Effects of norepinephrine and glyceryl trinitrate on cerebral haemodynamics: transcranial Doppler study in healthy volunteers.

BACKGROUND: The effects of vasoactive substances on cerebral haemodynamics are not fully known. We studied the effects of norepinephrine and glyceryl trinitrate (GTN) on cerebral haemodynamics in healthy volunteers. METHODS: The effects of norepinephrine (n=10) and GTN (n=10) on the middle cerebral artery flow velocity (MCAFV), cerebral autoregulation, reactivity to carbon dioxide, and estimated cerebral perfusion pressure (eCPP) were studied using transcranial Doppler ultrasound. Established methods were used for calculating zero flow pressure (ZFP). Measurements were made at baseline, and after i.v. infusion of the study drug to the endpoints of 25% increase in mean arterial pressure (MAP) for norepinephrine (0.02-0.1 microg kg(-1) min(-1)), or 15% decrease in MAP for GTN (0.5-2.5 microg kg(-1) min(-1)). RESULTS: The MCAFV remained unchanged with norepinephrine, but decreased slightly with GTN {from [median (inter-quartile range)] 53 (38, 62) to 48 (33, 52) cm s(-1)}. Cerebrovascular reactivity did not change significantly with either drug. The eCPP did not change significantly with norepinephrine, but increased significantly with GTN [from 49 (32, 54) to 62 (47, 79) mm Hg]. ZFP increased with norepinephrine [from 39 (28, 48) to 56 (46, 62) mm Hg] and decreased with GTN [from 35 (30, 49) to 12 (-7, 20) mm Hg]. CONCLUSIONS: Norepinephrine, despite increasing arterial pressure, did not increase the eCPP. The eCPP increased significantly with GTN, despite decreased MAP. Cerebral vascular tone is an important determinant of CPP during pharmacologically induced changes in arterial pressure.

Effects of ephedrine, dobutamine and dopexamine on cerebral haemodynamics: transcranial Doppler studies in healthy volunteers.

BACKGROUND: Sympathomimetic drugs are assumed to have no direct effects on cerebral haemodynamics on the basis of animal experiments; there is little evidence of their direct effects in humans. This study aimed to address this issue. METHODS: The effects of ephedrine, dobutamine, and dopexamine on cerebral autoregulation, cerebral vascular reactivity to carbon dioxide, estimated cerebral perfusion pressure, and zero flow pressure (ZPF) were studied in 10 healthy volunteers using transcranial Doppler ultrasound. The strength of autoregulation was measured using the transient hyperaemic response test. The reactivity to carbon dioxide was measured as the change in middle cerebral artery flow velocity with a step change in end-tidal carbon dioxide. For the estimated cerebral perfusion pressure and the ZFP, established formulae were used which utilized instantaneous values of arterial pressure and middle cerebral artery flow velocity. Measurements were made at baseline and after i.v. infusion of the study drug to an endpoint of 25% increase in mean arterial pressure (MAP) (ephedrine, dobutamine) or cardiac index (dopexamine). RESULTS: There was no significant change in the strength of autoregulation (from (mean (SD)) 1.07 (0.16) to 1.07 (0.18); from 1.07 (0.16) to 1.03 (0.19); from 1.04 (0.12) to 1.04 (0.25)), reactivity to carbon dioxide (from 40% (8) to 36 (10); from 37 (12) to 37 (11); from 45 (12) to 43 (11)) with ephedrine, dobutamine, or dopexamine, respectively. Despite a clinically significant increase in MAP with ephedrine and dobutamine and a clinically significant increase in cardiac index with dopexamine, the estimated cerebral perfusion pressure did not change significantly (from 81 (38) to 60 (16) mm Hg with ephedrine; from 67 (22) to 63 (11) mm Hg with dobutamine; from 87 (27) to 79 (17) mm Hg with dopexamine). The ZFP increased significantly with ephedrine (from 29 (10) to 44 (11) mm Hg) and dobutamine (from 35 (14) to 43 (10) mm Hg) but not dopexamine (from 3 (23) to 11 (22) mm Hg). CONCLUSIONS: Sympathomimetic agents do not significantly change cerebrovascular homeostasis as assessed by the transient hyperaemic response test, reactivity to carbon dioxide and estimated cerebral perfusion pressure.

Cerebral haemodynamics in pregnancy and pre-eclampsia as assessed by transcranial Doppler ultrasonography.

BACKGROUND: Altered cerebral circulation, as reported during normal pregnancy, and in patients with pre-eclampsia, can be associated with changes in cerebral vascular reactivity and/or cerebral autoregulation. The aim of our study was to perform a comparative assessment of cerebral haemodynamics, including vascular reactivity and autoregulation, in pre-eclamptic patients, healthy pregnant women, and healthy non-pregnant women. METHODS: Thirty patients with pre-eclampsia were recruited. Age- and height-matched healthy pregnant (n=30) and non-pregnant control (n=30) groups were also recruited. Monitoring included transcranial Doppler ultrasonography, end-tidal carbon dioxide and non-invasive arterial pressure measurement. Cerebral autoregulation was assessed by performing the transient hyperaemic response (THR) test. The cerebrovascular reactivity to carbon dioxide (CRCO(2)) was assessed by measuring middle cerebral artery blood flow velocity (MCAFV) after induced changes in end-tidal carbon dioxide. Estimated cerebral perfusion pressure (eCPP) and critical closing pressure (CrCP) were calculated using established formulae. Statistical analysis included ANOVA with Tukey's pairwise comparisons. RESULTS: Mean arterial pressure (MAP) was increased in pre-eclampsia (P<0.05). Mean MCAFV was lower in healthy pregnancy (P<0.05), but in pre-eclampsia it was similar to the non- pregnant group. When compared with the non-pregnant group, mean eCPP was higher in the healthy pregnant and pre-eclamptic groups (P<0.05). There were no meaningful differences in cerebral autoregulation or CRCO(2). CONCLUSIONS: Healthy pregnancy increases eCPP, presumably by decreasing CrCP. In pre-eclampsia, eCPP is maintained at the same level as in healthy pregnancy despite an increased MAP. Pre-eclampsia has no significant effect on cerebral autoregulation or CRCO(2).

Scrotal and abdominal skin necrosis complicating intravenous vasopressin therapy for bleeding esophageal varices.

Two patients with severe liver disease developed scrotal necrosis after intravenous vasopressin infusion for bleeding esophageal varices. One of these patients also developed anterior abdominal wall skin necrosis. Although ischemic complications secondary to vasopressin are probably not totally avoidable, attention to hypovolemia, concomitantly administered pressor drugs, patient position, and points of local pressure may decrease the likelihood of these previously unreported complications.

Bullet embolization to the heart. Report of a case and review of the literature on indications for removal of intracardiac foreign bodies.

The hospital course of a young man with a bullet migration through the venous system to the right ventricle is reviewed. The intraoperative management of foreign bodies to the heart using x-ray image intensifier is employed.