Biomedical subjects
Publications and source records attributed to A Hurwitz.
Adequate heparinization is considered to prevent stroke in pregnant women with prosthetic heart valves. A 21-year-old pregnant woman with a Starr-Eduards prosthetic mitral valve and atrial fibrillation experienced repeated cerebral embolic events despite full heparinization.
Increasing doses of clonidine enhanced the retention of sulfobromophthalein (BSP) in plasma and liver, while reducing elimination of this dye into bile. The ED50 of clonidine for these effects was 0.05 to 0.2 mg/kg s.c. In clonidine-treated mice which were warmed to reverse drug-induced hypothermia, plasma and liver BSP levels were raised as compared to saline-treated mice. Clonidine also raised plasma and liver levels of the BSP analog, dibromosulfophthalein, which is not conjugated before biliary elimination. Hepatic glutathione levels, activity of glutathione-S-transferase and ratios of conjugated to unconjugated BSP were not affected by clonidine. In mice with cannulas in their common bile ducts to prevent duct spasm, clonidine reduced the amounts of BSP eliminated into bile. Thus, the alpha-2 adrenoceptor agonist, clonidine, raised plasma and liver levels of anionic dyes and reduced their levels in bile by mechanisms other than altered conjugation, hypothermia or bile duct spasm.
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The management of preterm rupture of membranes (ROM) is controversial. Some advise immediate delivery and others advocate conservative approach in the hope of decreasing morbidity and mortality rates associated with prematurity. A retrospective review of 75 pregnancies with preterm ROM treated conservatively was performed to delineate the relative risk factors. All patients with preterm ROM were placed at bed rest until either labor or chorioamnionitis prompted delivery. Chorioamnionitis developed in 25% of the cases. The percentage of women developing chorioamnionitis increased with duration of ROM. Fetal morbidity and mortality was not increased in the group with chorioamnionitis. Hyaline membrane disease (HMD) and intra ventricular hemorrhage (IVH) were the major causes of neonatal death in the entire group of preterm ROM. There was a significant relationship between neonatal mortality and birth weight. The smaller the birth weight, the greater the risk of neonatal death. Our data support the conservative approach to preterm ROM especially in the very low birth weight group where extreme caution must be taken before a decision is made to terminate pregnancy.
Uterine anomalies are one of the various processes in the pelvic organs which present themselves as adnexal masses in pregnancy. In pregnancy associated with congenital uterine anomalies, complications are likely to occur. Ultrasonography is of great importance in early recognition of the anomalies, which can prevent unnecessary surgical intervention. A case of ultrasonic detection of uterus didelphys with unicavitary pregnancy is described.
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Morphine, 20 mg X kg-1, sc, halved the plasma clearance of sulfobromophthalein (BSP) while tripling hepatic tissue levels of this dye. Since narcotics depress respiration, effects of hypoxia, hypercapnia, and acidosis on BSP disposition were studied. Ambient gases breathed by rats were adjusted to achieve blood gas levels identical to those of morphine-induced respiratory depression. Saline-treated rats breathing room air had PAO2 of 87 +/- 3 mmHg (mean +/- SE) and PaCO2 of 40 +/- 2 mmHg. After intraarterial injection of BSP, 100 mg X kg-1, plasma clearance of this dye was 7.1 +/- 1.1 ml X min-1 and BSP levels in the liver at 40 min after injection were 163.3 +/- 19.8 micrograms X g-1. After morphine, 20 mg X kg-1, PaO2 decreased to 47 +/- 4 mmHg and PaCO2 increased to 89 +/- 5 mmHg. In these rats BSP clearance dropped to 3.5 +/- 0.4 ml X min-1, and 40-min liver dye levels were increased to 596.4 +/- 60.4 micrograms X g-1. Similar hypoxia and hypercapnia caused by breathing 9% O2 and 8% CO2 in the absence of morphine caused plasma BSP clearance to be decreased to 4.4 +/- 0.2 ml X min-1 and 40-min hepatic BSP to be increased to 292.5 +/- 31.8 micrograms X g-1. Hypercapnia and acidosis alone did not affect BSP disposition, while hypoxia without hypercapnia decreased its plasma clearance to 5.5 +/- 0.3 ml X min-1 and increased liver levels to 339.1 +/- 35.1 micrograms X g-1. Hypoxia was reversed completely in morphine-treated rats by placing them in 40% O2. In these animals, despite normal oxygen, plasma BSP clearance was decreased to 4.4 +/- 0.6 ml X min-1, and liver BSP was increased to 497.9 +/- 65.6 micrograms X g-1. Thus, respiratory depression with hypoxia may contribute to morphine-induced effects on BSP disposition, but altered blood gases cannot account fully for these narcotic effects.
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A case is described of antenatal detection of a placental mass by ultrasound in a patient with hydramnios due to chorioangioma and who had a sinusoidal-like pattern and positive oxytocin challenge test (OCT). The importance of frequent fetal heart rate monitoring in cases of suspected chorioangioma is emphasized.
Ascending morphine doses above 5 mg/kg s.c. progressively reduced plasma clearance of sulfobromophthalein (BSP) and raised hepatic levels of this dye in rats. The narcotic reduced the elimination constant of BSP without affecting its volume of distribution. Because abdominal surgery markedly reduced plasma clearance of BSP, no further effect of morphine could be shown in rats with bile cannulas. In duct-cannulated animals morphine had no effect on BSP concentration in bile, but did raise hepatic BSP levels while reducing bile flow and biliary BSP content. The narcotic also lowered the biliary transport maximum of BSP. The effects on BSP disposition were demonstrated acutely after morphine administration but had subsided completely by 1 and 2 days after giving narcotic. The present findings suggest that morphine impaired the secretion of BSP into bile by a mechanism not involving biliary occlusion and thereby enhanced retention of this dye in liver and plasma.
We studied the growth of calcium oxalate monohydrate (COM) crystals in stirred suspensions by following the changes in ionic conductivity of supersaturated solutions at 25 +/- 0.02C. At a pH of 6.9-7.2, in the presence of polyphosphate ion, crystallization proceeded by an initial rapid step followed by a markedly reduced growth rate as compared with that in pure supersaturated solution. The initial surge was reduced as the polyphosphate concentration reached 1.6 X 10(-6) M, which can be interpreted as evidence of either surface nucleation or the incomplete adsorption of inhibitor at the active growth sites. In spontaneous precipitation experiments made in the presence of polyphosphate ions, the formation of calcium oxalate dihydrate and trihydrate is favored together with appreciable coprecipitation of additive ions.
The quarternary ammonium antimuscarinic drugs propantheline bromide and clidinium bromide, given orally at the usual therapeutic doses, delayed gastric emptying of a swallowed radiolabeled liquid meal as measured by a gamma camera. Delay of emptying was dose dependent. If an identical meal was given by gastric tube, there was no slowing of emptying by propantheline in the group as a whole. Six subjects who emptied the intubated meal more quickly with placebo had slowed emptying after 30 mg propantheline. In five others, intubation alone slowed gastric emptying while the addition of 30 mg propantheline caused a paradoxical acceleration of gastric emptying. Clidinium bromide, 5 mg, delayed gastric emptying to the same extent as 15 mg propantheline bromide without the marked suppression of salivary secretion induced by the latter.
The authors studied the elimination of disulfiram and its metabolites for 24 hours after disulfiram administration in five healthy male alcoholic volunteers. Using high-performance liquid chromatography, they found that a single 500-mg dose resulted in a gradual increase in plasma disulfiram and its metabolites, with peak levels generally occurring 8 hours after dosing. There was considerable interpatient variability (e.g., in one volunteer no disulfiram was detected during the entire 24-hour sampling period). The authors also found that breath carbon disulfide was 9.1% of the dose of disulfiram administered, which is less than that expected theoretically.
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alpha-Adrenoceptor blockade after placebo and 5-mg oral doses of prazosin was assessed in five normal subjects over a range of phenylephrine infusion rates. Systolic blood pressure during a 400-microgram/min infusion of phenylephrine at 3 hr after placebo or prazosin was 172.8 +/- 6.2 and 108.7 +/- 4.4 mm Hg (p less than 0.05). The phenylephrine effects were blocked from 1 hr to at least 7 hr after prazosin. The drug-sensitivity ratio, an indicator of alpha-adrenoceptor blockade, before prazosin was 1.1, rising to 4 at 1 hr, 4.9 at 3 hr, 5.7 at 5 hr, and 4 at 7 hr after oral prazosin. The highest prazosin plasma concentration after a 5-mg oral dose was 29.3 +/- 6.6 ng/ml. It occurred 1 hr after prazosin. The elimination half-life was 2.9 +/- 0.3 hr. After oral prazosin the alpha-adrenoceptor blockade response did not correlate with prazosin plasma concentration.
The double sampling method for measuring gastric volumes is analysed mathematically. It is shown to cause magnification of randomly occurring analytical errors in dye concentration. The errors which arise in calculated gastric volume depend on extent of analytical error, concentration of dye initially placed in the stomach, repetition of analysis cycle, and ratio of volume of added dye to gastric volume. By starting with dye-free water and doubling the concentration of dye added in serial volume determinations the error in calculated volume is markedly reduced and no longer increases with successive measurements. These modifications reduce the limitations inherent in the method as originally described.
Morphine administration reduces phenol red clearance in mice. Increasing subcutaneous morphine doses from 10 to 40 mg/kg caused a progressive increase in plasma phenol red concentrations and reduced dye elimination in urine. Intravenous phenol red given at 50 to 200 mg/kg was cleared from plasma at 24 to 30 microliters/min/kg b. wt. At these dosages of dye plasma clearance of phenol red was reduced at least 33% by morphine pretreatment (20 mg/kg s.c.). Lowered dye clearance by morphine was reflected in smaller apparent volumes of phenol red distribution. The morphine effect on the elimination constant (kel) of phenol red was variable. The narcotic caused a rise in kel at the lowest phenol red dose and lowered this constant at the high phenol red dose. Like morphine, hydromorphone and methadone had an antidiuretic effect in mice and reduced renal elimination of phenol red. Naloxone had no effect on phenol red disposition but reversed completely the effect of morphine. This finding shows that the effect of the narcotic was not due to competition or displacement from transport sites. Morphine did not cause a change in urine pH. Since the urine did not become more acidic after morphine, back diffusion of undissociated due is not likely as the cause of its reduced renal elimination. Reduced renal elimination of phenol red by narcotics is probably due to reduced renal blood flow and glomerular filtration as shown by lowered p-aminohippurate and iothalamate clearance in mice.