Regional pulmonary blood flow in mitral disease studied by xenon radiospirometry.
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Regional lung perfusion was measured in the sitting position by 4 external detectors after intravenous injection of 133Xe in 24 patients with mitral valve disease and in 8 people with no cardiopulmonary disease acting as normal controls. Right- and left-sided heart catheterization was carried out on the patients on the following day. Mitral valve stenosis was found in 9, mitral valve regurgitation in 8, and both stenosis and regurgitation in the remaining 7. Regional lung perfusion in the normal people fell linearly from the basal to the apical sections of the lungs. The perfusion distribution in patients with mitral valve disease and a pulmonary capillary vein (PCV) pressure lower than 15 mmHg (2-0 kPa) did not differ significantly from that of the controls. A redistribution of the regional perfusion, with an increase in the apical perfusion and a fall in the basal perfusion of the lungs, was seen in patients with a raised PCV pressure. The hyperperfusion of the apical lung sections correlated with the mean pressure in the pulmonary artery (r=+0-795, P less than 0-001), while the basal hypoperfusion correlated with the PCV pressure (r=0-842, P less than 0-001). The PCV pressure can be predicted with an exactitude of +/- 7 mmHg (0-9 kPa) (95% confidence limits). Neither the cardiac index nor the pulmonary vascular resistance correlated with the changes in perfusion. Xenon radiospirometry is a rapid and reliable method for evaluating PCV pressure before or after operation in patients with mitral valve disease. (+info)
Heterogeneous capillary recruitment among adjoining alveoli.
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Pulmonary capillaries recruit when microvascular pressure is raised. The details of the relationship between recruitment and pressure, however, are controversial. There are data supporting 1). gradual homogeneous recruitment, 2). sudden and complete recruitment, and 3). heterogeneous recruitment. The present study was designed to determine whether alveolar capillary networks recruit in a variety of ways or whether one model predominates. In isolated, pump-perfused canine lung lobes, fields of six neighboring alveoli were recorded with video microscopy as pulmonary venous pressure was raised from 0 to 40 mmHg in 5-mmHg increments. The largest group of alveoli (42%) recruited gradually. Another group (33%) recruited suddenly (sheet flow). Half of the neighborhoods had at least one alveolus that paradoxically derecruited when pressure was increased, even though neighboring alveoli continued to recruit capillaries. At pulmonary venous pressures of 40 mmHg, 86% of the alveolar-capillary networks were not fully recruited. We conclude that the pattern of recruitment among neighboring alveoli is complex, is not homogeneous, and may not reach full recruitment, even under extreme pressures. (+info)
Hepatic regulation of renal function.
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Despite apparently conflicting reports in the past, the bulk of evidence presently available points to a significant role for the liver in the regulation of renal function. Hepatic regulation of renal function may involve both a hepatorenal reflex and a liver-borne diuretic factor (LBDF and/or 'glomerulopressin'). The hepatorenal reflex is elicited by an increase in intrahepatic pressure, and/or certain amino acids in portal venous blood. It is transmitted by serotonin in the liver and presumably by noradrenaline in the kidney. It leads to a marked decrease in renal blood flow, glomerular filtration and urinary flow rate. The evidence for the LBDF is still circumstantial. The LBDF may be stimulated by glucagon and adenosine. It leads to a marked increase of renal blood flow, glomerular filtration rate and urinary output. Amongst the conditions presumed to be associated with altered hepatic regulation of renal function are postprandial hyperfiltration, and the deterioration of renal function which occurs in liver disease, cardiac insufficiency and cardiovascular shock. (+info)
Familial and idiopathic colonic varices: an unusual cause of lower gastrointestinal haemorrhage.
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A patient is described presenting with an acute lower gastrointestinal haemorrhage as a result of extensive colonic varices. Further investigation revealed that there were no oesophageal varices or splenomegaly. Liver biopsy showed grade II fatty change only, with no other specific or significant pathological features. Transhepatic portography showed a raised portal pressure (20 mm/Hg) but the portal system was patent throughout. There was an abnormal leash of vessels in the caecum thought to represent a variceal plexus. This patient was diagnosed as having idiopathic colonic varices. This case is discussed together with nine other reports of idiopathic colonic varices from the published literature. Four of these reports describe idiopathic colonic varices in more than one member of the same family. Possible modes of inheritance, aetiology of variceal change, natural history, and prognosis are discussed. (+info)
Regular monitoring of access flow compared with monitoring of venous pressure fails to improve graft survival.
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Regular vascular access blood flow (Qa) surveillance is recommended to detect graft stenosis; however, there is little evidence that monitoring and correcting with angioplasty improves graft survival. This blinded, randomized, controlled trial of 112 patients studied time to graft thrombosis and graft loss, comparing monthly Qa plus standard surveillance (dynamic venous pressure and physical examination) (treatment group) to standard surveillance alone (control group). Only the treatment group was referred for angiogram if Qa <650 ml/min or a 20% decrease in Qa from baseline. Percutaneous angioplasty was performed for stenosis >50%. The rate of graft thrombosis per patient-year at risk was 0.41 and 0.51 in the control and treatment groups, respectively. Fifty-one interventions (0.93/patient-years at risk) were performed in the treatment group versus 31 interventions (0.61/patient-years at risk) in the control group. There was no difference in time to graft loss (P = 0.890). In a multivariate analysis, aspirin (ASA) therapy at baseline was associated with an 84% reduction in risk of graft thrombosis (odds ratio [OR], 0.14; P = 0.002). Higher baseline Qa (OR, 0.84; P = 0.05) and longer interval since graft insertion (OR, 0.97; P = 0.07) were associated with a decrease in graft thrombosis. Results reveal that graft surveillance that uses Qa increases the detection of stenosis, compared with standard surveillance; however, intervention with angioplasty does not improve the time to graft thrombosis or time to graft loss. (+info)
Prospective evaluation of chronic venous insufficiency based on foot venous pressure measurements and air plethysmography findings.
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PURPOSE: The purpose of this study was to evaluate lower extremity venous function in patients with chronic venous insufficiency, with foot venous pressure (FVP) measurements and air plethysmography (APG). METHODS: Eighty-five limbs of 63 patients with a history of chronic venous insufficiency (CVI) from 1995 to 1999 were studied. FVP parameters studied included ambulatory venous pressure (AVP), percent decrease in FVP with manual calf compression (%drop), ratio of increase in FVP over 4 seconds after release of compression (4SR%), and time to 90% recovery of FVP were measured. APG parameters studied included functional venous volume, 90% refilling time (VFT90), venous filling index, ejection fraction, and residual volume fraction. RESULTS: Venous filling index and 90% refilling time were significantly decreased in limbs with stasis syndrome compared with the control group. AVP, %drop, and 4SR% also showed significantly decrease in limbs with stasis syndrome compared with those without it. AVP, %drop, and 4SR% were significantly different for the primary group compared with the secondary group, whereas no differences were found with regard to any APG parameter. CONCLUSIONS: APG enables prediction of the presence of CVI, whereas FVP measurements are more useful for evaluation of clinical severity of CVI. (+info)
Why is the measurement of jugular venous pressure discredited?
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Every doctor should be able to make a probable diagnosis of congestive heart failure by clinical examination. The most revealing clinical sign is an elevated jugular venous pressure. The measurement of this pressure was introduced by Lewis in 1930 and refined and standardised by Borst and Molhuysen in 1952. Still, this method has fallen into disuse and is thought to be not very sensitive for diagnosing congestive heart failure. A study of the methods described in the literature reveals that variations in technique are responsible for great differences in normal values. It is argued that smaller elevations of jugular venous pressure can only be measured reliably by adhering strictly to the conditions put forward by Borst and Molhuysen. In this way the sensitivity will improve considerably. A plea is made for an intensive training in this method for doctors and medical students. (+info)
A new in vitro model of venous hypertension: the effect of pressure on dermal fibroblasts.
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PURPOSE: Venous hypertension leads to venous stasis ulcers. White cell activation, protein leakage from pressurized capillaries, and cytokine imbalances have all been implicated as indirect effects of venous hypertension that contribute to dermal changes seen in chronic venous insufficiency. The direct effect of increased tissue pressures on dermal elements has not been investigated. Prior studies have shown that fibroblasts isolated from venous ulcers have altered growth rates, morphologies, and protein production similar to senescent or aged fibroblasts. We hypothesize that neonatal fibroblasts (NNFs) cultured in conditions of increased atmospheric pressure will demonstrate altered cell function when compared with those grown at normal atmospheric pressure (ATM). METHODS: A pressure incubator was used to culture populations of NNFs at ATM, 60 mm Hg over ATM (ATM + 60 mm Hg), and 120 mm Hg over ATM (ATM + 120 mm Hg). NNF population growth rates were determined by periodic flow cytometry analysis over a 2-week period. Light microscopy and digital imaging were used to evaluate cell morphology. Senescence-associated B-galactosidase (SA-beta-Gal) activity was determined using the X-Gal stain. Fibronectin production was assessed by exposing cells sequentially to anti-fibronectin antibodies and Oregon Green-conjugated goat anti-mouse secondary antibodies. Flow cytometry then was used to determine relative proportions of cells staining positively for fibronectin. Statistical analysis was accomplished with analysis of variance. RESULTS: Populations of cells grown under increased pressures (both ATM + 60 and ATM + 120) showed reduced growth rates (P <.001). Similarly, morphologies of cells grown under pressure had increased cytoplasm to nuclear ratios with abnormal nuclear shapes. Populations of cells grown under pressure had higher percentages of cells staining positive for fibronectin (ATM = 45%, ATM + 60 = 59%, ATM + 120 = 79%). After 14 days of growth under pressure, fibroblast populations did not demonstrate augmented productions of the senescence marker SA-beta-Gal (ATM =.5%, ATM + 60 =.25%, ATM + 120 =.75%). CONCLUSIONS: This study demonstrated that NNFs grown in culture under increased pressures undergo a transformation not seen in cells grown at atmospheric pressure. Cells grown under pressure demonstrated reduced growth rates, increased fibronectin production, and abnormal morphologies similar to fibroblasts isolated from venous ulcers. This study suggests that pressure elevations (like venous hypertension) can directly result in altered cell function and morphology that may contribute to the delayed wound healing seen in patients with venous ulcers. This model uses a pressurized incubator that may prove to be a valuable adjunct in studying the effects of venous hypertension. (+info)