Respiratory and cardiovascular effects in relation to plasma levels of midazolam and diazepam.

Sunzel, Maria; Paalzow, Lennart; Berggren, Lars; Eriksson, Ingrid

doi:10.1111/j.1365-2125.1988.tb03346.x

Cited by 62 publications

(25 citation statements)

References 23 publications

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“…In addition, they affect the ventilatory response curve to carbon dioxide by flattening the response. BZDs do not shift the curve to the right, like opioids, but a typical reaction to BZDs is a decrease in tidal volume (Sunzel et al, 1988). If the patient is given BZDs together with opioids, the risk of significant ventilatory depression is increased markedly because BZDs depress the reaction to hypoxia under hypercapnic conditions (Alexander and Gross, 1988;Tverskoy et al, 1989).…”

Section: Gabaergic Inhibition In Anesthesiologymentioning

confidence: 99%

Enhancement of GABAergic Activity: Neuropharmacological Effects of Benzodiazepines and Therapeutic Use in Anesthesiology

et al. 2011

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Section: Gabaergic Inhibition In Anesthesiologymentioning

confidence: 99%

Enhancement of GABAergic Activity: Neuropharmacological Effects of Benzodiazepines and Therapeutic Use in Anesthesiology

et al. 2011

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“…On one hand, our results justify the occurrence of cardiovascular side effects of midazolam used as a sedative or anesthetic. [6][7][8] On the other hand, they could indicate midazolam as a potential antihypertensive agent. The antihypertensive effects of midazolam are quite speculative because we did not conduct experiments with midazolam in in vivo models of hypertension, and midazolam-induced vasodilation occurs at concentrations that are too high for general clinical practice.…”

Section: Discussionmentioning

confidence: 99%

“…Nonetheless, the vascular effects of midazolam could be useful in emergency/urgency situations, such as in hypertensive crises. Specifically, under intravenous infusion, midazolam can reach micromolar concentrations in plasma 6 and exert its vasodilative and sedative properties, which could be beneficial in the treatment of hypertensive crises.…”

Section: Discussionmentioning

confidence: 99%

“…4 BDZs can reduce blood pressure in experimental 5 and clinical settings. 6 In addition, BDZs can reduce blood pressure both indirectly, by central inhibition of the autonomic neurocardiac system and the control of the baroreflex, 7,8 and directly, by dilating the blood vessels in the vascular beds of animal models. 4,[9][10][11] Nonetheless, the mechanism by which BDZs stimulate vasodilation remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…For this purpose, we used aortic rings of C57/BL6 mice, and we chose the BDZ midazolam because of its demonstrated vascular effects. 6,20 …”

Section: Introductionmentioning

confidence: 99%

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Involvement of endothelium-dependent and -independent mechanisms in midazolam-induced vasodilation

et al. 2011

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Benzodiazepine (BDZ) infusion has been shown to reduce blood pressure in both humans and animals. Although the inhibitory effects of BDZ on the central nervous system have been well documented, less is known about the direct effects of BDZ on the vascular bed. The aims of this study were to assess the effects of the BDZ midazolam on the vascular system in C57/BL6 mouse aortic rings and to investigate the mechanisms of its direct vascular action. We found that midazolam induced reversible, dose-dependent vasodilation in potassium-and phenylephrine-precontracted rings. In rings that were precontracted with potassium or phenylephrine, treatment with 10 lmol l À1 midazolam increased vasodilation by 15 and 60%, respectively, compared with baseline. Vasodilation increased by 80 and 87%, respectively, after treatment with 50 lmol l À1 midazolam. Only the low concentration of midazolam (10 lmol l À1 ) induced endothelium-dependent vasodilation in phenylephrine-precontracted rings. Vasodilation increased by 60% in rings with endothelium and by 20% in rings without endothelium. Conversely, only the high concentration of midazolam (50 lmol l À1 ) reduced the CaCl 2 -induced vasoconstriction of aortic rings with EC 50 (the concentration giving 50% of the maximal effect) values of 1 and 6 mmol l À1 for vehicle-and midazolam-treated rings, respectively. Furthermore, the incubation of phenylephrine-precontracted rings with an inhibitor of the nitric oxide synthase (NOS) NG-nitro-L-arginine methyl ester or the inhibitors of central or peripheral type BDZ receptors (flumazenil or PK 11195, respectively) produced no change in midazolam-induced vasodilation. Thus, low concentrations of midazolam induce vasodilation via an endothelium-dependent mechanism that does not involve NO production. In contrast, high concentrations of midazolam induce vasodilation via an endothelium-independent mechanism that implies reduced sensitivity of aortic rings to calcium ions. Additionally, neither the central c-amino-butyric acid receptor type A nor the peripheral type BDZ receptors seem to be involved in the mechanism of midazolam-induced vasodilation.

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Cardiovascular Disease

Congdon¹

2014

Canine and Feline Anesthesia and Co‐Existing Disease

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Respiratory and cardiovascular effects in relation to plasma levels of midazolam and diazepam.

Cited by 62 publications

References 23 publications

Enhancement of GABAergic Activity: Neuropharmacological Effects of Benzodiazepines and Therapeutic Use in Anesthesiology

Enhancement of GABAergic Activity: Neuropharmacological Effects of Benzodiazepines and Therapeutic Use in Anesthesiology

Involvement of endothelium-dependent and -independent mechanisms in midazolam-induced vasodilation

Cardiovascular Disease

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