Clinical evaluation of a PHMB-impregnated biocellulose dressing on paediatric lacerations.

OBJECTIVE: To evaluate the clinical benefits, primarily tolerability and reduction in pain levels, associated with the use of a PHMB-impregnated biosynthetic cellulose dressing (Suprasorb X + PHMB) on paediatric heel lacerations. METHOD: These lacerations were caused when children, who were being transported on their parents' bicycles, got their heels trapped in the wheel spokes. Where these injuries just comprised skin contusion and laceration, treatment had previously comprised cleansing followed by application of conventional dressings and moist wound healing dressings. However, the high incidence of infection necessitated regular dressing changes, which caused parents and children stress and anxiety. This clinical evaluation assessed the benefits of a new treatment protocol, where the PHMB-impregnated biocellulose dressing was applied and left in situ until epithelialisation occurred. A cork splint was used for 3 days to prevent pes equinus and to let the ankle joint rest. Change in wound size (cm²), incidence of local infection, wound bed characteristics and pain levels (measured on a 0-10 paediatric pain scale) were assessed at 3-day intervals during the 14-day treatment period. Satisfaction with the dressing was also evaluated. RESULTS: Twenty children (mean age 5.6 years (± 1.33) were recruited into the study and included in the analysis. The mean baseline wound area was 8.60cm² (± 6.57). The mean time to complete wound closure was 12.95 days (± 7.69) with a mean total of 4.70 visits (± 1.56). The mean VAS pain score was 9.55 (± 0.69), compared with 0.15 (± 0.37) on day 14 (p<0.003). At the second visit (after 3 days) 17 of the 20 children were reported to be free of pain. No cases of local infection were noted. CONCLUSION: The dressing was found to be child and parent friendly. The evaluation also showed that it was well tolerated and achieved good healing outcome. It has now been incorporated into the clinic's treatment protocol for these wounds. CONFLICT OF INTEREST: None. The authors have no relevant financial interest in this article. All authors were involved in the critical revision of the manuscript for important intellectual content.

Critical sarcomere extension required to recruit a decaying component of extra force during stretch in tetanic contractions of frog skeletal muscle fibers.

29 single frog skeletal muscle fibers were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a critical length change (average: 16.6 nm per one-half sarcomere) that was independent of velocity of stretch and of sarcomere length between 1.8 and 2.8 microns. After stretch there was an early decaying force component with a force-extension curve similar to that during stretch, which disappeared over approximately 2 s. This component was removed by a small, quick release, leaving a longer-lasting component. The critical amplitude of release required to produce this result was found by clamping the fiber to a load at which there was zero velocity of shortening. This amplitude increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch, and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch required to reach the breakpoint of force enhancement during stretch but was also independent of sarcomere length. The force drop accompanying the critical release showed a small increase up to an optimum magnitude at 2.4--2.7 microns sarcomere length, with a decrease at longer lengths.

Residual force enhancement after stretch of contracting frog single muscle fibers.

Single fibers from the tibialis anterior muscle of Rana temporaria at 0.8-3.8 degrees C were subjected to long tetani lasting up to 8 s. Stretch of the fiber early in the tetanus caused an enhancement of force above the isometric control level which decayed only slowly and stayed higher throughout the contraction. This residual enhancement was uninfluenced by velocity of stretch and occurred only on the descending limb of the length-tension curve. The absolute magnitude of the effect increased with sarcomere length to a maximum at approximately 2.9 micrometers and then declined. The phenomenon was further characterized by its dependence on the amplitude of stretch. The final force level reached after stretch was usually higher than the isometric force level corresponding to the starting length of the stretch. The possibility that the phenomenon was caused by nonuniformity of sarcomere length along the fiber was examined by (a) laser diffraction studies that showed sarcomere stretch at all locations and (b) studies of 9-10 segments of approximately 0.6-0.7 mm along the entire fiber, which all elongated during stretch. Length-clamped segments showed residual force enhancement after stretch when compared with the tetanus produced by the same segment held at the short length as well as at the long length. It is concluded that residual force enhancement after stretch is a property shown by all individual segments along the fiber.

The effect of hyperosmolality on the rate of heat production of quiescent trabeculae isolated from the rat heart.

We have measured the rate of heat production of isolated, quiescent, right ventricular trabeculae of the rat under isosmotic and hyperosmotic conditions, using a microcalorimetric technique. In parallel experiments, we measured force production and intracellular calcium concentration ([Ca2+]i). The rate of resting heat production under isosmotic conditions (mean +/- SEM, n = 32) was 100 +/- 7 mW (g dry wt)-1; it increased sigmoidally with osmolality, reaching a peak that was about four times the isosmotic value at about twice normal osmotic pressure. The hyperosmotic thermal response was: (a) abolished by anoxia, (b) attenuated by procaine, (c) insensitive to verapamil, ouabain, and external calcium concentration, and (d) absent in chemically skinned trabeculae bathed in low-Ca2+ "relaxing solution." Active force production was inhibited at all osmolalities above isosmotic. Passive (tonic) force increased to, at most, 15% of the peak active force developed under isosmotic conditions while [Ca2+]i increased, at most, 30% above its isosmotic value. We infer that hyperosmotic stimulation of resting cardiac heat production reflects, in large part, greatly increased activity of the sarcoplasmic reticular Ca2+ ATPase in the face of increased efflux via a procaine-inhibitable Ca(2+)-release channel.

Human resources for control of tuberculosis and HIV-associated tuberculosis.

The global targets for tuberculosis (TB) control were postponed from 2000 to 2005, but on current evidence a further postponement may be necessary. Of the constraints preventing these targets being met, the primary one appears to be the lack of adequately trained and qualified staff. This paper outlines: 1) the human resources and skills for global TB and human immunodeficiency virus (HIV) TB control, including the human resources for implementing the DOTS strategy, the additional human resources for implementing joint HIV-TB control strategies and what is known about human resource gaps at global level; 2) the attempts to quantify human resource gaps by focusing on a small country in sub-Saharan Africa, Malawi; and 3) the main constraints to human resources and their possible solutions, under six main headings: human resource planning; production of human resources; distribution of the work-force; motivation and staff retention; quality of existing staff; and the effect of HIV/AIDS. We recommend an urgent shift in thinking about the human resource paradigm, and exhort international policy makers and the donor community to make a concerted effort to bridge the current gaps by investing for real change.

Pump function of the feline left heart: changes with heart rate and its bearing on the energy balance.

Pump function of the feline left heart was determined by measuring the relationship between mean left ventricular pressure and mean left ventricular output, obtained by changing the arterial load on a beat-to-beat basis. The effect of a change in heart rate from 120 to 160 beats . min-1 was studied and a parallel shift of the pump function graph was found. Care was taken to keep left ventricular end-diastolic pressure constant with the change in frequency. If the mean pressure and output values obtained at 160 beats . min-1 were multiplied by the ratio between the two frequencies (0.75), almost complete superposition of the two graphs was obtained. Changes in arterial load also caused changes in oxygen consumption, mean external power and external efficiency of the heart. We plotted these variables, altered them as a function of mean left ventricular output for easy comparison with the pump function graph. It was found that oxygen consumption decreases with increasing output. Mean external power and efficiency attain maxima for different values of mean output. If the left heart in the intact animal is controlled to function at its maximum power output, this can therefore not be achieved at the optimum efficiency level. The results of the present study and those obtained earlier were compared with the behaviour of a time varying compliance model.

An analogue device for the measurement of cardiovascular variables.

An analogue device is described which is designed to analyse repetitive signals. It measures peak amplitudes, time to peak values, areas, and values at a preset time. The results can be displayed or recorded on a beat-to-beat basis, or an average can be taken over up to 31 consecutive beats.

How to quantify an arterial stenosis: a study on the femoral arteries of dog and man.

The blood supply to the femoral bed was studied in anaesthetised dogs before and after producing arterial stenoses. The blood supply system consisted of the vessels proximal to the site of measurement in the femoral artery and was characterised by a supply graph, which related mean perfusion pressure to mean flow. The different pressures and flows were obtained using an artificial periphery, the impedance of which was changed from beat to beat. The supply graph was approximated by a parabola with two parameters: the intercepts with the pressure and flow axes, the latter indicating the maximum mean flow. For constant aortic pressure the maximum mean flow appeared to be linearly related to the cross sectional area of the stenosed section (r = 0.98). Maximum mean flow was already considerably reduced before the stenosis became critical--that is, before physiological flow was measurably diminished. The change in maximum mean flow was therefore used to quantify the haemodynamic effects of stenoses that were less than critical. Blood supply graphs of the superficial femoral arteries were determined also in seven patients undergoing a femoropopliteal bypass operation. The maximum mean flow correlated well with the degree of obstruction determined from the preoperative angiograms (r = 0.90).

Measurement of left ventricular wall stress.

Forces in the myocardial wall can be measured in several ways or calculated using certain simplifying assumptions. In this study we investigated the reliability of two measurement methods, one of which was introduced by Feigl et al (1967), whereas the other method was developed in our laboratory. Both methods were tested in actively contracting skeletal muscle and beating hearts of open-chest dogs by comparing the force transferred from the muscle to the transducer under various circumstances. It appeared that changes in muscle length, be it through initial length changes or through shortening during contractions, had a great influence on the transfer of force to the transducer, for both methods, in both preparations. In the heart a decrease in internal left ventricular diameter of 15% resulted in a 50% reduction of force transferred to the transducer, independent of whether the length took place as a change in filling or as a change in ejection volume. In skeletal muscle the length-dependent effects during shortening were larger and those resulting from initial length changes were more variable than in beating hearts. That the effects of muscle length changes are of such magnitude means that, if no other errors exist, they alone would invalidate that until principally different methods of measuring wall stress in the myocardium are discovered, attempts at accurate calculation of myocardial wall stress are a better approach than wall stress measurements.

Changes of microsphere density with time in myocardial infarcts in dogs.

The density of microspheres injected before occlusion of a coronary artery, in the infarcted region [I], was compared with that of healthy, normal myocardium [N], from the same dog. The [I]/[N] ratio was measured at different days after infarction up to 2 weeks. The ratio was below unity before the ninth day and above that thereafter. The changes in microspheres density can be explained on the basis of microsphere loss from necrotic tissue and changes in infarct mass.

Reflection in the systemic arterial system: effects of aortic and carotid occlusion.

Experiments were performed in seven closed-chest anaesthetized male dogs to determine the role of pulse wave reflection in the pattern of flow and pressure in the ascending aorta. Ten days after implantation of an electromagnetic flow transducer around the ascending aorta a balloon catheter was placed in the descending aorta via the femoral arteries. At the same time a tip manometer was introduced into the ascending aorta. Aortic occlusions at three different sites caused pressure pulses with secondary systolic rises and flow pulses with biphasic deceleration. Secondary rises occurred 45 +/- 9.0 ms after the initial pressure rise for high aortic occlusion; this time was 75 +/- 8.5 ms for occlusion at the level of the diaphragm and 114 +/- 16.5 ms for occlusion near the level of the renal arteries. These times approximate the times in which the pulse travels from the tip manometer to the inflated balloons and back. Forward and reflected pressure and flow waves were calculated from reflection coefficients. Aortic occlusion caused larger reflected waves and the recorded wave forms were caused by the summation of forward and backward waves, the latter contributing the secondary pressure rise and the increased flow deceleration. Occlusion of both carotid arteries showed no specific reflection site but reflected waves were larger. This increased reflection can probably be explained as the result of greater total reflection from distributed sites under increased peripheral resistance.

Control of cardiac output in exercising dogs using different types of workload.

The system which controls cardiac output was studied in dogs during exercise on the treadmill. The aim was to investigate whether the pattern of the workload influences the control system. To measure cardiac output, electromagnetic flow probes were implanted at least 10 days before the exercise study. During the experiments cardiac output was computed on a beat-to-beat basis. We compared changes in cardiac output resulting from stepwise, sinusoidally and randomly varying workloads, obtained by changing treadmill velocity accordingly. The time constants found with sinusoidally and randomly varying workloads were 11.6 and 10.0s respectively. The time constants of the alteration in cardiac output resulting from a step function was 9.9s for the positive step and 15.6s for the negative step. However when the stepwise change in workload was between a velocity of 0.67 and 1.56 m.s-1 positive and negative steps yielded the same time constant (13.5 s). It is concluded that the pattern of the workload has no influence on the control system of cardiac output during exercise.

Geometry and pump function in cardiac ventricular hypertrophy.

Ventricular pump function can be quantified by the inverse relation between pressure and output, i.e., the pump function graph, which is obtained by varying arterial load without changing end-diastolic volume, inotropic state and heart rate. The ratio of pressure and output, i.e., the peripheral resistance, can be represented in the same graph by a line through the origin. The 2 pressure-output relations intersect in the working point, i.e., the pressure and flow at the prevailing steady state. In normal, anesthetized cats the ventricle appears to be matched to the arterial load in the sense that the working point is found at the optimal power, i.e., the optimal value of the product of pressure and output along the pump function graph. To maintain this matching criterion during pressure overload, the ventricular volume has to remain the same while thickening of the wall takes place: concentric hypertrophy. With volume overload, matching would be preserved with eccentric hypertrophy. Because volume and pressure overloads typically lead to eccentric and concentric hypertrophy, respectively, the matching criterion may be a valuable predictor of the geometric changes found with changes in load. This idea was further investigated experimentally by determining the position of the working point in the perinephritic cat that had 1 kidney removed and the other wrapped in cellophane for 15 to 26 weeks. The working point was no longer found at the optimal power, indicating that either matching was permanently comprised or that the ventricle was still trying to restore matching.

Why smaller animals have higher heart rates.

Diastolic blood pressure is the main driving pressure for coronary perfusion. Diastolic pressure depends on mean pressure and the ratio of the decay time of aortic pressure in diastole (tau) and the duration of diastole (Td). The ratio of tau, a morphological, arterial parameter, and Td, a functional, cardiac parameter, is the same in all mammals. This could mean that smaller animals have higher heart rates i.e. shorter duration of diastole to match the shorter time constant of the diastolic pressure decay and to guarantee adequate coronary perfusion.

Stretch of contracting muscle fibres: evidence for regularly spaced active sites along the filaments and enhanced mechanical performance.

Single frog skeletal muscle fibres were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a mean critical length change of 16.6 nm per half sarcomere that was independent of stretch velocity and sarcomere length. The early decaying extra force after stretch (component 2) was removed by a small quick release, leaving a longer lasting component (component 3). The amplitude of release required increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch (above). Component 3 occurred at sarcomere lengths above 2.3 microns and was amplitude dependent. The final force after stretch was usually higher than the isometric force at the starting length of the stretch. Non-uniformity as a cause of this component was examined by (a) laser diffraction studies which showed sarcomere stretch at all locations and (b) 0.6-0.7 mm long segments along the entire fibre which all elongated during stretch. After stretch the sarcomeres and segments were significantly more stable than during control isometric tetani. Segments which were clamped by a servo system demonstrated component 3. Shortening during contraction followed by stretch back to the starting length led to nearly as much force enhancement as stretch alone, suggesting that component 3 is not due to a passive elastic element recruited during activation. An increase in temperature decreased components 1 (velocity dependent force during stretch) and 2 but increased component 3. The critical length features of component 2 suggest a cross-bridge mechanism. However, the sarcomere length dependence of all components differs from that of isometric force and from predictions based on filament overlap.

The energetics of work and heat production by single muscle fibres from the frog.

During active shortening the heat rate in isolated muscle fibres is greater than during isometric contraction, and increases with velocity of shortening (V), but at a decreasing rate as the maximum velocity (V0) is approached. For shortening at V less than 0.25 V0 the amount of extra heat produced during a period of shortening is proportional to the distance shortened, but for rapid shortening (V greater than 0.5 V0) the extra heat increases less than proportionally with the distance shortened. After a period of shortening the higher heat rate returns to the isometric level over a period of several hundred milliseconds. A similar period of increased heat rate is seen after a quick release. After shortening 10% of muscles slack length at 0.1 V0 the amount of heat produced during tension redevelopment is similar to that after a quick release. But after more rapid shortening there is less heat production than after a quick release.

['Public health status and perspectives' 1997. I. Introduction]. / 'Volksgezondheid toekomst verkenning' 1997. I. Introductie.

The 'Public health status and forecasts' 1997 presents a comprehensive and integrated overview of health, disease and health care in the Netherlands, to which more than 250 experts contributed. On the basis of the findings, policy recommendations are formulated regarding target groups, planning, prevention, health care, monitoring and research.