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T K Rowles

Publications and source records attributed to T K Rowles.

10 recordsLinked to original sources
PubMed1995

Thermoregulation of the intra-abdominal testes of the bottlenose dolphin (Tursiops truncatus) during exercise.

Dolphins possess a vascular countercurrent heat exchanger (CCHE) that functions to cool their intra-abdominal testes. Spermatic arteries in the posterior abdomen are juxtaposed to veins returning cooled blood from the surfaces of the dorsal fin and tail flukes. In this study, we investigated the effect of exercise on CCHE function in the bottlenose dolphin. The CCHE flanks a region of the bowel in the posterior abdomen and influences colonic temperatures. A rectal probe housing a linear array of seven copper-constantan thermocouples was designed to measure colonic temperatures simultaneously at positions anterior to, within and posterior to the region of the colon flanked by the CCHE. Immediately after vigorous swimming, temperatures at the CCHE decreased relative to resting and pre-swim values: post-swim temperatures at the CCHE were maximally 0.5 degrees C cooler than pre-swim temperatures. These data suggest that the CCHE has an increased ability to cool the arterial blood supply to the testes when the dolphin is swimming. This ability could offset the increased thermal load on the testes is an exercising dolphin. To the best of our knowledge, this is the first report of deep body cooling in an exercising mammal that is not undertaking a dive.

Animals↗
PubMed1994

Ridogrel improves maternal/fetal homeostasis in an ovine model of pregnancy-induced hypertension.

The effects of ridogrel (a thromboxane synthetase inhibitor/endoperoxide receptor antagonist) were assessed in an ovine model of pregnancy-induced hypertension. Maternal serum prostacyclin and thromboxane levels were quanitiated using RIA, and maternal and neonatal coagulation status was assessed. Pregnancy and neonatal outcome were recorded. Ridogrel, (E)-5-[[[3-pyridinyl)[3-(trifluoromethyl)phenyl]methylen]amin++ +] oxy]pentanoic acid, was administered in one bolus dose at 0.1 or 1.0 mg/kg IV, three hours following the onset of a 27 hour magnesium sulfate infusion given hypertensive ewes to prevent maternal seizures. At both doses, ridogrel improved neonatal outcome (0% neonatal mortality in each ridogrel group versus 67% neonatal mortality in the magnesium sulfate group), and ridogrel at 0.1 mg/kg IV normalized birth weights. Abnormalities of maternal platelet function (abnormal or no response to collagen), occurring during the ovine syndrome, resolved following ridogrel treatment. Ridogrel's effects on maternal and neonatal coagulation were more dramatic at the 0.1 mg/kg IV dose. Ridogrel appeared to be beneficial in this model of pregnancy-induced hypertension.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Morphological alterations of neurons and astrocytes in guinea pigs exposed to low levels of inorganic lead.

Both astrocytes and neurons potentially undergo structural and functional alterations in the brains of animals exposed to low levels of lead (Pb). No morphometric studies of astrocytes have been reported to date in animals in low Pb exposure. In the present study, morphometric measurements of astrocytes and pyramidal neurons in the frontoparietal cortex were made in guinea pigs exposed postnatally (5 or 10 days) or prenatally (gestational day 22 to birth) to low Pb levels. Although few significant effects of Pb treatment were detected by the rigorous statistical model applied, a recurring trend was noted for postnatal Pb treatment to increase astrocyte maximum diameter (dmax). In addition, prenatal Pb treatment was associated with increased apical and basal dendritic length, increased total apical dendrites per cell and an increased basal branching complexity in neurons.

Animals↗
PubMed1992

Toxicology of carbaryl and aldicarb on brain and limb cultures of chick embryos.

A variety of carbamates have been developed since the 1960s for use as broad-spectrum insecticides. An easy and inexpensive in vitro assay using chick-embryo derived cells was examined for its capability to screen and test the toxicity of these compounds. Chick embryo brain and limb bud cultures were treated with different concentrations of either carbaryl or aldicarb with or without activation (+/- S-9) for 5 days. Viability and cytotoxicity using the neutral red assay, and carbamate effects on cell migration and colony spread were measured. S-9 decreased the effects of carbaryl and aldicarb on brain cell cytotoxicity at exposures of 15-60 ppm and 40-200 ppm, respectively, as indicated by increased concentrations of neutral red. Viability of brain cell cultures was not altered by aldicarb, but was decreased by carbaryl plus S-9 in concentrations of greater than 40 ppm. In limb cultures, carbaryl without S-9 was significantly toxic at 8-25 ppm, but only concentrations of greater than 25 ppm of carbaryl plus S-9 significantly affected cytotoxicity. In contrast, aldicarb without S-9 caused no effect on limb cell cytotoxicity at concentrations of 40-200 ppm, but aldicarb plus S-9 significantly reduced cellular cytotoxicity at concentrations of greater than 160 ppm. Carbaryl +/- S-9 decreased the spread of both brain and limb colonies; aldicarb +/- S-9 caused a significant increase in the spread of the brain but not limb colonies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldicarb↗
PubMed1989

Interaction of lead and zinc in cultured astroglia.

Astroglia take up lead (Pb) in vivo and in vitro. In view of the fact that zinc affects both tissue deposition of Pb and clinical signs of Pb intoxication, the present study was carried out to test the effects of various Zn levels on lead toxicity in astroglia. Primary cultures of astroglia from 1- to 3-day-old neonatal rats were divided into three groups and cultured in Waymouth's 752/l medium with 0, 1, or 2 microM ZnCl2. Each group was further divided into two subgroups which were treated with either 0, 29.9, or 32.5 mumol of Pb acetate. Cultures were assayed for viability and metal content after 1 and 3 days of continuous exposure to Pb (designated days 1 and 3) as well as 10, 17, and 24 days after the initiation of a 3-day exposure to Pb. The Trypan blue dye exclusion viability assay showed no significant differences between controls and Pb-treated groups except on day 3, at which time the 0 and 2 microM Zn groups treated with Pb had reduced viability. 3H-Leucine incorporation into acid-precipitable proteins (cpm/micrograms protein) was unaffected by Pb or Zn except on days 1 and 17, when cultures given 2 microM Zn and no Pb showed increased incorporation. Pb-treated cultures showed a reduction in cell number which was partially offset in a dose-dependent manner by the presence of Zn in the medium but not enough to mask completely the reduction caused by Pb. Pb produced the following effects on intracellular trace metal concentrations: (1) increased intracellular [Pb]. (2) increased intracellular [Fe], (3) increased intracellular [Cu], and increased intracellular [Zn]. By day 24, intracellular Cu concentrations were normal, but intracellular [Zn] and [Pb] remained elevated in all Pb-treated subgroups. Furthermore, intracellular Fe levels remained increased in the Pb-treated subgroup cultured with 0 microM Zn. Zinc showed a protective effect by (1) reducing intracellular Pb levels and (2) delaying or preventing the Pb-induced increase in intracellular [Fe] and [Zn] but not the increase in intracellular [Cu]. These effects became more pronounced with increasing extracellular Zn concentrations, although intracellular Zn levels did not increase in response to extracellular levels. Increased dietary zinc in rats is known to reduce Pb accumulation in organs. Our results extend this observation to cells in culture and, furthermore, suggest that the Pb-Zn interaction is complex and not simply a substitution of Pb by Zn at the point of absorption through the plasma membrane.

Animals↗
PubMed1989

Low level lead neurotoxicity in a pregnant guinea pigs model: neuroglial enzyme activities and brain trace metal concentrations.

Specific activities of the astroglial marker glutamine synthetase (GS), and the oligodendroglial marker glycerol-3-phosphate dehydrogenase (GPDH) were measured in the spinal cord of fetal guinea pigs and their dams following chronic exposure to low levels of lead (Pb) during gestation. In addition, the effects of Pb on intracellular trace metals (Cu, Fe, Zn) were measured in the blood, cerebellum and forebrain. Aminolevulinic acid dehydratase (ALAD) and zinc protoporphyrin IX (ZPP) were measured in order to monitor established parameters of Pb-exposure. Pregnant guinea pigs were orally administered 0, 5.5 or 11 mg Pb/kg body weight for 30 or 40 days commencing on day 22 of gestation. Blood Pb levels produced in dams and fetuses were at or near the currently identified "no effect" levels for children (10-30 micrograms/dl). These Pb blood levels produced a significant (P less than 0.05) dose-dependent decrease in GS and GPDH activity in the dams and fetuses. Fe and Zn concentrations in blood, cerebellum and forebrain of both dams and fetuses were significantly (P less than 0.05) decreased in a dose-dependent manner. However, Cu concentrations in the blood, cerebellum and forebrain were decreased in the dams but increased in the fetuses in a dose-dependent fashion. The alteration of trace metal concentrations is a proposed mechanism of Pb neurotoxicity. Blood ALAD activity was significantly (P less than 0.05) decreased and ZPP levels were significantly (P less than 0.05) increased, as expected in Pb-exposed animals. This study presents the first biochemical evidence for the alteration of neuroglial function at low levels of Pb exposure and focuses attention on the fetus as an important Pb target.

Animals↗
PubMed1989

Lead toxicity in neuroglia.

In this article we evaluate evidence that neuroglia (astroglia and oligodendroglia) are primary targets for lead toxicity in the central nervous system or mediate its pathogenesis. An integrated overview of morphologic and biochemical evidence from clinical cases, experimental animals, and cell culture models is attempted. Our review encompasses both high-level lead exposure that produces lead encephalopathy and low-level lead exposure that is associated with cognitive deficits. We also discuss the selection of toxicologically relevant lead doses for cell culture studies. The evidence is compelling that both astroglia and oligodendroglia respond directly or indirectly to lead exposure in ways that could impair brain function. However, at this time more is understood about the responses of astroglia than those of oligodendroglia. Though oligodendroglia appear sensitive to lead in cell culture, as measured by loss of viability and enzyme activity, it is not clear whether their responses to Pb exposure in vivo are primary or secondary to other tissue and cell damage. Astroglia show a definitive primary response in vivo and in vitro to high-level lead exposure, the uptake and storage of Pb intracellularly, possibly by Pb- binding macromolecules. Astroglia also exhibit reactive gliosis, but probably as a secondary response to other tissue damage by high lead levels. The hypothesis that astroglia serve a protective function in the brain by acting as a lead depot in encephalopathy is well supported by several whole animal and cell culture studies. In addition, alterations of glutamine synthetase activity, which have been reported in the astroglia of animals chronically exposed to low levels of lead, bear further investigation.

Animals↗
PubMedDate not supplied

Preeclampsia.

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Animals↗