No abstract

There is a high mortality and morbidity in patients with subarachnoid hamorrhage (SAH) following rupture of cerebral arterial aneurysms. The reason for this is not definitely established but it is associated with constriction of the major cerebral arteries. This cerebral arterial spasm (CAS) is a salient feature of the clinical condition, and appears as a pronounced constriction of one or more of the major cerebral arteries (Fig 1). It may

1 The pharmacological similarity between human basilar artery and a number of isolated tissues (rat colon, anococcygeus, stomach fundus and aorta and guinea-pig ileum and colon) has been assessed during investigations of the aetiology of cerebral arterial spasm. 2 The responses of each of the six tissues to human normal and abnormal cerebrospinal fluid (CSF) and to human serum were compared with those of the human isolated basilar artery. 3 These studies revealed the presence of a vasodilator factor in CSF from subarachnoid haemorrhage patients and several tissues may be of use for further work in identifying the vasoactive substances in CSF. 4 No tissue displayed exactly the same spectrum of biological reactivity as the human basilar artery. The rat stomach fundus showed the closest similarity and was further studied for similarities in drug-induced responses. 5 The rat stomach fundus, like the human basilar artery, was contracted by 5-hydroxytryptamine, prostaglandin F2X and histamine and relaxed by dopamine. However, noradrenaline relaxed the fundus but contracted the basilar artery.

1Kryptopyrrole (2, 4-dimethyl, 3-ethylpyrrole) inhibited conduction in rat sciatic nerve by a local anaesthetic action. 2 Tone and both spontaneous and electrically-induced contractions of guinea-pig ileum were also inhibited by kryptopyrrole. The concentration of kryptopyrrole required for 50% inhibition of a maximum twitch tension (ID50) was 0.085 mm.3 Oxidation products of kryptopyrrole with chromatographic properties similar to those of urinary constituents reported in schizophrenia and hepatic porphyrias had little or no effect at similar concentrations. 4 Dose-response curves to exogenous acetylcholine in guinea-pig ileum were shifted to the right by kryptopyrrole, with loss of parallelism and reduction in the maximum contraction. 5 Acetylcholine overflow from ileal segments at rest and during electrical stimulation was reduced by kryptopyrrole. 6 These results on ileal segments are consistent with kryptopyrrole having both a post-junctional site of action, presumably directly on the muscle, and a pre-junctional site reducing the output of acetylcholine from the myenteric plexus. 7 The significance of these findings is discussed in relation to a possible clinical pathological role for these compounds.