Capillary refill and core-peripheral temperature gap as indicators of haemodynamic status in paediatric intensive care patients.
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OBJECTIVES: Capillary refill time is an important diagnostic adjunct in the acute resuscitation phase of the shocked child. This study assesses its relation to commonly measured haemodynamic parameters in the postresuscitation phase when the child has reached the intensive care unit, and compares this with core-peripheral temperature gap. METHODS: Ninety standardised measurements of capillary refill time were made on 55 patients, who were divided into postcardiac surgery (n = 27), and general (n = 28), most of whom had septic shock (n = 24). A normal capillary refill time was defined as < or = 2 seconds. Measured haemodynamic variables included: cardiac index, central venous pressure, systemic vascular resistance index, stroke volume index (SVI), and blood lactate. Seventy measurements were made on patients while being treated with inotropes or vasodilators. RESULTS: Capillary refill time and temperature gap both correlated poorly with all haemodynamic variables among post-cardiac surgery children. For general patients, capillary refill time was related to SVI and lactate; temperature gap correlated poorly with all variables. General patients with a prolonged capillary refill time had a lower median SVI (28 v 38 ml/m2) but not a higher lactate (1.7 v 1.1 mmol/l). A capillary refill time of > or = 6 seconds had the best predictive value for a reduced SVI. CONCLUSION: Among ventilated, general intensive care patients, capillary refill time is related weakly to blood lactate and SVI. A normal value for capillary refill time of < or = 2 seconds has little predictive value and might be too conservative for this population; septic shock. (+info)
Vascular and stromal features in the skin of the lower limb in patients with chronic critical limb ischaemia (CLI) and oedema.
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OBJECTIVE: peripheral oedema is often observed in limbs affected by chronic critical limb ischaemia (CLI) and is mainly subcutaneous in distribution. Previous work has shown that capillary filtration coefficient (CFC) in limbs with CLI and oedema was twice as great as that in the contralateral limb. These changes might be due to morphological changes. Transmission electron microscopy (TEM) was used to examine the morphological features of the capillary walls and surrounding stromal tissues in the skin of these limbs. MATERIAL AND METHODS: eight patients with unilateral CLI and peripheral pitting oedema (four men, four women, a mean age of 81+/-6.9 years) was studied. Skin biopsies were taken from the pulp of the first toe, interdigital space between the first and second digits and dorsal part of forefoot just prior to amputation. RESULTS: stromal oedema and dilated capillaries were most prominent in the distal part of the foot. Some of the capillaries were filled with blood cells and some were empty. The endothelium of the dilated vessels was elongated and distended. In some patients a number of capillaries were collapsed with degenerate endothelial cells. <<<>>>, i.e. large openings, were found between the elongated oedematous endothelial cells. The basal lamina was thickened in all patients. Stromal haemorrhage and degeneration were seen in approximately 50% of patients. CONCLUSION: CLI causes ultrastructural changes in the capillary endothelium and surrounding stroma. The presence of large gaps between endothelial cells as well as an increased capillary pressure may enhance transcapillary transudation, and are most likely the causative factors in the formation of the ischaemic oedema. The stromal haemorrhage as well as degeneration probably signifies a terminal stage of CLI. (+info)
Fluid flow induces upregulation of synthesis and release of tissue factor pathway inhibitor in vitro.
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Fluid flow modulates the synthesis and secretion by endothelial cells (ECs) of several proteins that control the hemostatic properties of the vessel wall. Tissue factor pathway inhibitor (TFPI), also synthesized by ECs, is the main downregulator of tissue factor-dependent procoagulant activity. In the present study, we investigated the effect of physiological shear stress on the expression, distribution, and release of TFPI in cultured ECs. The EA.hy926 cell line was grown in a hollow-fiber perfusion system and exposed for variable times to different shear values: 0.27 dyne/cm(2) (minimal flow), 4.1 dyne/cm(2) (venous flow), and 19 dyne/cm(2) (moderate arterial flow). Step increase of the shear stress from 0.27 to 19 dyne/cm(2) induced a sharp increase of TFPI released into the medium and a parallel decrease and redistribution of cell-associated TFPI, which suggests that an acute release of TFPI occurred from the cellular pools. During 24 hours of high shear stress, cell-associated TFPI antigen and mRNA increased time-dependently. Subjecting ECs to steady shear stress for 72 hours also upregulated the expression and production of TFPI, in direct correlation with the degree of the shear. The secretion of TFPI was enhanced 1.9-fold under venous flow and 2.4-fold under arterial flow compared with minimal flow. Equally, cell-associated TFPI antigen and cell surface TFPI activity increased proportionally with the shear stress. The expression of TFPI mRNA, as determined by Northern blotting, increased up to 2-fold in ECs under venous flow and up to 3-fold under arterial flow. These results suggest that shear forces regulate TFPI by modulating its release and gene expression in ECs in vitro. (+info)
Decrease in coronary blood flow reserve during hyperlipidemia is secondary to an increase in blood viscosity.
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BACKGROUND: During maximal hyperemia, capillaries provide the greatest resistance to flow. A major determinant of capillary resistance is viscosity. We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperlipidemia is secondary to increased blood viscosity and not abnormal coronary vasomotion. METHODS AND RESULTS: Maximal hyperemia was induced in 9 dogs using adenosine. Serum triglyceride levels were increased by incremental doses of Intralipid. A good correlation was noted between serum triglyceride levels and blood viscosity (r=0.82). Neither total coronary blood volume nor myocardial blood volume changed with increasing serum triglyceride levels, indicating lack of vasomotion. Myocardial vascular resistance (MVR) increased with increasing triglyceride levels (r=0.84), while hyperemic myocardial blood flow (MBF) decreased (r=-0.64). The decrease in hyperemic MBF was associated with a decrease in blood velocity (r=-0.56). These findings were confirmed with direct intravital microscopic observations in the mice cremaster muscle. CONCLUSIONS: Increasing lipid levels in a fully dilated normal coronary bed causes no change in large or small vessel dimensions. Instead, the increase in blood viscosity causes capillary resistance to rise, which attenuates hyperemic CBF. Therefore, the abnormal CBF reserve associated with hyperlipidemia is due to increase blood viscosity and not abnormal vascular function. (+info)
Capillary and cell wall permeability to potassium in isolated dog hearts.
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From venous tracer-dilution curves recorded after 36 pulse injections of 42KCl and 131I-labeled albumin into the coronary artery inflow of 15 isolated canine heart preparations, we calculated maximal fractional extractions (Emax) and capillary permeability-surface area products (PScap) for 42K+ over a range of plasma flows (FP) from 0.3 to 1.7 ml min-1 g-u. At low FP (less than 1.0), Emax was 0.60 +/- 0.0l (mean +/- SD) and PScap was 0.72 +/- 0.20 ml min-1 g-1; at high FP (greater than 1.0), Emax decreased to 0.49 +/- 0.05 and PScap increased to 1.06 +/- 0.18. Continuous recording (gamma detector) of residual myocardial 42K+ in seven hearts showed that the mean fractional escape rate of tracer between 30 and 60 min after injection was 0.011-0.023 min-1; higher rates were observed at high FP, when the residue of 42K+ decreased to less than 10% of the injected dose by 60 min. Using PScap measured at high FP and considering the virtual intracellular volume of distribution for K+ to be 20 ml/g, we calculated the permeability-surface area product for sarcolemma (PScw) as 0.54-0.73 ml min-1 g-1, or about 50% of PScap. Considering sarcolemmal surface area (Scw) as 4,200 cm2/g and capillary surface area (Scap) as 500 cm2/g, cell permeability is low, with Pcw:Pcap being less than 0.08. (+info)
Postural changes in capillary pressure in the hallux of healthy volunteers.
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Capillary circulation is delicately regulated by microvascular constriction mechanisms, thereby controlling capillary perfusion and transmural pressure. The influence of posture on capillary flow has been investigated in both diseased and healthy people. However, its influence on capillary pressure has rarely been investigated. We measured capillary pressures in the supine and sitting positions in the hallux of healthy volunteers. The capillaries in the eponychium of the hallux were punctured by using a micropipette connected to a micropressure system (900A, WPI). Also, peripheral arterial and venous pressures were measured in both positions. The rise in systolic capillary pressure from supine to sitting position (32 mmHg; from 39 to 71 mmHg, respectively) was significantly (P < 0.001) smaller than the rise in systolic arterial toe pressure (57 mmHg, from 87 to 144 mmHg, respectively) and venous pressure (41 mmHg, from 26 mmHg to 67 mmHg, respectively). This study shows that the postural rise in precapillary arteriolar pressure is not completely transmitted to the capillaries, probably because of activation of peripheral vasoconstriction mechanisms. (+info)
Effect of captopril on the release of the components of the renin-angiotensin system into plasma and lymph.
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The effects of captopril on the intrarenal renin-angiotensin system were assessed from measurements in arterial plasma, renal venous plasma, and renal lymph from salt-depleted dogs. In the basal state, immunoreactive angiotensin II (Ang II) in renal venous plasma averaged only 60 +/- 12% (P less than 0.01) of arterial plasma, although the concentration of Ang II in renal lymph was 2.0 +/- 0.4-fold (P less than 0.05) greater. The Ang II concentration of renal lymph incubated ex vivo at 37 degrees C doubled in 10 to 15 min, which was the time taken to collect renal lymph samples. Compared with arterial plasma, renal lymph contained lower concentrations (P less than 0.01) of renin substrate and angiotensin-converting enzyme but higher concentrations of active (5.3 +/- 2.1-fold) and inactive (8.9 +/- 3.2-fold) renin. Although captopril increased the secretion of active renin into renal venous plasma by six-fold, the secretion of total renin was unchanged because of a reciprocal fall in the secretion of inactive renin. The percent reduction in renal vascular resistance with captopril correlated with the percent fall in Ang II in renal lymph (r = 0.70). IN CONCLUSION: (1) all components of the renin-angiotensin system are represented in the renal interstitium, as reflected in lymph; (2) Ang II concentrations in renal lymph in vivo approximate arterial levels; (3) increased secretion of active renin into plasma during intrarenal infusion of captopril into denervated kidneys is due predominantly to renin activation; and (4) renal vascular resistance may depend on the concentration of Ang II in the renal interstitium. (+info)
A novel application of myocardial contrast echocardiography to evaluate angiogenesis by autologous bone marrow cell transplantation in chronic ischemic pig model.
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OBJECTIVES: We investigated the feasibility of myocardial contrast echocardiography (MCE) to evaluate regional perfusion after bone marrow cell transplantation. BACKGROUND: The myocardial microvessels improved by cell transplantation are too small to visualize with conventional angiography. METHODS: Fourteen mini-pigs from the Nippon Institute for Biological Science were used. The proximal left anterior descending coronary artery was ligated. One month later, nine pigs survived. Six pigs received autologous cell transplantation into the left ventricular anterior wall: bone marrow mononuclear cells (BMMNCs) (n = 3) and bone marrow stromal cells (BMSCs) (n = 3). The other three pigs received saline (control group, n = 3). The pigs were sacrificed one month later. Myocardial contrast intensity (MCI) with a contrast agent was measured using the SONOS 5500 system (Philips). Capillary density (CD) and MCI were measured at four areas: anteroseptum (nontransplanted infarct area), anterior wall (transplanted infarct area), septum (border zone), and lateral wall (normal). We compared the anteroseptum with the anterior wall by MCI and CD. RESULTS: In the BMMNC and BMSC subsets, the CD of the anterior wall was higher than that of the anteroseptum (p < 0.001). There was a linear relation between MCI and CD (acoustic unit [AU2] = 0.234 CD + 0.010, r = 0.92, p < 0.001). At one month after cell transplantation, MCI of the anterior wall increased in the BMMNC and BMSC subsets (p < 0.05), although it did not change in the control group. The ratio of wall thickness (systole/diastole) in the transplanted infarct area was larger than that in the nontransplanted infarct area (p < 0.01). CONCLUSIONS: Myocardial contrast echocardiography is useful to evaluate regional perfusion, which was enhanced by bone marrow cell transplantation. (+info)