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Biomedical subjects

S M Muldoon

Publications and source records attributed to S M Muldoon.

63 records · Page 4Linked to original sources
PubMed1978

Norepinephrine metabolism in canine saphenous vein: prevalence of glycol metabolites.

To examine the disposition of [3H]norepinephrine ([3H]NE) in adrenergically innervated veins, helical strips of canine saphenous veins were incubated in Krebs-Ringer solution containing D,L[3H]NE (2 X 10(-7) M) for 2 h. [3H]NE and its metabolites were measured in extracts of veins and in superfusate (Krebs-Ringer) collected during basal conditions and during release of [3H]NE evoked by electrical stimulation (1-8 Hz), tyramine (5 X 10(-6) to 5 X 10(-4) M), or high concentrations of potassium (35-100 meq/liter). During basal conditions, the efflux from veins comprised mainly metabolits of [3H]NE, especially 3,4-dihydroxphenylglycol (DOPEG) and 3-methoxy-4-hydroxyphenylglycol (MOPEG); this pattern was unchanged by cocaine treatment, and monoamine oxidase inhibition reduced the formation of DOPEG. During evoked release of NE, the major metabolites in the perfusate were DOPEG, MOPEG, and normetanephrine, and their proportions differed with the stimulus used: O-methylated metabolites in the perfusate always increased more than did the deaminated catechol compounds; DOPEG and MOPEG were released in greater amounts than the corresponding acids; and cocaine treatment caused a higher content of all metabolites except DOPEG. 3-Methoxy-4-hydroxymandelic acid was also formed by the vein but was retained in the tissue.

Animals↗
PubMed1977

Alpha-adrenergic blocking properties of droperidol on isolated blood vessels of the dog.

Concentrations of droperidol which caused a shift to the right of the dose-response curve to noradrenaline in the pulmonary artery and the saphenous vein of the dog did not affect myogenic activation by K+; they did not inhibit spontaneous activity of portal-mesenteric veins. Droperidol inhibited the contractile response to nerve stimulation, but did not affect the evoked release of 3H-noradrenaline. These experiments indicate that the vasodilator properties of smaller doses of droperidol are a result of its ability to block alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1976

Effects of amide-linked local anesthetics on adrenergic neuroeffector junction in cutaneous veins of dog.

When changes in isometric tension of helical strips of dog saphenous veins were recorded, etidocaine caused a dose-dependent depression of the contractile responses to nerve stimulation, norepinephrine and K+. The response to nerve stimulation was significantly more depressed than that to exogenous norepinephrine. Similar results were obtained with lidocaine. In preparations incubated in solutions containing 3H-norepinephrine and mounted for superfusion and isometric tension recording, etidocaine depressed the contractions and diminished the release of 3H-norepinephrine evoked by nerve stimulation. Thus, in addition to an inhibitory effect on the responses of smooth muscle cells, amide-linked local anesthetic agents such as etidocaine depress adrenergic neurotransmission in the blood vessel wall, which helps explain their vasodilator properties in the intact organism. In unstimulated preparations and during contractions caused by K+, etidocaine increased the efflux of 3H-norepinephrine and deaminated metabolites. After incubation with the monamine oxidase inhibitor, pargyline, etidocaine augmented markedly the efflux of 3H-norepinephrine. During responses to tyramine, it augmented the release of 3H-norepinephrine more than the efflux of deaminated compounds. This suggests that etidocaine augments the leakage of norepinephrine out of the storage vesicles, making more catecholamines available for intraneuronal deamination.

Amides↗
PubMed1975

Venomotor changes caused by halothane acting on the sympathetic nerves.

Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of morepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephrine and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth muscle cells.

Anesthesia, Inhalation↗
PubMedDate not supplied

Effect of prolonged dietary administration of vanadate on blood pressure in the rat.

Vanadate, a potent naturally occurring Na+,K+-ATPase inhibitor thought to have a role in regulating Na+-K+ pump activity, was fed to uninephrectomized rats drinking tap water or a 1% solution of sodium chloride for as long as 56 weeks. Feeding was achieved by adding sodium orthovanadate to normal rat chow equivalent to 100 or 200 ppm vanadium by weight. In the rats drinking tap water, systolic pressure gradually increased over a period of several weeks and then was sustained in a dose-related manner for the duration of the treatment. The increased pressure was not associated with changes in water intake, urine output, or urinary sodium excretion but correlated positively with plasma vanadium levels ranging from 0.04 to 0.27 microgram/ml. Increased pressure was associated with increased heart-to-body-weight ratio but did not appear to occur in a small group of animals drinking the 1% solution of sodium chloride. These findings, considered in the light of others, indicate that vanadate deserves continued study in relation to hypertension.

Animals↗
PubMedDate not supplied

Sequential blood volume changes in patients undergoing total hip arthroplasty.

Adequacy of transfusion based exclusively on clinical observations of hemodynamic changes and quantities of blood lost during total hip arthroplasty (THA) in 15 adults was tested by serial measurements of 51-Cr red-cell volume (RCV), 125-I RISA plasma volume (PV), and peripheral hematocrit (Hv) determined immediately before and 2 and 48 hours after operation. Blood transfusion and intravenous-fluid therapy were based on clinical observations and designed to restore blood volume (BV) to within 10 percent of its preoperative level prior to the isotopic determination 2 hours postoperatively. (When that determination showed a BV less than 90 percent, transfusions were given to restore it to between 90 and 100 percent). Isotopic data 2 hours after operation showed that the BV reduction--thought clinically to be less than 10 percent in every case--averaged 21.6 percent (range: 6 to 39 percent) and was shared by RCV and PV. Isotopic measurements 48 hours after operation showed that patients whose BV at 2 hours was within 10 percent of the preoperative BV were able to compensate for an average continuing RCV reduction of 23.9 percent by expansion of PV, resulting in an average BV reduction of 11.4 percent. Hv was a valuable guide for transfusion therapy at 48 hours, but not 2 hours after operation. In view of inadequacy of blood replacement based on clinical observations and the magnitude and variability of the 2 hour postoperative isotopically measured BV reductions in our patients, we recommend obtaining a derived BV by measuring PV and Hv preoperatively and 2 hours postoperatively as a further guide to transfusion therapy for each patient under-going THA. This is simpler and more practical than the two-isotope technique and is more sensitive than clinical observation alone. If clinical observation had been supplemented with a derived BV in our 15 cases, 80 percent instead of 30 percent would have had their BV restored to within 10 percent of the preoperative BV.

Adult↗