Are there gender differences in the use of peak flow meters?

To determine if there are gender differences in correct use of peak flow meters (PEM), third-year doctor of pharmacy students (n = 83; 52 females, 31 males) were instructed in a classroom on correct use of a PFM, including demonstrations. Students were then immediately divided into five groups, given a PFM, and assessed for three attempts in private individual sessions. Males had superior performance on the first attempt for total score (p < 0.05) and for "inhale fully" (p < 0.05). On the second attempt, the total score was not different, but males scored higher on "exhale as fast and as hard as you can" (p < 0.05). Controlled gender studies examining use of PFM in adult and pediatric patients with asthma are warranted.     

Functional hepatic flow in patients with liver cirrhosis

AIM:To evaluate hepatic reserve function by investigatingthe change of functional hepatic flow and total hepatic flowin cirrhotic patients with portal hypertension.METHODS:HPLC method was employed for the determinationof concentration of D-sorbitol in human plasma and urine.Thefunctional hepatic flow (FHF) and total hepatic flow (THF)were determined by means of modified hepatic clearanceof D-sorbitol combined with duplex doppler color sonographyin 20 patients with cirrhosis and 10 healthy volunteers.RESULTS:FHF,evaluated by means of the D-sorbitol clearance,was significantly reduced in patients with cirrhosis in comparisonto controls (764.74±167.91 Vs i 195.04±242.97 mL/min,P<0.01).While THF was significantly increased in patientswith cirrhosis in comparison to controls (1605.23±279.99vs 1 256.12±198.34 mL/min,P<0.01).Portal blood flow andhepatic artery flow all were increased in cirrhosis comparedto controls (P<0.05 and P<0.01).D-sorbitol total clearancewas significantly reduced in cirrhosis compared to control(P<0.01),while D-sorbitol renal clearance was significantlyincreased in cirrhosis (P<0.05).In controls FHF was similar toTHF (1195.05±242.97 vs 1 256.12±198.34 mL/min,P=0.636),while FHF was significantly reduced compared with THF incirrhosis (764.74±167.91 vs 1605.23±279.99 mL/min,P<0.01).CONCLUSION:Our method that combined modified hepaticclearance of D-sorbitol with duplex doppler color sonographyis effective in the measurement of FHF and THF.FHF canbe used to estimate hepatic reserve function.     

Can regurgitant flow damage the left atrial endothelium in patients with prosthetic mechanical heart valves?

BACKGROUND AND AIM OF THE STUDY: Previous in-vitro studies of mechanical heart valves (MHVs) in the closed position demonstrated the formation of regurgitant flows, with bubbles and jets forming vortices during each systole. The study aim was to determine whether the regurgitant flow observed in patients with MHVs can damage the left atrial endothelium, due to shear stresses exerted on the endothelial layers. This objective has been accomplished by appropriate in-vitro simulation experiments. METHODS: In these experiments, leakage flow through several commercial MHVs was investigated. The geometry of the set-up closely resembled that of the left atrial anatomy. Water was forced through the slit of a closed MHV and directed toward the hemispherical cup coated with fluorescent paint. The flow field between the valve and the cup was photographed using high-speed videography, from which local velocities were measured, using digital particle imaging velocimetry. Qualitative damage to the surface of the cup was assessed from the amount of fluorescent paint removed from the cup. RESULTS: The experimental results and calculations indicated that flows through the gaps of the closed valves were sufficient to generate strong vortices, with velocities near the atrial wall in the range of 0.5 to 4.0 m/s, depending on the valve. This led to high shear stresses on the left atrial wall, which far exceeded physiologically acceptable levels. CONCLUSION: The calculated shear stresses exceeded by orders of magnitude the maximum physiologically tolerated stresses. This suggests that shear stresses associated with regurgitant jets in MHVs may damage the endothelial cells, leading to the activation of the inflammatory reaction, enhanced procoagulation, platelet activation and aggregation, and mechanical cell denudation.     

Is the blood flow in the left ventricle during the isovolumic relaxation period a useful parameter of left ventricular systolic and early diastolic performance?

Left ventricular (LV) early diastolic performance is determined by LV behavior in the late systole to early diastole and may relate to the physical potential of patients. Isovolumic relaxation flow (IRF) velocity was obtained by continuous Doppler echocardiography in the left ventricle from the apex in 26 patients with atypical chest pain and 63 patients with coronary artery disease (CAD) with or without prior myocardial infarction (MI) who underwent cardiac catheterization. In each patient, a time constant of LV relaxation (tau) was calculated from the LV pressure waves obtained by a catheter-tipped micromanometer. The LV end-systolic volume index was measured using contrast left ventriculography. IRF velocity in patients having CAD with prior MI (24.8 +/- 5.4 cm/s) was significantly less than in those with atypical chest pain (41.2 +/- 9.6 cm/s). It was also significantly less than in patients having CAD without prior MI (37.3 +/- 6.8 cm/s). IRF velocity significantly correlated with the time constant tau (r = -0.42, p < 0.001) and LV end-systolic volume index (r = -0.84, p < 0.001). This study indicates that IRF velocity obtained by continuous Doppler echocardiography in the left ventricle provides important information regarding LV systolic performance and early diastolic performance.     

Lessons learned from the TIMI trials in rescue interventions for elderly patients after failed fibrinolytic therapy:look beyond the TIMI flow

In ST-segment elevation myocardial infarction (STEMI ), acute reperfusion of the infarct-related artery (IRA) is the main goal in the early minutes after the patient seeks medical attention. Fibrinolytic therapy (FT) and/or primary coronary intervention (PCI) were proven to be effective in opening the IRA.     

Incorporating flow cytometry and next-generation sequencing in the diagnosis of CMML. Are we ready for prime?

In the last version of the WHO classification of myeloid malignancies, flow cytometry and molecular investigation are listed as potentially useful, yet non-essential diagnostic tools in hard-to-recognize chronic myelomonocytic leukemias (CMML). Flow recognition of CMML was initially based on an increase in the fraction of peripheral blood, CD14⁺,CD16^- classical monocytes ≥94% of total monocytes. An associated inflammatory disease can preclude the detection of classical monocyte fraction increase by inducing accumulation of CD14⁺,CD16⁺ intermediate monocytes. In such a situation, decrease in the Slan⁺,CD14^low,CD16⁺ non-classical monocyte fraction below 1.7% still supports CMML diagnosis. This robust, two-step flow cytometry assay identifies CMML with a very high sensitivity. Otherwise, detection of one or several acquired gene mutations with high variant allele frequency supports the diagnosis of CMML, oligomonocytic CMML or clonal monocytosis of clinical significance. Together, recent investigations support integration of flow cytometry analysis of peripheral blood monocyte subsets and new generation sequencing of a panel of 20–30 recurrently mutated genes in the diagnostic work-up of CMML.     

Acidosis in muscle tissue distal to vascular contusion despite unchanged global blood flow in rats: an uncoupling of microvascular blood flow and metabolism?

Studies using a contusion trauma model have shown that the femoral artery of the rat remains patent in 85% despite a severe vessel injury. A significant increase in tissue oxygenation (PtO2) has been found despite only a minor effect on blood flow (<20% decrease) on the muscle surface distal to the injury indicating a disturbed relationship between microvascular blood flow and metabolism. The aim of the present study was to further study the interplay between microvascular blood flow and metabolism within the distal muscle using an ethanol clearance technique (blood flow) in conjunction to the determination of an ischemia marker (lactate) by use of microdialysis. Although skeletal muscle blood flow remained unaltered as assessed by ethanol clearance, skeletal muscle lactate levels increased significantly (P<0.001) post-trauma in both legs. The increase was initially higher, faster and the increase over time larger in the trauma leg as compared to the control leg (P<0.001). These findings indicate a systemic effect of the trauma. Further, it suggests a functional impairment of the relationship between microvascular blood flow and/or muscle metabolic processes when the trauma is directed towards the supplying blood vessel. The reason for this anaerobic insult as found in this study compared to the presence of a local increase in PtO2 in the trauma leg as shown in our previous study is suggestive of an microvascular blood flow and tissue metabolism uncoupling.     

Post–conditioning reduces infarct size in the isolated rat heart: Role of coronary flow and pressure and the nitric oxide/cGMP pathway

We aimed to assess the role of the nitric oxide (NO)–cGMP pathway in cardioprotection by brief intermittent ischemias at the onset of reperfusion (i.e., post–conditioning (Post–con)). We also evaluated the role of coronary flow and pressure in Post–con. Rat isolated hearts perfused at constant– flow or –pressure underwent 30 min global ischemia and 120 min reperfusion. Post–con obtained with brief ischemias of different duration (modified, MPost–con) was compared with Post–con obtained with ischemias of identical duration (classical, C–Post–con) and with ischemic preconditioning (IP). Infarct size was evaluated using nitro–blue tetrazolium staining and lactate dehydrogenase (LDH) release. In the groups, NO synthase (NOS) or guanylyl–cyclase (GC) was inhibited with LNAME and ODQ, respectively. In the subgroups, the enzyme immunoassay technique was used to quantify cGMP release. In the constant–flow model, M–Post–con and C–Post–con were equally effective, but more effective than IP in reducing infarct size. The cardioprotection by M–Post–con was only blunted by the NOS–inhibitor, but was abolished by the GC–antagonist. Post–ischemic cGMP release was enhanced by MPost–con. In the constant–pressure model IP, M–Post–con and C–Post–con were equally effective in reducing infarct size. Post–con protocols were more effective in the constant–flow than in the constant–pressure model. In all groups, LDH release during reperfusion was proportional to infarct size. In conclusion, Post–con depends upon GC activation, which can be achieved by NOS–dependent and NOS–independent pathways. The benefits of M– and CPost–con are similar. However, protection by Post–con is greater in the constant–flow than in the constant–pressure model.