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Biomedical subjects

F Coceani

Publications and source records attributed to F Coceani.

At least 109 records · Page 6Linked to original sources
PubMed1980

Prostaglandin E2 catabolism in the spinal nerve roots of the cat.

Catabolism of prostaglandin (PG) E2 was studied in homogenates of spinal cord and spinal nerve roots of the cat. Spinal roots enzymatically converted PGE2 to a product (metabolite I) with the chromatographic mobility of 15-keto-PGE2. Little metabolic degradation occurred in the spinal cord; however, incubation of PGE2 with combined spinal cord and nerve root tissue yielded a second metabolite (metabolite II) in addition to metabolite I. Metabolite II was identified as 15-keto-13, 14-dihydro-PGE2. These results prove that spinal nerve roots, unlike the spinal cord, contain 15-hydroxyprostaglandin dehydrogenase (15-PGDH) which is the major and rate-limiting enzyme in the inactivation of prostaglandins. The location and functional significance of 15-PGDH in peripheral nerves remain to be elucidated.

Animals↗
PubMed1980

Direct pulmonary vascular responses to prostaglandins in the conscious newborn lamb.

The effects of prostaglandins PGD2, PGE1, PGE2, PGF2 alpha, and PGI2 on pulmonary vascular tone were investigated in normoxic and hypoxic unsedated newborn lambs with chronically implanted flow probes around right and left pulmonary arteries. Prostaglandins were injected into only one pulmonary artery, and direct effects of the compounds were determined by comparing the flow changes in the injected vs. the uninjected lung. PGD2 and PGF2 alpha were direct pulmonary vasoconstrictors, whereas PGE1, PGE2 and PGI2 were direct pulmonary dilators. Hypoxia augmented the vasodilation of PGE1 and PGI2 and diminished the constriction of PGD2 and PGF2 alpha; it also lowered the threshold for PGI2-induced dilation. While the E-type prostaglandins and PGI2 were both local dilators, they differed in that the systemic dilatory effects of the E-type agents exceeded their pulmonary effects, whereas the opposite occurred with PGI2. These results demonstrate that prostaglandins can act locally on pulmonary vascular smooth muscle tone in vivo and that the level of oxygenation or base-line vascular tone influences the pulmonary vascular responses to the PGs. Among the dilator prostaglandins, PGI2 appears to be more effective on the pulmonary rather than the systemic vascular bed under hypoxic conditions.

Animals↗
PubMed1980

Indomethacin-induced pulmonary vasoconstriction in the conscious newborn lamb.

The pulmonary vascular effects of indomethacin were studied in chronically-instrumented conscious newborn lambs, 2-12 wk old. Flows were measured in right and left pulmonary arteries; indomethacin was injected into only one lung; and constriction or dilation was assessed from the proportion of pulmonary flow directed to the injected vs. the noninjected lung. Indomethacin was a pulmonary vasoconstrictor in all animals, its threshold dose being 0.01 mg/kg. The constriction after a dose of 0.1 mg/kg was associated with plasma indomethacin levels sufficient to inhibit prostaglandin (PG) synthesis. However, chronic indomethacin therapy (3 mg/kg per day orally) for 3 days, though resulting in similar plasma indomethacin levels, altered neither base-line pulmonary tone nor the pulmonary vascular responses to hypoxia, acetylcholine, bradykinin, or histamine. Pretreatment with indomethacin did abolish the pulmonary effects of a further intravenous dose of the drug. Our results indicate that production of a pulmonary PG may help to maintain normal vessel relaxation. However, the neonatal lung adapts to chronic inhibition of PG synthesis, maintaining normal vascular tone and homeostasis. Pulmonary PGs may play a role in, but are not essential for, normal neonatal pulmonary vascular control.

Animals↗
PubMed1980

Direct pulmonary vascular responses in the conscious newborn lamb.

Electromagnetic flow probes were placed around the right and left pulmonary arteries (RPA and LPA) of nine newborn lambs. Preliminary in vitro and in vivo experiments delineated the accuracy and limitations of this method of flow measurement and the value in vivo of a balloon occlusive zero. Six to nine days after surgery, catheters were placed in the aorta and a branch pulmonary artery permitting simultaneous measurements of RPA and LPA flow, pulmonary arterial pressure, and aortic pressure. Vasoactive agents were injected into one lung, and a shift in blood flow distribution reflected direct active vasoconstruction or vasodilation in that lung. With a normal arterial oxygen tension, acetylcholine had no direct effect on the pulmonary vessels, but indirectly lowered pulmonary resistance via its systemic effects. Histamine was a potent direct pulmonary vasoconstrictor, bradykinin was a weak direct dilator, norepinephrine was a direct constrictor, prostaglandin E1 was a direct dilator, and prostaglandin F2a was a direct constrictor. These results demonstrate the feasibility of isolating the direct pulmonary vascular effects of certain pharmacologic agents using a double pulmonary artery flow probe preparation, agents using a double pulmonary artery flow probe preparation, without the use of anesthetics or extracorporeal perfusion circuits.

Acetylcholine↗
PubMed1980

The pulmonary vascular effects of three prostaglandin I2 analogs in conscious newborn lambs.

Pulmonary and systemic vascular effects of three stable prostaglandin (PG) I2 analogs were studied in normoxic and hypoxic conscious newborn lambs. The three agents were : (5E)-6a-carba-PGI2 (analog I); 9-deoxy-9 alpha, 6-nitrilo-PGF1 hydrochloride (analog II); and (2E,5S)-9-deoxy-5,9 alpha-epoxy-13,14-dihydro-delta 1-PGF1 (analog III). Each component was injected into either a branch pulmonary artery or the ascending aorta. Locally induced alterations in pulmonary vascular tone were assessed from changes in the ratio of blood flow to the injected lung over total flow (delta Qinj/Qt). Each compound was a systemic vasodilator, with thresholds from 1 to 3 micrograms/kg. However, analog III was without local pulmonary vasoactivity, and analog I was a pulmonary vasodilator only at the highest dose used (30 micrograms/kg) and in hypoxic lambs. Analog II, in contrast, was a pulmonary vasodilator in both hypoxic (threshold = 3 micrograms/kg) and normoxic (threshold = 10 micrograms/kg) lambs. Moreover, only analog II mimicked PGI2 during hypoxia by decreasing vascular resistance in the injected lung more than systemic resistance. These results demonstrate that PGI2 analogs are vasodilators with variable activity on the pulmonary and systemic circulations of the newborn lamb. Of the three analogs tested, only analog II resembles PGI2 in being more specific for the pulmonary as opposed to the systemic circulation. Analog II, however, is less active than PGI2 in this regard.

Animals↗
PubMed1979

Does 15-hydroxy prostaglandin dehydrogenase contribute to prostaglandin inactivation in brain?

15-Methyl prostaglandin E2, a compound which is not a substrate for 15-hydroxy prostaglandin dehydrogenase, is a more potent pyretic agent than prostaglandin E2 when injected into the third ventricle of conscious cats. This finding raises the possibility that 15-hydroxy prostaglandin dehydrogenase contributes to prostaglandin inactivation in brain, notwithstanding its low activity.

Animals↗
PubMed1979

Pulmonary and systemic vascular responses to 6-keto-PGE1 in the conscious lamb.

6-Keto-PGE1 is a potent direct dilator of the pulmonary and systemic circulations of the newborn lamb under both normoxic and hypoxic conditions. Its threshold dose is similar to that of PGI2 and PGE1. Under hypoxia, 6-keto-PGE1 appears equally effective on the pulmonary and systemic circulations, while under normoxia it predominantly affects the systemic circulation.

Alprostadil↗
PubMed1979

Direct and indirect pulmonary vascular effects of tolazoline in the newborn lamb.

The pulmonary vascular effects of tolazoline were studied in unsedated newborn lambs during normal oxygenation and hypoxia. Direct and indirect pulmonary vascular responses were analyzed separately. During normal oxygenation, tolazoline (1 mg/kg) given into a branch pulmonary artery increased cardiac output while decreasing systemic and pulmonary resistances. Pulmonary flow distribution did not change, suggesting that the fall in pulmonary resistance was due to an indirect rather than a direct action of the drug. Tolazoline had similar effects on systemic and pulmonary resistances in the hypoxic lamb; however, there was a shift in blood flow toward the injected lung, indicating local pulmonary vasodilation induced by the drug. In either case, tolazoline did not alter the resistance ratio between the injected lung and the systemic circulation. We conclude that tolazoline is a direct pulmonary vasodilator in the hypoxic lamb, but does not appear to lower the pulmonary to systemic resistance ratio.

Animals↗