Experimental vasoconstriction of cerebral arteries by prostaglandins

Yamamoto, Y.; Feindel, William; Wolfe, L. S.; Katoh, Hiroshi; Hodge, Charles P.

doi:10.3171/jns.1972.37.4.0385

Cited by 136 publications

(26 citation statements)

References 18 publications

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“…PGE 2 injected intraarterially or intravenously causes cerebral vasodilatation in dogs and cats 4 -6 but when applied topically causes vasoconstriction in cats. 6 Yamamoto et al 1 have demonstrated that PGE, decreases cerebral blood flow in dogs, but Steiner et al 2 and Nakano et al 4 found the opposite in humans and dogs. Allen et al 17 have shown a PGE,-induced contraction of isolated cerebral arterial segments from humans and dogs, while the present study demonstrated marked relaxation of dog as well as human cerebral arteries in response to PGE^ Such an inconsistency in the response of cerebral vessels to PGE, is not believed to be due to species difference but possibly to the ability of PGEi to induce both contraction and relaxation.…”

Section: Modification By Aspirin Of Response To Pgsmentioning

confidence: 99%

Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate.

Toda¹,

Miyazaki²

1978

Stroke

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SUMMARY In helically cut strips of dog cerebral, coronary, mesenteric and femoral arteries, the contractile response to prostaglandin (PG) F 2( , and E 2 , relative to contractions induced by 30 mM K + , did not appreciably differ, whereas relaxations induced by PGE, relative to those induced by 10 * M papaverine were significantly different; the least in cerebral arteries and the greatest in mesenteric arteries. The relaxation of human cerebral arteries in response to PGE, was similar to that of dog cerebral arteries. Treatment for 60 min with polyphloretin phosphate (3 X 10" and 10 ' g/ml) suppressed the contractile response to PGF 2( , and E 2 but did not alter the response to 25 mM K + . The relaxing effect of PGE, was not influenced. Aspirin (5 X 10" and 2 X 10 ' M) significantly potentiated the contractile response to PGF to and E 2 but did not alter the relaxation induced by PGE,. In contrast, contractions induced by serotonin were attenuated. It is concluded that dog cerebral, coronary, mesenteric and femoral arteries relaxed differently in response to PGE,. It appears that arterial responses to vasoconstricting PCs, but not to the vasodilating PG, are significantly attenuated by polyphloretin phosphate and potentiated by aspirin.PROSTAGLANDINS (PGs) induce changes in systemic blood pressure, regional blood flow and tone of vascular smooth muscle. Alterations induced by a variety of PG derivatives differ markedly, and even the same PGs sometimes elicit opposite actions on vessels from various species. Different responses of cerebral vessels to PGEi and E 2 have been reported, 16 however, it is generally agreed that PGF 2a causes constriction in cerebral vessels.The ability of polyphloretin phosphate (PPP) to antagonize the effect of PGE 2 on intraocular pressure was first demonstrated by Beitch and Eakins.7 PPP does not antagonize all actions of PGs on uterine, tracheal and bronchial smooth muscles. "10 Aspirinlike anti-inflammatory agents inhibit the biosynthesis of PGs in isolated tissues and whole animals, 11 ' 12 but the interaction between PGs and aspirin or indomethacin, related to responses of vascular smooth muscles, has not been clarified.The present study was undertaken to compare the actions of PGE,, E 2 and F 2a on isolated dog cerebral arteries with their actions on coronary, mesenteric and femoral arteries and to analyze the antagonistic action of PPP in these arteries. Alterations in the response of the arteries to PGs after aspirin and indomethacin application were also investigated. MethodsMongrel dogs of both sexes, weighing 7 to 15 kg, were anesthetized with intraperitoneal injections of sodium pentobarbital in a dose of 50 mg/kg and sacrificed by bleeding from common carotid arteries. The brain and heart were rapidly removed. Basilar and middle cerebral arteries (0.5 to 0.8 mm outside diameter) and ventral interventricular branches of the left coronary artery (0.6 to 0.9 mm) were isolated. Distal portions of the mesenteric (0.5 to 0.8 mm) and femoral arteries (0.5 to 0.8 mm) were also...

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Section: Modification By Aspirin Of Response To Pgsmentioning

confidence: 99%

Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate.

Toda¹,

Miyazaki²

1978

Stroke

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“…Stroke Vol 14, No 2, 1983 CHEMICAL FACTORS OF THE PATHOGENESIS of cerebral vasospasm following subarachnoid hemorrhage include serotonin, 1-3 catecholamines 4 " 6 and prostaglandins [7][8][9] that are released from the subarachnoid hematoma 10 " and cerebral vessel. 7,812 These substances produce contractions of cerebral and extracerebral vessels by increasing the release of Ca + + from intracellular storage sites and the transmembrane influx of Ca + + .…”

mentioning

confidence: 99%

Mechanisms of relaxant action of nicardipine, a new Ca++-antagonist, on isolated dog cerebral and mesenteric arteries.

Yamamoto¹,

Ohta²,

Toda³

1983

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SUMMARY In helically-cut strips of cerebral and mesenteric arteries contracted with prostaglandin (PG) F^, carbocyclic thromboxane A 2 (cTxA 2 ) or K + , the addition of nicardipine caused a dose-related relaxation. Nicardipine-induced relaxation was greater in cerebral than in mesenteric arteries when contracted with PGF 2a and cTxA 2 , but did not appreciably differ in the arteries contracted with K + . Cerebral arteries contracted with hemolysate and PGF 2a relaxed in response to nicardipine to a similar extent. The contractile response to PGF 2a was attenuated by pretreatment with nicardipine, the attenuation being greater in cerebral than in mesenteric arteries. Ca ++ -induced contractions in cerebral and mesenteric arteries previously exposed to Ca + + -free media and depolarized by excess K + were attenuated by nicardipine to a similar extent. PGF 2a -induced contractions of cerebral arteries exposed to Ca + + -free media were attenuated by nicardipine, whereas those of mesenteric arteries were unaffected. Attenuations by nicardipine of the Ca + + -induced contraction in PGF 2a -treated cerebral arteries were greater than those seen in mesenteric arteries. It may be concluded that nicardipine produces a greater relaxation of cerebral arteries than mesenteric arteries, possibly due to a greater inhibition of the Ca + + -influx and to a decrease in the release of Ca + + from intracellular storage sites in cerebral arteries. As far as the concentrations used are concerned, nicardipine appears to attenuate the inward movement of Ca + + across cell membrane in mesenteric arterial smooth muscle, but not the release of intracellular^ stored Ca + + .Stroke Vol 14, No 2, 1983 CHEMICAL FACTORS OF THE PATHOGENESIS of cerebral vasospasm following subarachnoid hemorrhage include serotonin, 1-3 catecholamines 4 " 6 and prostaglandins 7-9 that are released from the subarachnoid hematoma 10 " and cerebral vessel. 7,812 These substances produce contractions of cerebral and extracerebral vessels by increasing the release of Ca + + from intracellular storage sites and the transmembrane influx of Ca + + . 1314 Ca ++ -antagonists which preferentially interfere with the Ca ++ -influx relax cerebral arterial smooth muscle previously contracted with these vasoconstrictors to a greater extent than extracerebral arteries, 15 ' 16 and the ability of the antagonists to effectively relieve the experimentally-induced cerebral vasospasm has been demonstrated. 17 Nicardipine has recently been reported to interfere with the uptake of 45 Ca ++ by rabbit aortae, 18 to increase the cerebral blood flow in dogs, monkeys and human patients, 19 and to relieve the experimentallyinduced cerebrovascular spasm in cats.20 At vasodilatory concentrations, this drug produces less bradycardia, A-V conduction block and decreased cardiac contractility. 21The present study was undertaken to clarify the action and the mechanism of action of nicardipine on isolated dog cerebral and mesenteric arteries stimulated by PGF 2a , cTxA 2 , hemolysate and K + , ...

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“…I~ In contrast, Yamamoto et al reported that PGE~ decreased CBF in dogs. 19 However recent studies by Kitaguchi et al and Sha et al claimed that PGE I did not increase CBF in anaesthetized humans. 4,6 Even though we did not measure cerebral blood flow in this study, the lack of alteration in SjvO2, rSO 2 and EEG suggested that PGE 1 did not provoke major alteration in blood flow and metabolism in brain during the induced hypotension.…”

Section: Discussionmentioning

confidence: 99%

Cerebral oxygénation during prostaglandin E1 induced hypotension

et al. 1998

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Purpose: To evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E t(PGEI) during fentanyl-oxygen anaesthesia. Methods: Ten patients who underwent elective cardiac surgery received infusion of PGE I . After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO2) estimated by INVOS 3100 R, PGE, was continuously infused at 0.25-0.65 ~g'kg -*'min -t (mean dosage: 410 -+ 41.4 mg'kg -* -min -*) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO 2. Thirty minutes from the start of drug infusions, administration of PGE, was stopped. The same parameters were measured again I 0, 30 minutes after the stop of drug infusion. Results: PGE, decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE, increased mixed venous saturation, but in contrast did not effect internal jugular pressure, internal jugular oxygen saturation and rSO 2. Conclusions: These results suggest that PGE, is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.Objectif : l~valuer les effets de l'hypotension, induite par la prostaglandine E,(PGE~), sur l'oxygEnation c&Ebrale pendant l'anesthEsie avec fentanyl et oxygEne. M&hodes : Dix patients qui devaient subir une chirurgie cardiaque Elective ont re~u une perfusion de PGE i. Apt& avoir procEdE ~ la gazomEtrie art&ielle de base, ~ celle du sang veineux mEIE et ~ celle de la veine jugulaire interne, EvaluE rhEmodynamie systEmique et la saturation en oxygEne cErEbral regional (SO2r) par INVOS 3100R, la PGE, a EtE administrEe en perfusion intraveineuse continue ~ 0,25-0,65/~g'kg -l'min -l (dosage moyen : 410 +_ 41,4 ~g.min-i). Dix, 20 et 30 minutes apr& le debut des perfusions de medicaments, les gaz du sang dEj~ cites ont &6 obtenus simultanEment avec la mesure de l'hEmodynamie systEmique et laSOzr. Trente minutes aprEs le debut des perfusions, l'administration de la PGE I a EtE arr&Ee. Les m~mes paramEtres ont EtE mesurEs encore aprEs I0 et 30 minutes apr~s rarr& de la perfusion de medicament. R~sultats : La PGE i abaisse la tension art&ielle moyenne (TAM) ~. 70 % de sa valeur de base environ (P < 0,05). La PGE, augmente la saturation en oxygEne du sang veineux m~IE mais, au contraire, n'a pas d'effet sur la tension de la veine jugulaire interne, sur la saturation en oxygEne de cette veine et sur la SO2r. Conclusion : Ces rEsultats montrent que la PGE, est un medicament appropriE pour induire de l'hypotension parce que le couplage dEbit/mEtabolisme du cerveau et l'oxygEnation cEr~brale rEgionale ont EtE maintenus pendant l'hypotension.

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Experimental vasoconstriction of cerebral arteries by prostaglandins

Cited by 136 publications

References 18 publications

Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate.

Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate.

Mechanisms of relaxant action of nicardipine, a new Ca++-antagonist, on isolated dog cerebral and mesenteric arteries.

Cerebral oxygénation during prostaglandin E1 induced hypotension

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