Effect of Dihydroergotamine on Subdural Intracranial Pressure and Cerebral Haemodynamics
Dihydroergotamine (DHE) acts as a non-competitive agonist at vascular 5-hydroxytryptamine receptors. Experimental studies indicate that DHE is a constrictor of the venous capacitance vessels and, in in vitro studies, DHE induces concentration-dependent co
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Abstract Dihydroergotamine (DHE) acts as a non-competitive agonist at vascular 5-hydroxytryptamine receptors. Experimental studies indicate that DHE is a constrictor of the venous capacitance vessels and, in in vitro studies, DHE induces concentration-dependent contraction in human cerebral arteries and veins. Theoretically, DHE is more effective in the treatment of increased ICP than hyperventilation and is less dangerous because it predominantly acts on the cerebral venous pool, which contains a larger blood volume than the arterial pool. In this chapter DHE and the results of a study dealing with the effect of DHE on arterial blood pressure, subdural ICP, cerebral perfusion pressure, cerebral blood flow and the cerebral metabolism in patients subjected to craniotomy for supratentorial brain tumours is discussed.
Treatments of increased ICP, tension of dura or brain swelling during craniotomy include therapy that increases CVR, such as hyperventilation and indomethacin, hypnotic agents, such as barbiturates or propofol and osmotic therapy (mannitol and hypertonic saline); also CSF drainage and evacuation of cystic processes, head elevation or rTp can be used (Miller and Leech 1975; Bedford et al. 1980; Bundgaard et al. 1996; Cenic et al. 2000; Tankisi et al. 2002). Each of these measures has advantages and disadvantages. Controlled hyperventilation is often of limited value since patients with intracerebral space-occupying lesions may have impaired or abolished cerebrovascular reactivity to changes in PaCO2. The effect of hyperventilation follows the changes in PaCO2, but maximal effect will only occur after 10–15 min and adaption to the effect takes place during continuous hypocapnia (Raichle and Plum 1972); adverse effects such as serious decrease in CBF have been reported (Cold 1989; Muizelaar et al. 1991). A precipitous decrease in CBF has also been found after i.v. indomethacin, but unlike hyperventilation this drug increases CPP. The effect of repeated mannitol infusion has also been questioned, and a rebound effect at a high repeated dose is well known (Kaufmann and Cardoso 1992). Barbitu-
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12 Effect of Dihydroergotamine on Subdural Intracranial Pressure
rates and propofol may induce cardiovascular depression with a decrease in CPP, and CSF drainage is often impossible because of difficult access to the ventricular system. Dihydroergotamine (DHE) acts as a non-competitive agonist at vascular 5-hydroxytryptamine receptors (Glusa and Markwardt 1984; Müller-Scheweinitzer and Rosenthaler 1987; Müller et al. 1988). Experimental studies indicate that DHE is a constrictor of the venous capacitance vessels (Mellander and Nordenfelt 1970; Müller-Scheweinitzer and Rosenthaler 1987) and, in in vitro studies, DHE induces concentration-dependent contraction in human cerebral arteries and veins (Nilsson et al. 1997). The Lund group have shown that in patients with severe head injury a bolus dose of DHE reduces ICP and increases CPP (Grände 1989; Asgeirsson et al. 1994, 1995). The ICP-reducing effect of DHE start
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