Cerebrovascular response to hypotension in hypertensive rats: effect of antihypertensive therapy
Hoffman, W.E.; Miletich, D.J.; Albrecht, R.F.
Anesthesiology 58(4): 326-332
1983
ISSN/ISBN: 0003-3022 PMID: 6837973 Document Number: 212817
The possibility that antihypertensive therapy in spontaneously hypertensive rats (SHR) will reverse the shift in cerebral autoregulation and improve cerebrovascular performance during sodium nitroprusside[SNP]-induced hypotension was tested. Four-month-old SHR and Wistar Kyoto controls (WKY) were tested using 4 groups. One group each of SHR and WKY received 10 wk of antihypertensive drug treatment using the vasodilators minoxidil and hydralazine combined with a .beta.-adrenergic blocker, propranolol. A 3rd and 4th group of SHR and WKY, respectively, received 10 wk of sham treatment (n = 15). Systolic pressure was measured weekly by tail cuff occlusion. Anitihypertensive drug treatment significantly decreased blood pressure in SHR and WKY over the 10-wk treatment period. At the end of 10 wk, cerebral blood flow (CBF) was measured under control conditions (ketamine anesthesia plus hexamethonium pretreatment) and during SNP-induced hypotension to mean pressure levels of 82-92 mmHg and 54-58 mmHg. CBF was measured with radioactive microspheres and cerebral O2 consumption (CMRO2) was calculated as the product of CBF and arterial-sagittal sinus blood O2 content difference. Antihypertensive therapy did not significantly alter CBF in SHR or WKY measured under control conditions compared with sham-treated controls. Decreasing blood pressure to 82-92 mmHg produced a 49% decrease in CBF in sham-treated SHR (P < 0.05) but no significant change in CBF in sham- or antihypertensive-treated WKY or antihypertensive-treated SHR. At a mean blood pressure level of 54-58 mmHg, CBF decreased significantly in all SHR and WKY test groups, and decreased significantly more in sham- (69%) than in antihypertensive-treated SHR (49% P < 0.05). Long-term antihypertensive therapy may reverse the shift in cerebral autoregulation produced by chronic hypertension.