Effects of Prostaglandins F2  and E2 on the Bovine Circulation

Anderson, Fred; Kralios, Alexandros C.; Tsagaris, Theofilos J.; Kuida, Hiroshi

doi:10.3181/00379727-140-36609

Cited by 18 publications

(5 citation statements)

References 4 publications

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“…In near-term pregnant sheep, PGE, and PGF2, had no significant effects on the maternal or fetal circulations, suggesting that sheep are insensitive to prostaglandins (3). In unanesthetized calves, however, PGF2, administration produced a significant increase in pulmonary artery pressure, but no discernible effects on systemic arterial pressure (4). PGE2 in the same species produced a fall in systemic arterial pressure, which was attributed to arteriolar dilatation since cardiac output was not affected.…”

Section: Responses After Ganglionic and P-adre-mentioning

confidence: 92%

Effects of Ganglionic and -Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid

Kot

Johnson

Ramwell

et al. 1975

Experimental Biology and Medicine

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The bisenoic prostaglandins, PGE2 and PGF2a, increase myocardial contractile force, but have opposite effects on systemic arterial pressure in the dog (1). PGE, produces a vasodepressor response and PGF,, produces a pressor response. Arachidonic acid (AA), the precursor of the bisenoic prostaglandins, has variable effects on myocardial contractile force, but consistently produces a decline in systemic arterial pressure (2).The specific objectives of the present study were to determine whether the cardiac responses to these agents observed in the dog are due to direct action on the heart or are reflex in nature, and to examine blood pressure and cardiac responses to these agents after blockade of the autonomic ganglia and the @receptors of the heart. Materials and Methods. Mongrel dogs were anesthetized with sodium pentobarbital (30 mg/kg) and maintained on intermittent positive respiration with a Harvard respirator. A left thoracotomy was performed and a Walton-Brodie strain gauge arch was sutured to the right ventricular wall for measurement of myocardial contractile force. A femoral artery and vein were catheterized; the former for direct measurement of systemic arterial pressure and the latter for administration of test substances into the inferior vena cava. Through a midline neck incision both common carotid arteries were isolated and tagged with loose ligatures.The sodium salt of arachidonic acid (5, 8, 1 1, 14-eicosatetraenoic acid; > 99 % pure from porcine liver; Sigma) was prepared by dissolving the free acid in sodium carbonate (100 mM) with constant stirring under nitrogen in the absence of light. The resulting solution was water clear and 1 Supported in part by the Educational Foundation of America.was stored for no more than 2 days in the dark under nitrogen. The prostaglandins used in this study were generously supplied by the Upjohn Company. Solutions in ethanol (1 mg/ml) were evaporated to dryness under nitrogen, and the residue was dissolved in normal saline. Hexamethonium chloride (Schwarz/Mann) was prepared in aqueous solution in a concentration of 50 mg/ml. Practolol (Practol) was generously supplied by Ayerst Laboratories, Inc.Test substances were administered as bolus injections intravenously in the following dose levels; AA 300 pg/kg and 900These doses were selected because our previous studies indicated that such levels administered intravenously produced a profound change in systemic arterial pressure from which recovery always rapidly ensued. AA 300 pg/kg is equidepressor with PGE2 5 pg/kg (2). Sufficient time was allowed to elapse (approx 5 min) between each injection to permit systemic arterial pressure and myocardial contractile force to return to control values.Following observation of the initial response to each of these agents, ganglionic blockade was produced with hexamethonium chloride 2 mg/kg given intravenously. Both common carotid arteries were temporarily occluded just prior to, and shortly after, the administration of the hexamethonium to verify that the baroreceptor reflex...

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Section: Responses After Ganglionic and P-adre-mentioning

confidence: 92%

Effects of Ganglionic and -Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid

Kot

Johnson

Ramwell

et al. 1975

Experimental Biology and Medicine

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“…Though the effect of exogenously administered prostaglandin E (PGE) on the pulmonary circulation has been studied both in various species of animal and in healthy man (Bergstrom et al, 1959(Bergstrom et al, , 1965Hauge et al, 1967;Carlson et al, 1969;Hyman, 1969;Sobel and Robinson, 1969;Anderson et al, 1971;Koss et al, 1973;Kadowitz et al, 1974), the part it plays in the regulation of the pulmonary circulation in disease has not yet been analysed. It has been assumed that PGE, which is liberated and metabolised in the lungs, fulfils the role of a local mediator influencing the pulmonary circulation in hypoxaemia or in anaphylactic reactions (Bergofsky, 1974).…”

mentioning

confidence: 99%

Effects of prostaglandin E1 on pulmonary circulation in patients with pulmonary hypertension.

Szczeklik¹,

Dubiel²,

Mysik³

et al. 1978

Heart

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in a dose of 0-02 ,ug/kg per min resulted in a significant fall in the pulmonary arterial pressure (P < 0.001), total pulmonary resistance (P < 0 001), left ventricular end-diastolic pressure (P < 0.001), and aortic pressure (P < 0.01), and an increase in the pulmonary blood volume (P < 0.01), cardiac index (P < 0.01), and heart rate (P < 0'05). No significant differences were noted in stroke volume index or left ventricular dP/dt at 50 mmHg after prostaglandin E1. These results indicate that exogenously administered prostaglandin E1 causes active vasodilatation of the pulmonary vascular bed and has no inotropic action on the cardiac muscle.Though the effect of exogenously administered prostaglandin E (PGE) on the pulmonary circulation has been studied both in various species of animal and in healthy man (Bergstrom et al., 1959(Bergstrom et al., , 1965Hauge et al., 1967;Carlson et al., 1969;Hyman, 1969;Sobel and Robinson, 1969;Anderson et al., 1971;Koss et al., 1973;Kadowitz et al., 1974), the part it plays in the regulation of the pulmonary circulation in disease has not yet been analysed. It has been assumed that PGE, which is liberated and metabolised in the lungs, fulfils the role of a local mediator influencing the pulmonary circulation in hypoxaemia or in anaphylactic reactions (Bergofsky, 1974).The effect of exogenous PGE on the pulmonary vascular bed can be usefully studied in patients with mitral stenosis, in whom pulmonary vasoconstriction resulting from chronic hypoxaemia plays an important part in the development of pulmonary hypertension (Bergofsky, 1974). Subjects and methodsThe effect of prostaglandin E1 (PGE1) was studied in 20 patients, 4 men and 16 women, ranging Received for publication 13 March 1978 in age from 19 to 59 years (average 36-7 years). Mitral stenosis was present in all with mitral regurgitation also in 2 patients. The diagnosis was established by clinical examination and haemodynamic study, and was confirmed at operation in all cases. Heart failure was grade 2 and was found in 4 cases, grade 3 in 11, and grade 4 in 5, according to the NYHA classification. All the patients had pulmonary arterial hypertension: the mean value of the mean pulmonary arterial pressure was 38-5 + 15-2 mmHg, and the total pulmonary resistance was 808-2 + 387 dynes s cm-5 (10.1 ± 4-8 units). The majority of patients were receiving a digitalis preparation and a thiazide diuretic, but for 2 weeks before the investigation non-steroidal anti-inflammatory drugs were not given.A prostaglandin solution was prepared immediately before the injection by dissolving PGE1 (Upjohn Co. Ltd) in a 95 per cent ethanol solution.The appropriate dose of this solution was then diluted in 120 ml of 0 9 per cent saline. The preparation was administered by continuous intravenous infusion, using a Unipan peristaltic pump, in doses of [0][1]

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“…It has been established that the factors influencing the state of PTS in patients after coronary artery bypass grafting (CABG) are: the duration of cardiopulmonary bypass, blood loss during surgery, the number of platelets in the blood, hypocapnia. The factors influencing the aggregation ability of platelets are: the duration of cardiopulmonary bypass, the number of platelets, the degree of "emptying" of platelet alpha granules of platelets, the functional state of PTS [1][2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…According to the literature, the prostacyclin -thromboxane system (PTS) is one of the leading systems of neurohumoral regulation, which determines both the state of central and peripheral hemodynamics and platelet -vascular hemostasis (2,3,4,6,9). Prostacyclin has a powerful antiaggregatory and vasodilating effect (4,5,7,9).…”

Section: Introductionmentioning

confidence: 99%

The state of the prostacyclin-thromboxane system in patients after aorto-coronary bypass surgery

Kattakhanova,

Kanataeva

2023

BIO Web Conf.

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In order to clarify the role of the prostacyclin-thromboxane system (PTS) in the development of acute circulatory disorders in the early postoperative period after coronary artery bypass surgery, its condition was studied in 86 patients with coronary artery disease. In patients with the development of vascular insufficiency and shock, a decrease in the level of thromboxane in the blood was revealed, while in patients with arterial hypertension, elevated concentrations of thromboxane in the blood were determined in the absence of changes in the level of prostacyclin. There were no significant differences in the content of prostacyclin and thromboxane between groups of patients with uncomplicated postoperative course and with the development of such complications as heart failure and hypovolemia.

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Effects of Prostaglandins F2 and E2 on the Bovine Circulation

Cited by 18 publications

References 4 publications

Effects of Ganglionic and -Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid

Effects of Ganglionic and -Adrenergic Blockade on Cardiovascular Responses to the Bisenoic Prostaglandins and their Precursor Arachidonic Acid

Effects of prostaglandin E1 on pulmonary circulation in patients with pulmonary hypertension.

The state of the prostacyclin-thromboxane system in patients after aorto-coronary bypass surgery

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