Pharmacokinetics of tulathromycin in nonpregnant adult ewes

2014 ◽  
Vol 38 (4) ◽  
pp. 414-416 ◽  
Author(s):  
K. Washburn ◽  
V. R. Fajt ◽  
J. F. Coetzee ◽  
S. Rice ◽  
L. W. Wulf ◽  
...  
Keyword(s):  
Nonpregnant Adult

Dose-Response Aggregometry in Maternal/Neonatal Platelets

1988 ◽  
Vol 60 (02) ◽  
pp. 314-318 ◽  
Author(s):  
A M A Gader ◽  
H Bahakim ◽  
F A Jabbar ◽  
A L Lambourne ◽  
T H Gaafar ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Dose Response ◽  
Lag Phase ◽  
Phase Slope ◽  
Multiple Doses ◽  
Nonpregnant Adult ◽  
Aggregation Of Platelets

SummaryThe aggregation of platelets collected from maternal/neonatal pairs (n = 240) at the time of childbirth, was studied in response to multiple doses of ADP, collagen, arachidonic acid and ristocetin. Similar responses were obtained from healthy nonpregnant adult controls for comparison. The lag phase, slope of the aggregation curves as well as maximum aggregation (MA%) were recorded and analysed. Neonatal and adult platelets exhibited more enhanced responses to decreasing doses of ADP, arachidonic acid and ristocetin, than maternal platelets. These enhanced responses were exhibited more consistantly in the slopes of the aggregation curves than in MA%. Although neonatal platelets have shown longer lag phase in their responses to collagen, the rate of the aggregation reaction was significantly faster than maternal platelets, with no differences in MA%. These results contradict many previous reports suggesting impaired aggregation responses of neonatal platelets to these agonist. The possible reasons for these contradictions were discussed.

Cerebral artery KATP- and KCa-channel activity and contractility: changes with development

2000 ◽  
Vol 279 (6) ◽  
pp. R2004-R2014 ◽  
Author(s):  
Wen Long ◽  
Lubo Zhang ◽  
Lawrence D. Longo
Keyword(s):  
Channel Blocker ◽  
Cerebral Arteries ◽  
Dependent Manner ◽  
Channel Activity ◽  
Channel Opener ◽  
Channel Inhibition ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca ◽  
Near Term ◽  
Nonpregnant Adult

The present study was designed to test the hypothesis that in cerebral arteries of the fetus, ATP-sensitive (KATP) and Ca2+-activated K+channels (KCa) play an important role in the regulation of intracellular Ca2+ concentration ([Ca2+]i) and that this differs significantly from that of the adult. In main branch middle cerebral arteries (MCA) from near-term fetal (∼140 days) and nonpregnant adult sheep, simultaneously we measured norepinephrine (NE)-induced responses of vascular tension and [Ca2+]i in the absence and presence of selective K+-channel openers/blockers. In fetal MCA, in a dose-dependent manner, both the KATP-channel opener pinacidil and the KCa-channel opener NS 1619 significantly inhibited NE-induced tension [negative logarithm of the half-maximal inhibitory concentration (pIC50) = 5.0 ± 0.1 and 8.2 ± 0.1, respectively], with a modest decrease of [Ca2+]i. In the adult MCA, in contrast, both pinacidil and NS 1619 produced a significant tension decrease (pIC50 = 5.1 ± 0.1 and 7.6 ± 0.1, respectively) with no change in [Ca2+]i. In addition, the KCa-channel blocker iberiotoxin (10−7 to 10−6 M) resulted in increased tension and [Ca2+]i in both adult and fetal MCA, although the KATP-channel blocker glibenclamide (10−7 to 3 × 10−5 M) failed to do so. Of interest, administration of 10−7 M iberiotoxin totally eliminated vascular contraction and increase in [Ca2+]i seen in response to 10−5M ryanodine. In precontracted fetal cerebral arteries, activation of the KATP and KCa channels significantly decreased both tension and [Ca2+]i, suggesting that both K+ channels play an important role in regulating L-type channel Ca2+ flux and therefore vascular tone in these vessels. In the adult, KATP and the KCa channels also appear to play an important role in this regard; however, in the adult vessel, activation of these channels with resultant vasorelaxation can occur with no significant change in [Ca2+]i. These channels show differing responses to inhibition, e.g., KCa-channel inhibition, resulting in increased tension and [Ca2+]i, whereas KATP-channel inhibition showed no such effect. In addition, the KCa channel appears to be coupled to the sarcoplasmic reticulum ryanodine receptor. Thus differences in plasma membrane K+-channel activity may account, in part, for the differences in the regulation of contractility of fetal and adult cerebral arteries.

scholarly journals Regulation of Ca2+sensitization by PKC and rho proteins in ovine cerebral arteries: effects of artery size and age

1998 ◽  
Vol 275 (3) ◽  
pp. H930-H939 ◽  
Author(s):  
Sergey E. Akopov ◽  
Lubo Zhang ◽  
William J. Pearce
Keyword(s):  
G Protein ◽  
Cerebral Arteries ◽  
Rho Kinase ◽  
Cerebrovascular Reactivity ◽  
Rho Proteins ◽  
Experimental Conditions ◽  
Fetal Sheep ◽  
Middle Cerebral Arteries ◽  
Near Term ◽  
Nonpregnant Adult

G protein-regulated Ca2+ sensitivity of vascular contractile proteins plays an important role in cerebrovascular reactivity. The present study examines the intracellular mechanisms that govern G protein-regulated Ca2+ sensitivity in cerebral arteries of different size and age. We studied β-escin-permeabilized segments of common carotid, basilar, and middle cerebral arteries from nonpregnant adult and near-term fetal sheep. Activation of protein kinase C (PKC) by (−)-indolactam V or a phorbol ester produced receptor-independent increases in Ca2+ sensitivity. Such increases were more marked in immature arteries and were inversely correlated with artery size in both mature and immature arteries. However, inhibitors of PKC did not significantly affect increases in Ca2+ sensitivity in responses to either serotonin (5-hydroxytryptamine, 5-HT) or guanosine 5′- O-(3-thiotriphosphate) (GTPγS). Alternatively, deactivation of rho p21, a small G protein associated with Rho kinase, by exotoxin C3 fully prevented increases in Ca2+ sensitivity in responses to 5-HT or GTPγS in both adult and fetal arteries of all types. Neither inhibitors of PKC nor exotoxin C3 altered baseline Ca2+ sensitivity. We conclude that patterns of receptor- and/or G protein-mediated modulation of Ca2+ sensitivity are dependent on an intracellular pathway that involves activation of small G proteins and Rho kinase. In contrast, PKC has little, if any, role in agonist-induced Ca2+ sensitization under the present experimental conditions.

Protein deprivation in primates. I. Nonpregnant adult rhesus monkeys

1974 ◽  
Vol 27 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Arthur J. Riopelle ◽  
Charles W. Hill ◽  
Su-Chen Li ◽  
Robert H. Wolf ◽  
Herman R. Seibold ◽  
...  
Keyword(s):  
Rhesus Monkeys ◽  
Protein Deprivation ◽  
Nonpregnant Adult

Physiological variations in ovine cerebrovascular calcium sensitivity

1997 ◽  
Vol 272 (5) ◽  
pp. H2271-H2281 ◽  
Author(s):  
S. E. Akopov ◽  
L. Zhang ◽  
W. J. Pearce
Keyword(s):  
Biogenic Amines ◽  
G Protein ◽  
Calcium Sensitivity ◽  
Cerebrovascular Reactivity ◽  
Arterial Diameter ◽  
Fetal Sheep ◽  
Near Term ◽  
Nonpregnant Adult ◽  
Physiological Variations ◽  
Dependent Mechanism

Cerebrovascular reactivity to biogenic amines varies in relation to both arterial diameter and age. The present study examines the hypothesis that these patterns of reactivity are secondary to corresponding variations in the Ca2+ sensitivity of the contractile proteins. To test this hypothesis, we permeabilized segments of common carotid (Com), basilar, main branch middle cerebral, and second-branch middle cerebral (MCA-B) arteries from nonpregnant adult and near-term fetal sheep using beta-escin. Permeabilization methods were carefully validated and adjusted for each artery type. Baseline myofilament Ca2+ sensitivity in both adults and fetuses increased significantly from the Com to the MCA-B and was generally higher in fetuses than in adults. Serotonin dose dependently increased Ca2+ sensitivity via a G protein-dependent mechanism in all arteries. The magnitudes of this effect did not vary among artery types but were significantly greater in fetal than in adult arteries. This effect of serotonin was mimicked by guanosine 5'-O-(3-thiotriphosphate), a nonhydrolyzable analog of guanosine 5'-triphosphate, and its effects were also much greater in fetal than in adult arteries. We conclude that patterns of cerebrovascular reactivity to biogenic amines were determined, at least in part, by underlying variations in baseline myofilament Ca2+ sensitivity and/or its alteration by G protein-dependent mechanisms.

scholarly journals α1-Adrenergic receptor subtype function in fetal and adult cerebral arteries

2010 ◽  
Vol 298 (6) ◽  
pp. H1797-H1806 ◽  
Author(s):  
Ravi Goyal ◽  
Ashwani Mittal ◽  
Nina Chu ◽  
Lubo Zhang ◽  
Lawrence D. Longo
Keyword(s):  
Adrenergic Receptor ◽  
Cerebral Arteries ◽  
Age Groups ◽  
Critical Factor ◽  
Receptor Subtype ◽  
Erk Activation ◽  
Wb 4101 ◽  
Intracellular Ca ◽  
Nonpregnant Adult ◽  
And Function

In the developing fetus, cerebral artery (CA) contractility demonstrates significant functional differences from that of the adult. This may be a consequence of differential activities of α1-adrenergic receptor (α1-AR) subtypes. Thus we tested the hypothesis that maturational differences in adrenergic-mediated CA contractility are, in part, a consequence of differential expression and/or activities of α1-AR subtypes. In CA from fetal (∼140 days) and nonpregnant adult sheep, we used wire myography and imaging, with simultaneous measurement of tension and intracellular Ca2+ concentration ([Ca2+]i), radioimmunoassay, and Western immunoblots to examine phenylephrine (Phe)-induced contractile responses. The α1A-AR antagonists (5-MU and WB-4101) completely inhibited Phe-induced contraction in adult but not fetal CA; however, [Ca2+]i increase was reduced significantly in both age groups. The α1D-AR antagonist (BMY-7378) blocked both Phe-induced contractions and Ca2+ responses to a significantly greater extent in adult compared with fetal CA. In both age groups, inhibition of α1A-AR and α1B-AR, but not α1D-AR, significantly reduced inositol 1,4,5-trisphosphate responses to Phe. Western immunoblots demonstrated that the α1-AR subtype expression was only ∼20% in fetal CA compared with the adult. Moreover, in fetal CA, the α1D-AR was expressed significantly greater than the other two subtypes. Also, in fetal but not adult CA, Phe induced a significant increase in activated ERK1/2; this increase in phosphorylated ERK was blocked by α1B-AR (CEC) and α1D-AR (BMY-7378) inhibitors, but not by α1A-AR inhibitors (5-MU or WB-4101). In conclusion, in the fetal CA, α1B-AR and α1D-AR subtypes play a key role in contractile response as well as in ERK activation. We speculate that in fetal CA α1B-AR and α1D-AR subtypes may be a critical factor associated with cerebrovascular growth and function.

Dynamic stiffness of rabbit mesotubarium smooth muscle: effect of isometric length

1978 ◽  
Vol 234 (1) ◽  
pp. C14-C26 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Dynamic Stiffness ◽  
Muscle Tension ◽  
Muscle Length ◽  
Isometric Tension ◽  
Published Data ◽  
Tension Level ◽  
Tension Peak ◽  
Nonpregnant Adult

The dynamic stiffness of mesotubarium smooth muscle from nonpregnant adult rabbits was measured continuously during isometric contraction by applying small (0.5 percent of the muscle length) sinusoidal length perturbations and measuring the amplitude and phase of the resulting tension perturbations. Stiffness during contraction was directly proportional to muscle tension; during relaxation stiffness at all tensions was significantly increased as compared to the values encountered during the rise of tension. Peak isometric tension and dynamic stiffness (determined at a common tension level) both decreased at shorter muscle lengths; the relative falloff in stiffness was significantly less than the tension decrease. Varying levels of muscle activation (obtained by changing stimulus strength and by applying quick releases to active muscle) had little effect on the measured elastic modulus. Comparisons of these results with published data on single-cell contractile properties imply a cellular locus for a portion of the measured stiffness.

Effect of maturation on hepatic adenosine triphosphate

1965 ◽  
Vol 208 (4) ◽  
pp. 628-632 ◽  
Author(s):  
Steven Schenker ◽  
James F. O'Donnell
Keyword(s):  
Adenosine Triphosphate ◽  
Guinea Pigs ◽  
Quantitative Data ◽  
Limiting Factors ◽  
Liver Protein ◽  
Metabolic Processes ◽  
Atp Concentration ◽  
Neonatal Liver ◽  
Nonpregnant Adult ◽  
Rate Limiting

Inasmuch as there are no quantitative data as to adenosine triphosphate (ATP) concentration in fetal and neonatal liver, a method for estimating the nucleotide in developing animals was devised and validated and the results obtained are reported here. The hepatic ATP levels, means ± sd, of fetal, one-day-old, nonpregnant adult, and pregnant guinea pigs were, respectively, 19.25 ± 3.36, 24.67 ± 3.90, 23.83 ± 2.98, and 26.12 ± 4.05 µmoles/g liver protein. In comparable groups of rats, which mature less rapidly, the values for ATP were 28.40 ± 3.24, 30.24 ± 2.72, 23.34 ± 2.17, and 22.62 ± 3.24 µmoles/g liver protein. It is concluded that 1) hepatic ATP concentration is specific for a species and does not appear to correlate primarily with its maturity, and 2) the levels of ATP in fetal and neonatal guinea pigs and rats are sufficiently similar to those in adult animals as not to be likely rate-limiting factors for hepatic ATP-dependent metabolic processes.

Sign in / Sign up

Export Citation Format

Share Document