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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether magnesium sulfate and promethazine interact to cause hypotension in gravid ewes. Fifteen experiments were performed in five chronically instrumented animals between 125 and 130 days of timed gestation (term = 145 days). In one group of experiments each animal received magnesium sulfate (4 gm intravenous bolus followed by 4 gm/hr intravenous infusion) then promethazine (50 mg intravenously). In a second group each animal received magnesium sulfate then saline solution as a control. In a third group each animal received saline solution then promethazine. Infusion of magnesium sulfate increased the mean (+/- SEM) serum magnesium concentration to 5.7 +/- 0.6 and 6.6 +/- 0.6 mg/dl in the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups, respectively. Magnesium sulfate slightly decreased maternal mean arterial pressure (p less than 0.05) and increased cardiac output (p less than 0.05) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups. Otherwise there were no significant changes in maternal mean arterial pressure or cardiac output in any group. Promethazine increased maternal heart rate (p = 0.0001) in both the magnesium sulfate-promethazine and saline solution-promethazine groups. Magnesium sulfate increased uterine blood flow (p less than 0.01) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups, but promethazine blunted the increase in uterine blood flow associated with magnesium sulfate. Similarly, magnesium sulfate decreased uterine vascular resistance (p less than 0.01) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups, but promethazine eliminated the decrease in uterine vascular resistance associated with magnesium sulfate. Maternal and fetal arterial blood gas and acid-base values did not change in any group, except that there was a small, near-significant decrease (p = 0.06) in fetal pH 10 minutes after promethazine was given in the magnesium sulfate-promethazine group. We conclude that magnesium sulfate and promethazine did not interact to cause maternal hypotension in normovolemic gravid ewes. However, promethazine increased maternal heart rate and blunted the increase in uterine blood flow associated with magnesium sulfate.
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PMID:Magnesium sulfate and promethazine do not interact to cause hypotension in gravid ewes. 240 57

Evidence in vitro and in humans suggest that Mg2+ can alter systemic and renal vascular tone. However, the mechanism of these effects is not known. The role of vasodilator prostaglandin release and Ca2+ flux in Mg2+-induced changes in blood pressure and renal blood flow was studied in 10 normal subjects maintained on a fixed 80-mEq Na+ and K+ diet. Magnesium sulfate infused at 200 mg/hr for 3 hours reduced systolic and diastolic blood pressure within 1 hour (from 119 +/- 2 [SEM] to 109 +/- 4 mm Hg systolic; from 74 +/- 3 to 64 +/- 4 mm Hg diastolic; p less than 0.02). This hypotensive response was seen in all subjects and persisted for 3 hours. The pulse rate did not change, but renal blood flow (p-aminohippurate clearance) increased (from 902 +/- 78 to 1108 +/- 130 ml/min/1.73 m2; p less than 0.05). The Mg2+ infusion produced a significant increase in the excretion of the stable prostaglandin I2 (PGI2) metabolite 6-keto-PGF1 alpha (from 96 +/- 12 to 154 +/- 16 ng/g creatinine; p less than 0.01). In contrast, urinary PGE2 was not altered (328 +/- 75 vs 399 +/- 145 ng/g creatinine; p greater than 0.6). To evaluate the functional role of PGI2 release, the cyclooxygenase inhibitors indomethacin (75 mg) or ibuprofen (600 mg) were given before the Mg2+ infusion. Both cyclooxygenase blockers, given in doses that inhibited immunoreactive 6-keto-PGF1 alpha release, completely prevented the Mg2+-induced decline in blood pressure and increased renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that prostacyclin mediates the vascular action of magnesium in humans. 243 56