Fetal umbilical artery flow velocity waveforms and placental resistance: clinical significance

Summary. Since the umbilical arteries carry fetal blood to the placenta we studied flow velocity waveforms in these vessels with a simple continuous wave Doppler system to assess placental blood flow. The ratio of peak systolic to least diastolic (A/B) flow velocity was measured as an index of placental flow resistance. In 15 normal pregnancies there was a small but significant decrease in this ratio through the last trimester. The A/B ratio was measured on 436 occasions in 168 high-risk pregnancies. In 32 of 43 fetuses subsequently shown to be small for gestational age there was an increase in placental flow resistance with reduced, absent or even reversed flow in diastole. This finding was also present in the one fetus which died in utero . Serial studies in patients with fetal compromise indicated increasing flow resistance, a reverse of the normal trend. These results were not available to the clinician yet of 24 fetuses born before 32 weeks 13 had a high A/B ratio, and all of them were born electively. Maternal hypertension was associated with an increase in fetal placental flow resistance. The umbilical artery A/B ratio provides a new and non-invasive measure of fetoplacental blood flow resistance.     

Randomized controlled trial of oral captopril, of oral isosorbide mononitrate and of intravenous magnesium sulphate started early in acute myocardial infarction: safety and haemodynamic effects: ISIS-4 (Fourth International Study of Infarct Survival) Pilot Study Investigators

The purpose of this randomized controlled study was to assessthe haemodynamic effects, safety and tolerability in acute myocardialinfarction (AMI) of one month of oral captopril, one month oforal isosorbide mononitrate and 24 h of intravenous magnesium.It was carried out in four United Kingdom and six Polish hospitalsin consecutive phases; oral captopril vs oral mononitrate vsplacebo were compared among 400 patients in a ‘three-way’study; and then oral captopril vs placebo and oral mononitratevs placebo were compared among 474 patients in ‘2x2’and ‘2 x 2 x 2’ factorial studies (with 208 patientsin the latter study also randomized between intravenous magnesiumand open control). The factorial studies differed from the three-waystudy in that one group of patients was allocated both oralcaptopril and oral mononitrate, a higher maintenance dose ofcaptopril was used (following the same initial dose), and oncedaily controiled-release mononitrate was used. In the three-waystudy, the mean of the lowest systolic blood pressures recordedduring the first 4 h after randomization were (mmHg ±standard error): 104 ± 2 captopril vs 105 ± 1mononitrate vs 112 ±2 placebo (P<0.001 for captoprilor for mononitrate vs placebo), and in the factorial studieswere 105 ± 1 captopril vs 110 ± 1 placebo (P<0.01)and 106 ± 1 mononitrate vs 108 ±1 placebo (NS).There was an excess of hypotension recorded among patients allocatedactive treatment (captopril>mononitrate>placebo) and therewas a small, but significant, excess of cardiogenic shock withcaptopril compared with control in the factorial study. However,in these studies, neither captopril nor mononitrate were associatedwith any overall increase in the incidence of hypotension consideredsevere enough to lead to treatment being stopped. No other seriouscomplications were observed, and compliance with study tabletsat hospital discharge was not significantly different betweenthe active and placebo groups. Patients allocated magnesiumin the 2 x 2 x 2 factorial study had a slightly lower mean systolicblood pressure just after the initial 15 min bolus injection(126 ± 2 magnesium vs 134 ± 3 control; P<0.05)but there were no significant differences during the subsequent24 h maintenance infusion period. Apart from some facial flushing,magnesium did not appear to be associated with any complications.These pilot studies indicate that, although the study treatmentregimens produced moderate early reductions in blood pressure,they were all generally well tolerated when started in the acutephase of MI.     

Structural relationships between immune cells and longitudinal muscle during a Trichinella spiralis infection in the rat intestine

A Trichinella spiralis infection produces an acute inflammatory reaction and tissue damage in the mucosa, and, in addition, functional changes occur in the external muscle layers. The aim of the present study was to characterize structural changes in the musculature that occur during early infection, and to identify relationships between immune cells and muscle cells, as part of an ongoing investigation into the immune modulation of motor function in the gut. Rats were infected with T. spiralis larvae and the gut fixed at 12 h, 24 h, 48 h and 6 days post-infection for electron microscopy of the longitudinal muscle. Macrophages and lymphocytes penetrated the longitudinal musculature 12-24 h post-infection. Distinct contacts were observed between specific cell types; cellular protrusions from macrophages or lymphocytes made close apposition contacts with smooth muscle cells. Resident macrophages in the subserosal space, fibroblast-like cells as well as smooth muscle cells showed marked activation during inflammation. Fibroblast-like cells were frequently seen intercalated between lymphocytes and smooth muscle cells, hence they may mediate communication between immune cells and the musculature.