Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH

Abstract

Nimodipine was given as an intracarotid slow bolus injection in six patients with subarachnoid hemorrhage (SAH) due to rupture of a cerebral aneurysm, with angiographically demonstrated vasospasm. The patients were followed by serial angiograms for demonstration of the effect of nimodipine on vasospasm. After angiography, all patients were treated with a constant venous infusion of this new calcium antagonist. Although the therapeutic regimen was started only a few hours after onset of vasospasm, there was no change in cerebral vessel caliber detectable on angiograms following the intracarotid injection. Three patients died, two patients finally recovered with neurological deficits due to cerebral ischemia, and one patient with asymptomatic vasospasm remained symptom-free. Although nimodipine may act to prevent cerebral vasospasm after SAH, the authors believe that the intracarotid application is not effective after vasospasm has occurred.

Intra-Arterial Nimodipine for Severe Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Influence on Clinical Course and Cerebral Perfusion

“…37 IAN in patients with severe vasospasm has been reported by several authors. [24][25][26] Data from a larger series by Biondi et al 18 demonstrated that IAN is effective and safe for the treatment of vasospasm after SAH. In this trial, 25 patients treated The present study completes the examination of the effectiveness of IAN by additionally investigating the cerebral perfusion by means of repeated PCT.…”

“…23 Intra-arterial nimodipine (IAN) in patients with severe vasospasm has been reported by several authors. [24][25][26] Data from a larger series by Biondi et al 18 suggested that IAN is effective and safe for the treatment of vasospasm after SAH. However, no information regarding the influence of IAN on cerebral perfusion is available.…”

Nimodipine‐induced changes in the distribution of carotid blood flow and cardiac output in pentobarbitone‐anaesthetized pigs

“…The dihydropyridine derivative nimodipine appears to have a preferential action on cerebral vessels; it antagonizes vasoconstrictor effects of 5-hydroxytryptamine (5-HT), blood and carboxylic thromboxane A2 on the rabbit basilar artery more effectively than on the rabbit saphenous artery (Towart, 1981;Towart & Perzborn, 1981;Towart et al, 1982). Clinically, nimodipine has shown potential in the therapy of cerebral vascular spasm following subarachnoid haemorrhage (Auer et al, 1982;Grotenhuis et al, 1984;Kostron et al, 1984) and in the treatment of migrainous headaches (Gelmers, 1983;Meyer & Hardenberg, 1983).…”

Nimodipine has no effect on the cerebral circulation in conscious pigs, despite an increase in cardiac output

“…In order to eliminate possible complications introduced by the use of anaesthetic drugs, we have investigated the vascular responses in various tissues to nimodipine in conscious instrumented pigs. Particular attention has been devoted to regional cerebral blood flows in view of growing clinical evidence that the drug may exert a beneficial effect on a number of cerebral vascular disorders (Auer et al, 1982;Grotenhuis et al, 1984;Kostron et al, 1984;Gelmers et al, 1988) and in the treatment of migraine headaches (Gelmers, 1983;Meyer & Hardenberg 1983 1980). Briefly, the animals were sedated with ketamine HCI (30mgkg-1) and connected to a ventilator after endotracheal intubation.…”

“…1983; Meyer & Hardenberg 1983;Grotenhuis et al, 1984;Kostron et al, 1984;Gelmers et al, 1988). Though we grant that it remains difficult to extrapolate animal data to clinical situations, our results do question the assertion that nimodipine exerts its beneficial effects by enhancement of cerebral blood flow (Smith et al, 1983;Sahlin et al, 1987;Berger & Hakim, 1988;Lyden et al, 1988).…”