% at 72 h compared with controls. pIgR protein expression in the medullary thick ascending limb (TAL) decreased within 24 h and was nearly undetectable by 72 h. Urinary S-IgA and FSC concentrations decreased by 60% between days 3 and 6. pIgR mRNA and pIgR protein in the kidney returned to approximately 90% of control levels and urinary FSC and S-IgA concentrations returned to approximately 55% of control levels by day 7. We demonstrate that ischemic ARF decreases renal mucosal S-IgA transport in vivo and may contribute to the increased incidence of urinary tract infections. (+info)