Easily reversible hypoxemia and hypotension induced by nimodipine

Gerloni, Riccardo; Copetti, Roberto

doi:10.1097/00063110-200410000-00012

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…If one or more cardiotoxic phenotypes (heart rate change, abnormal heart rhythm including AV block, pericardial edema, abnormal circulation, hemorrhage and thrombosis) were observed in zebrafish treated with a known human cardiotoxic drug, the results in zebrafish would be regarded as comparable with the results in humans. Drug‐induced cardiovascular toxicity has been reported in patients administered with aspirin (Kent et al ., ), clomipramine hydrochloride (Hondeghem and Hoffmann, ), cyclophosphamide (Katayama et al ., ; Nakamura et al ., ), nimodipine (Gerloni and Copetti, ; Hui and Lau, ), quinidine (Falk, ; White, ), terfenadine (Eseverri, ; Hey et al ., 1996; Yap and Camm, ) or verapamil hydrochloride (Bronstein et al ., ; Lanteri‐Minet et al ., ). Gentamincin sulphate and tetracycline hydrochloride did not have known cardiovascular toxicity in humans.…”

Section: Resultsmentioning

confidence: 99%

“…Here we assessed the cardiovascular toxicity of seven known human cardiotoxic drugs and two non-cardiotoxic drugs in zebrafish using six specific phenotypic endpoints: heart rate, heart rhythm, pericardial edema, circulation, hemorrhage and thrombosis. Although these phenotypic endpoints for assessing Widen QRS and QT interval prolongation (Hondeghem and Hoffmann, 2003) Bradycardia, pericardial edema, slower and absent circulation Yes Cyclophosphamide Pericardial effusion, decreased systolic function, heart failure, cardiac tamponade and pericarditis (Katayama et al, 2009;Nakamura et al, 2010) Bradycardia, pericardial edema and slower circulation Yes Nimodipine Bradycardia, hypotension and hypoxemia (Gerloni and Copetti, 2004;Hui and Lau, 2005) Bradycardia, pericardial edema, slower and absent circulation Yes Quinidine QT interval prolongation, bradycardia and hypotension (Falk, 1992;White et al, 2007) Bradycardia, AV block, pericardial edema and slower circulation Yes Terfenadine QT interval prolongation, arrhythmias and torsades de pointes (Eseverri, 2000;Yap and Camm, 2002) Bradycardia, AV block, pericardial edema and slower circulation…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Human cardiotoxic drugs delivered by soaking and microinjection induce cardiovascular toxicity in zebrafish

Zhu¹,

Xu²,

He³

et al. 2013

J of Applied Toxicology

100

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Cardiovascular toxicity is a major challenge for the pharmaceutical industry and predictive screening models to identify and eliminate pharmaceuticals with the potential to cause cardiovascular toxicity in humans are urgently needed. In this study, taking advantage of the transparency of larval zebrafish, Danio rerio, we assessed cardiovascular toxicity of seven known human cardiotoxic drugs (aspirin, clomipramine hydrochloride, cyclophosphamide, nimodipine, quinidine, terfenadine and verapamil hydrochloride) and two non-cardiovascular toxicity drugs (gentamicin sulphate and tetracycline hydrochloride) in zebrafish using six specific phenotypic endpoints: heart rate, heart rhythm, pericardial edema, circulation, hemorrhage and thrombosis. All the tested drugs were delivered into zebrafish by direct soaking and yolk sac microinjection, respectively, and cardiovascular toxicity was quantitatively or qualitatively assessed at 4 and 24 h post drug treatment. The results showed that aspirin accelerated the zebrafish heart rate (tachycardia), whereas clomipramine hydrochloride, cyclophosphamide, nimodipine, quinidine, terfenadine and verapamil hydrochloride induced bradycardia. Quinidine and terfenadine also caused atrioventricular (AV) block. Nimodipine treatment resulted in atrial arrest with much slower but regular ventricular heart beating. All the tested human cardiotoxic drugs also induced pericardial edema and circulatory disturbance in zebrafish. There was no sign of cardiovascular toxicity in zebrafish treated with non-cardiotoxic drugs gentamicin sulphate and tetracycline hydrochloride. The overall prediction success rate for cardiotoxic drugs and non-cardiotoxic drugs in zebrafish were 100% (9/9) as compared with human results, suggesting that zebrafish is an excellent animal model for rapid in vivo cardiovascular toxicity screening. The procedures we developed in this report for assessing cardiovascular toxicity in zebrafish were suitable for drugs delivered by either soaking or microinjection.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Human cardiotoxic drugs delivered by soaking and microinjection induce cardiovascular toxicity in zebrafish

Zhu¹,

Xu²,

He³

et al. 2013

J of Applied Toxicology

100

View full text Add to dashboard Cite

show abstract

“…18,19 Two cases of hypoxemia due to nimodipine use have been reported in the literature. 20,21 Gerloni and Copetti 20 reported a case of hypoxemia after an accidental overdose of nimodipine (dose unknown). The patient was successfully treated with calcium gluconate.…”

Section: Minutes After Nimodipinementioning

confidence: 99%

Hypoxemia associated with nimodipine in a patient with an aneurysmal subarachnoid hemorrhage

Baker

Bastin²,

Cook³

et al. 2015

American Journal of Health-System Pharmacy

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“…Furthermore, Kieninger et al reported a brief impairment of the pulmonary gas exchange on the second day in comparison to the first day of the long-term continuous intra-arterial nimodipine infusion in patients with severe refractory cerebral vasospasm after SAH [12]. Gerloni et al presented a case report on hypoxemia and hypotension induced by accidental nimodipine overdose that supported the hypothesis suggested by Develin et al [7,10]. However, Bolt et al investigated the effect of calcium channel blockers including nimodipine on pulmonary shunting in anesthetized patients scheduled for aortocoronary bypass surgery.…”

Section: Discussionmentioning

confidence: 69%

The effect of nimodipine on pulmonary function in artificially ventilated patients with aneurysmal subarachnoid hemorrhage

et al. 2021

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Background Nimodipine is routinely administered in patients with aneurysmal subarachnoid hemorrhage (aSAH). However, the effect of nimodipine on oxygen exchange in the lungs is insufficiently explored. Methods The study explored nimodipine medication in artificially ventilated patients with aSAH. The data collection period was divided into nimodipine-dependent (ND) and nimodipine-independent (NID) periods. Values for arterial partial pressure of oxygen (PaO2) and fraction of inspired oxygen (FiO2) were collected and compared between the periods. Patients were divided in those with lung injury (LI), defined as median Horowitz index (PaO2/FiO2) ≤40 kPa (≤300 mmHg), and without and in those with lower respiratory tract infection (LRTI) and without. Results A total of 53 out of 150 patients were artificially ventilated, and in 29 patients, the Horowitz index could be compared between ND and NID periods. A linear mixed model showed that during ND period the Horowitz index was 2.3 kPa (95% CI, 1.0–3.5 kPa, P<0.001) lower when compared to NID period. The model suggested that in the presence of LI, ND period is associated with a decrease of the index by 2.8 kPa (95% CI, 1.2–4.3 kPa, P<0.001). The decrease was more pronounced with LRTI than without: 3.4 kPa (95% CI, 0.8–6.1 kPa) vs. 2.1 kPa (95% CI, 0.7–3.4 kPa), P=0.011 and P=0.002, respectively. Conclusions In patients with LI or LRTI in the context of aSAH, pulmonary function may worsen with nimodipine treatment. The drop of 2 to 3 kPa of the Horowitz index in patients with no lung pathology may not outweigh the benefits of nimodipine. However, in individuals with concomitant lung injury, the effect may be clinically relevant.

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Easily reversible hypoxemia and hypotension induced by nimodipine

Cited by 5 publications

References 30 publications

Human cardiotoxic drugs delivered by soaking and microinjection induce cardiovascular toxicity in zebrafish

Human cardiotoxic drugs delivered by soaking and microinjection induce cardiovascular toxicity in zebrafish

Hypoxemia associated with nimodipine in a patient with an aneurysmal subarachnoid hemorrhage

The effect of nimodipine on pulmonary function in artificially ventilated patients with aneurysmal subarachnoid hemorrhage

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