Biomedical subjects
R T Kelly
Publications and source records attributed to R T Kelly.
Temporal and receptor correlates of the estrogen response in sheep.
Uterine blood flow and uterine cytosol and nuclear estrogen receptors were measured at critical times during estradiol-induced vasodilatation in acute anesthetized and chronic conscious sheep preparations at estradiol bolus injection frequencies from 1 to 24 hours. During acute experiments, the uterine blood flow response was muted and cytosol estrogen receptor replenishment did not occur whereas full replenishment occurred in 12 hours in conscious ewes. In ewes treated with daily estradiol that had a stable daily uterine blood flow response, the uterine blood flow response 24 hours after uterine biopsy was similar to the preoperative one. Analysis of the duration of peak uterine blood flow levels and the rate of uterine blood flow descent from peak levels showed that an interval of 18 hours between estradiol injections was necessary for the uterine blood flow response to approximate that observed after 24 hours. These observations suggest: (1) that uterine vascular receptor replenishment is delayed compared with that of the total uterus; (2) that operative stress compromises cytosol estrogen receptor metabolism and possibly nuclear estrogen receptor function; (3) that the delayed maximum uterine blood flow response to estradiol in ewes previously untreated with estradiol is due to a trophic uterine effect of daily estradiol stimulation.
Variable decelerations during nonstress tests are not a sign of fetal compromise.
An examination of 908 fetal heart rate tests of 418 consecutive patients revealed brief variable decelerations in more than 50.7% of the patients. Although an association existed with nuchal cord location found at delivery, no association existed between these variable decelerations and fetal heart rate decelerations during labor, low Apgar scores at birth, or birth weight. We find no evidence to suggest that these brief variable decelerations are a sign of fetal compromise or an indication for obstetric intervention.
Catecholamine responses in fetal lambs subjected to hemorrhage.
We monitored plasma epinephrine and norepinephrine responses to hemorrhage of 20% of estimated blood volume in 11 chronically instrumented, unanesthetized fetal lambs. In addition, we performed control experiments--blood sampling but no hemorrhage--in five fetuses. Arterial blood gases, pH, mean arterial pressures, heart rates, and plasma norepinephrine and epinephrine levels were similar in both groups in the resting state. Arterial blood gases and pH did not change significantly during the experimental period in either group. Mean arterial pressure, heart rate, and plasma norepinephrine and epinephrine levels did not change in the control group during the experimental period. Hemorrhage was associated with a significant decrease in fetal mean arterial pressure, 39.8 +/- 1.2 to 29.6 +/- 2.1 mm Hg, and heart rate, 186 +/- 8 to 146 +/- 6 bpm (p less than 0.01 in both cases). There was a significant increase in plasma norepinephrine, 664.9 +/- 91.6 to 1384.8 +/- 216.7 pg/ml (p less than 0.02) and epinephrine, 224.6 +/- 43.6 to 681.7 +/- 199.0 pg/ml (p less than 0.01) with hemorrhage. These results demonstrate significant catecholamine responses to hypovolemia in the fetal lamb.
Vasopressin is important for restoring cardiovascular homeostasis in fetal lambs subjected to hemorrhage.
To determine if the posterior pituitary hormone vasopressin is important for maintaining fetal cardiovascular homeostasis during hypovolemic stress, in seven chronically catheterized fetal lambs we induced hemorrhage of 20% of estimated blood volume in the presence and in the absence of a potent antagonist to the pressor effects of vasopressin. The study was a paired crossover design with at least 48 hours separating experiments in the same animal. Injection of the vasopressin antagonist did not alter basal fetal heart rate or arterial blood pressure, but hemorrhage of 2% of estimated fetal blood volume per minute for 10 minutes produced a greater fall in blood pressure (13 +/- 2 versus 10 +/- 2 torr, p less than 0.05) when the blocker was present than when it was absent. Arterial blood pressure remained below control levels longer following hemorrhage when the fetuses were pretreated with the antagonist (49.7 +/- 6 versus 26.6 +/- 6 minutes, p less than 0.01), and the integrated fall in arterial blood pressure with hemorrhage was greatest (283 +/- 53 versus 169 +/- 57 mm Hg . min p less than 0.01) when the blocker was used. The fall in heart rate following hemorrhage was similar with and without blocker pretreatment. These results indicate that vasopressin plays a physiologic role in blood pressure regulation in fetal lambs during periods of hypovolemia.
Use of avidin-biotinylated horseradish peroxidase complex for visualization of spirochetes.
The use of avidin-biotinylated peroxidase as a simple technique for light microscopic visualization of spirochetes is described. The three major genera of spirochetes--Treponema, Borrelia, and Leptospira--were stained with the avidin complex.
A vasopressin antagonist blocks the norepinephrine and epinephrine responses to hemorrhage in the fetus.
In 8 chronically cannulated fetal lambs between 119 and 127 days gestation the resting plasma norepinephrine concentration was 528 +/- 77 pg X ml-1 and the resting plasma epinephrine concentration 159 +/- 42 pg X ml-1. Hemorrhage of 20% of estimated blood volume at 2% per min produced a 2.1-fold increase in plasma norepinephrine levels and a 3.4-fold increase in plasma epinephrine levels when the animals were pretreated with an injection of saline (1 ml). Plasma catecholamine levels returned toward control values following return of the shed blood. In contrast, hemorrhage of these animals following pretreatment with an antagonist of the pressor effect of vasopressin did not cause an increase in fetal plasma catecholamine levels. Thus, vasopressin may mediate the sympathetic responses to volume depletion in the fetus.
American Medical Association. American medicine in the 1980s.
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Particulate matter in the atmosphere.
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Asbetos--health hazards in perspective. Constructional uses.
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Interaction effects of achievement need and situational press on performance.
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Responsibility for rising health care costs.
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Physician associate program.
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Neuraminidase activities of clinical isolates of Diplococcus pneumoniae.
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Neuraminidase activity in Diplococcus pneumoniae.
Kelly, R. T. (Marquette University School of Medicine, Milwaukee, Wis.), D. Greiff, and S. Farmer. Neuraminidase activity in Diplococcus pneumoniae. J. Bacteriol. 91:601-603. 1966.-A method for the quantitation of neuraminidase in the presence of N-acetylneuraminic acid aldolase is described. The neuraminidase content of Diplococcus pneumoniae was found to be dependent on the media employed for growth; the highest enzyme activity per milligram of bacterial protein was obtained with Todd-Hewitt broth. Neuraminidase production was stimulated in D. pneumoniae by the addition of N-acetylneuraminlactose, N-acetylneuraminic acid, or N-acetylmannosamine to the growth medium. Three rough strains of D. pneumoniae, which were nonpathogenic for mice, lacked neuraminidase activity. Seven of 12 smooth strains contained neuraminidase; enzyme activity was not detected in the remaining 5 smooth strains. There was no correlation between the presence of neuraminidase activity and the capsular type or between neuraminidase production and animal virulence.
Cryotolerance of enzymes. I. Freezing of lactic dehydrogenase.
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