Impaired cerebral autoregulation in patients with malignant hypertension.
BACKGROUND
In patients with a malignant hypertension, immediate parenteral treatment with blood pressure-lowering agents such as intravenous sodium nitroprusside (SNP) is indicated. In this study, we evaluated static and dynamic cerebral autoregulation (CA) during acute blood pressure lowering with SNP in these patients.


RESULTS
In 8 patients with mean arterial pressure (MAP) >140 mm Hg and grade III or IV hypertensive retinopathy at hospital admission, middle cerebral artery blood velocity (MCA V) and blood pressure were monitored. Dynamic CA was expressed as the 0.1-Hz MCA V(mean) to MAP phase lead and static CA as the MCA V(mean) to MAP relationship during SNP treatment. Eight normotensive subjects served as a reference group. In the patients, the MCA V(mean) to MAP phase lead was lower (30+/-8 degrees versus 58+/-5 degrees , mean+/-SEM; P<0.05), whereas the transfer gain tended to be higher. During SNP treatment, target MAP was reached within 90 minutes in all patients. The MCA V(mean) decrease was 22+/-4%, along with a 27+/-3% reduction in MAP (from 166+/-4 to 121+/-6 mm Hg; P<0.05) in a linear fashion (averaged slope, 0.82+/-0.15% cm x s(-1) . % mm Hg(-1); r=0.70+/-0.07).


CONCLUSIONS
In patients with malignant hypertension, dynamic CA is impaired. An MCA V(mean) plateau was not detected during the whole SNP treatment, indicating loss of static CA as well. This study showed that during the whole rapid reduction in blood pressure with SNP, MCA V(mean) decreases almost one on one with MAP.
Immink
Rogier V
RV
Department of Physiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
van den Born
Bert-Jan H
BJ
van Montfrans
Gert A
GA
Koopmans
Richard P
RP
Karemaker
John M
JM
van Lieshout
Johannes J
JJ
D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D000306:Adrenal Cortex Neoplasms / Q000378:metabolism; D000328:Adult; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000503:physiopathology*; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology; D002277:Carcinoma / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005922:Glomerulonephritis, IGA / Q000150:complications; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D020768:Middle Cerebral Artery / Q000503:physiopathology; D009599:Nitroprusside / Q000494:pharmacology* / Q000627:therapeutic use; D010211:Papilledema / Q000209:etiology / Q000503:physiopathology; D012166:Retinal Hemorrhage / Q000209:etiology / Q000503:physiopathology
D000305:Adrenal Cortex Hormones; D000959:Antihypertensive Agents; D009599:Nitroprusside; D006854:Hydrocortisone