PubMed · 11846243
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Mark Slagle. 2002. Medication update.. https://pubmed.ncbi.nlm.nih.gov/11846243/
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HISTORY AND CLINICAL FINDINGS: A 78-year-old woman was admitted to the intensive care unit 9 hours after ingestion of 2 g of isosorbitmononitrate, 430 mg of amlodipine, 250 mg of benazepril and 600 mg of mirtazapin in suicidal intent. INVESTIGATIONS: Clinical findings and invasive monitoring showed signs of a hyperdynamic hemodynamic cardiovascular failure caused by toxic vasodilatation. TREATMENT AND COURSE: Despite of primary detoxication, intravenous volume infusion with calcium gluconate, glucagon and naloxone and administration (norepinephrine up to 2 micro g/kg/min) no hemodynamic stabilization was achieved. Only when the vasopressin-analogue argipressin was given peripheral vasodilatation was overcome and hemodynamic stabilization resulted. 10 hours after discontinuing argipressin and norepinephrine the patient developed a mesenteric ischemia, and she finally died on the third day after admission. CONCLUSION: In circulatory shock due to toxic vasodilatation the use of vasopressin analogue argipressin can be helpful as an ultima therapeutic measure in catecholamine refractory shock caused by vasodilatation. Attention must be paid to overwhelming vasoconstrictor effects resulting in mesenteric ischemia.
BACKGROUND: Supraspinal sympathetic control of leg vascular tone is lost in spinal cord-injured individuals, but this does not result in a reduced leg vascular tone: Leg vascular resistance is even increased. The aim of this study was to assess the alpha-adrenergic contribution to the increased vascular tone in the lower extremity in patients without central sympathetic control of leg circulation. METHODS AND RESULTS: Upper-leg vascular resistance responses to local infusion of incremental doses of phentolamine (a competitive antagonist of the alpha-adrenoceptor) into the femoral artery were determined in 10 spinal cord-injured individuals (SCI) and 8 healthy age-matched control subjects during local beta-adrenergic receptor blockade with propranolol. Basal leg vascular resistance was higher in SCI than in control subjects (41+/-6 arbitrary units [AU] versus 24+/-4 AU; P=0.034). The same accounts for minimal leg vascular resistance, assessed during reactive hyperemia, which was higher in SCI compared with control subjects (6.9+/-1.0 AU versus 2.5+/-0.2 AU; P<0.01). The maximal phentolamine-induced reduction in leg vascular resistance normalized to each individual's minimal resistance did not differ between the groups (68+/-17% and 51+/-4% for SCI and control subjects, respectively; P>0.1). A decline in mean arterial pressure was observed in both groups with increasing dosage of phentolamine. In response, baroreceptor-mediated vasoconstriction was observed in the noninfused leg of the control subjects, whereas in SCI individuals this reaction was absent. CONCLUSIONS: These results indicate that the alpha-adrenoceptor-mediated vascular tone in the leg is preserved in spinal cord-injured individuals without sympathetic supraspinal control.
We measured the effects of electrical stimulation of the central cut end of the lingual nerve on lower lip blood flow (LBF) and on arterial blood pressure in urethane-anesthetized, artificially ventilated, cervically vagosympathectomized rabbits. Different effects were observed depending on the stimulus frequency. Increasing the stimulus frequency above 5 Hz produced progressively larger ipsilateral LBF increases until the optimal frequency was reached at 20 Hz. In contrast, stimulation at above 0.5 Hz evoked progressively larger decreases in both contralateral LBF and arterial blood pressure until the optimal frequency was reached at around 10 and 2 Hz, respectively. Thus, the optimal stimulus frequencies for the ipsilateral LBF increase and the arterial blood pressure decrease were widely different. The lingual nerve-evoked change (i.e., fall) in arterial blood pressure showed a significant correlation with the contralateral LBF decrease, but not with the ipsilateral LBF increase. Prior administration of hexamethonium at 10 mg/kg markedly reduced both the ipsilateral LBF increase and arterial blood pressure decrease, although it was more effective against the former than against the latter. Pretreatment with scopolamine (muscarinic-receptor antagonist, 0.1 mg/kg), phentolamine (alpha-adrenoceptor antagonist, 0.1 mg/kg), or propranolol (beta-adrenoceptor antagonist, 0.1 mg/kg) failed to affect either response. However, 1.0 mg/kg phentolamine significantly reduced both responses (P<0.05). These results indicate that, in the rabbit, the LN-evoked reflex increase in ipsilateral LBF is (a) largely independent of any concomitant arterial blood pressure change and (b) probably due to active vasodilatation mediated via parasympathetic mechanisms. In contrast, the evoked decrease in contralateral LBF was proportional to the decrease in arterial blood pressure, suggesting that the former was secondary to the latter.