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Biomedical subjects

T N Tulenko

Publications and source records attributed to T N Tulenko.

44 records · Page 3Linked to original sources
PubMed1986

Alterations in canine coronary arteries produced by chronic cigarette smoking.

Segments of left circumflex coronary artery were obtained from beagles that had been exposed to cigarette smoke for 2 years and from nonsmoking controls. A ring sample from each was used to determine passive (0-Ca2+ and 2 mM EGTA) and active (75 mM K+) force-length relations. Other contiguous samples were used to determine collagen and elastin content, water content and distribution, and total electrolyte content. No significant differences were found in passive mechanical properties or the collagen and elastin content of arteries from the two groups of animals. Maximum values of active force development were found to be increased in arteries from smoking dogs as were values on the ascending part of the active force-length curve. Total water content and the distribution space of an extracellular marker (60Co-EDTA) were not significantly different among arteries from the two groups. This along with the similarity of total electrolyte contents suggests that values of cell volume were not different between the two groups and that the above differences in active force development represent alterations in smooth muscle cells at the subcellular level. These results suggest that the contribution of chronic smoking as one of a group of cardiac risk factors may be due to an effect of augmenting coronary artery smooth muscle contractility.

Animals↗
PubMed1983

Metabolism of C14 mevalonate by adult and fetal arteries.

The metabolism of mevalonate by the arterial wall was evaluated in fetal and adult maternal arteries of the New Zealand white rabbit. Freshly minced tissue from umbilical arteries, fetal aortas and adult maternal aortas was incubated in oxygenated Krebs Henseleit bicarbonate buffer at 37 degrees C in the presence of 5-14C-mevalonate or 5-14C-3-hydroxy-3-methylglutaryl-Coenzyme A (HMG CoA). After incubation, the arterial tissue lipids were extracted and total cholesterol and free fatty acids were purified by thin layer chromatography and assayed for 14C by liquid scintillation spectrometry and analyzed chemically. The conversion of labeled HMG CoA or mevalonate to cholesterol in fetal aorta was 15 fold greater than in maternal aorta and 5-10 fold greater than in fetal umbilical artery. In addition some 14C from HMG CoA became incorporated into palmitate, stearate and oleate while 14C from mevalonate appeared in palmitate and stearate in trace amounts. Similarly, conversion of label from both precursors to 14CO2 was greatest in fetal aorta followed by umbilical artery and maternal aorta of the term pregnant rabbit. Of particular interest was the observation of enhanced (3.5 fold) conversion of label from mevalonate to 14CO2 by maternal aortas at mid-gestation compared to aortas of late-term gestation. These results are consistent with the explanation that while mevalonate clearly serves as a precursor for cholesterol synthesis in arterial tissue, a finite degree of exclusion from the main stream sterol pathway also occurs. This "shunt" pathway may involve oxidation directly to CO2 or indirectly by way of fatty acids. The level of activity through this exclusion pathway in arterial tissue appears to be under physiologic control during pregnancy since a 3.5 fold increase in conversion to 14CO2 occurred in aortas obtained in midgestation compared to those obtained at term gestation.

Acyl Coenzyme A↗
PubMed1981

The actions of prostaglandins and cyclo-oxygenase inhibition on the resistance vessels supplying the human fetal placenta.

The resistance arteries supplying individual exchange villi of the full-term human fetal placenta were examined for their reactivity to various prostaglandins (PG's) as well as for their ability to synthesize biologically active PG's. PGA1, PGF2 alpha, PGE2 and PGE1 produced dose-dependent contractions between 10(-7) and 10(-5)M. The order of potency observed was PGA1 approximately PGF2 alpha greater than PGE2 greater than PGE1. TXB2 was without activity in this preparation. Prostacyclin (PGI2) produced a dose-dependent relaxation of pre-contracted strips between 10(-8)M and 10(-5)M. Arachidonic acid (A.A.) produced stable dose-dependent contractions (10(-5) M to 10(-3)M) which were totally abolished by pretreatment with 10(-7)M meclofenamate (MF). At no concentration of A.A. was any evidence of vascular relaxation observed. Larger concentrations of MF (greater than 10(-6)M) resulted in a non-specific depression of the placental vascular smooth muscle. Meclofenamate (10(-7)M) pretreatment of strips subjected to dose-response studies using PGF2 alpha, PGE2, bradykinin (B K) and angiotensin II (AII) revealed a significant reduction in tension developed to both BK and AII. This finding suggests that the vasoactive peptides BK and AII stimulate the synthesis of vasoconstricting PG's in the fetal placental resistance arteries which relax in response to PGI2 and contract in response to the other PG's tested.

Angiotensin II↗
PubMed1981

Fatty acid metabolism in human fetal placental vasculature.

The utilization of exogenous acetate and palmitate for the synthesis of vascular wall lipids was studied in isolated blood vessels of the human placenta under high- and low-oxygen conditions. Arteries and veins were obtained from fresh placental material and incubated in Krebs-Henseleit buffer (pH 7.4 at 37 degrees C) containing (in mM) either [2-14C]acetate, 0.11; [1-14C]palmitate, 0.43; or [16-14C]palmitate, 0.43. At the end of the 180-min incubation, neutral lipids accounted for 40%, and phospholipids 60%, of the 14C recovered. Following incubation with either precursor, 14C label was recovered mainly in 16-carbon fatty acids (FA) (35%) and 18-carbon FA (45%); less than 10% was recovered in less than or equal to 14-carbon FA and greater than or equal to 20-carbon FA. Estimates of synthesis rate however indicated that the 18- and 20-carbon FA had the highest turnover rates. Schmidt degradation analysis demonstrated considerable labeling of alkyl carbons after incubation with either carboxyl- or alkyl-labeled precursors, indicating that FA degradation products were used for de novo FA synthesis. Collectively, these findings suggest the presence of both de novo and chain elongation pathways. No differences were observed between arteries and veins, and anoxia had little influence on FA metabolism. Analysis of ATP levels demonstrated elevated concentrations of ATP present, accounting for the apparent lack of anoxic inhibition of FA metabolism.

Acetates↗
PubMedDate not supplied

Voltage-gated sodium channels in human aortic smooth muscle cells.

Whole-cell, voltage clamp methods were used to study inward currents in human aortic smooth muscle cells in culture. Cells were plated on glass coverslips, cultured in supplemented M-199 media with 5% serum and studied as primary cells and at passages 2-5. Inward currents were measured with a pipette solution containing Cs+ and TEA+ to block K+ currents and with 2.5 mM [Ca2+]0 in the perfusate. Inward currents activated at about -50 mV, peaked at about -15 mV and reversed at about +30 mV. Values of peak inward current averaged 14. 7 +/- 3.3 pA/pF and cell capacitance averaged 124 +/- 10 pF (n = 35). These currents activated rapidly with a time-to-peak current of 2.4 +/- 0.3 ms at a test potential of -10 mV from a holding potential of -80 mV. The current also inactivated rapidly with a time course that could be described by two components with time constants of 1.8 +/- 0.2 and 17.8 +/- 3.5 ms at -10 mV. The currents decreased when extracellular Na+ was reduced and were completely inhibited by 50 nM tetrodotoxin (TTX), suggesting that they represented voltage-gated Na+ currents (INa). Activation curves were characterized with a V0.5 = -16.6 +/- 2.4 mV and a slope factor k = -5.2 +/- 0.2 mV while inactivation curves were characterized with a V0.5 = -60.9 +/- 1.7 mV and a slope factor k = 8.8 +/- 0.4 mV. Lowering external [Ca2+] to zero increased the maximum INa, shifted its voltage dependence in the hyperpolarizing direction and increased the rate of INa inactivation. Increasing external [Ca2+] or [Mg2+]decreased INa and slowed its rate of inactivation. These studies demonstrate the presence of voltage-gated Na+ channels with high TTX sensitivity that are modulated by extracellular divalent cations in human aortic smooth muscle cells maintained in cell culture. Window currents were found in the voltage range of -50 to -20 mV, suggesting that these channels could contribute to the resting membrane potential.

Calcium↗
PubMedDate not supplied

Immediate and long-term effects of angioplasty-balloon dilation on normal rabbit iliac artery.

The present study was performed to determine the immediate (hours) and long-term (28-day) effects of angioplasty-balloon dilatation on arterial wall diameter, histology, response to vasoconstrictors, and passive mechanics. Dilated left iliac arteries of New Zealand rabbits were compared to control, right iliac arteries. In the immediate studies, dilation increased arteriographic diameter by 32%, denuded the endothelium, stretched and may have lysed smooth muscle cells, decreased arterial wall thickness, and increased passive stress and incremental elastic modulus. The dilated arteries failed to contract to norepinephrine or potassium chloride. In contrast, 28 days after dilation, arteriographic diameter had returned to normal, an intimal thickening had formed, passive stress and the incremental elastic modulus had decreased to below normal, and the arteries contracted, but to only 53% to 67% of control. Angioplasty had no long-term effect on arterial sensitivity (EC50) to potassium chloride or serotonin but did produce a decreased sensitivity (6X) to norepinephrine. These studies demonstrate that the effects of dilatation of the normal artery are partially reversible, suggest that restenosis after angioplasty is more likely to be due to intimal proliferation than increased arterial stiffness, and suggest that vasospasm of arteries after long-term recovery from the dilation is more likely to be mediated by serotonin than by norepinephrine.

Angioplasty, Balloon↗