Cerebral hemodynamics, blood gases, and electrolytes during breath-holding and the Valsalva maneuver.
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Biomedical subjects
Publications and source records attributed to F Gotoh.
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Serum dopamine-beta-hydroxylase (DBH) activity was measured in 34 patients with acute cerebrovascular disease. The serum level of DBH activity showed its highest value soon after the onset of stroke and then gradually decreased over the next few days. After reaching its lowest level, the DBH activity again showed a slight increase. There was no direct relationship between serum DBH activity and total serum protein, or blood pressure. In 8 of 12 patients, DBH activity in the cerebral venous blood was higher than that in the arterial blood. These results suggest that rapid release of DBH into the circulating blood occurred after stroke, presumably from sympathetic nerve endings in the vessels or organs, including the brain.
The influence of sympathetic nervous activity on cerebral circulation and cerebrovascular CO2 reactivity was investigated through inhibition of dopamine beta-hydroxylase (DBH). A PO2 electrode, a PCO2 electrode and a plate-type thermocouple-flowmeter were placed on the pial surface of the cat brain. Cerebrocortical PO2, PCO2, cerebrocortical blood flow and arterial blood pressure were continuously recorded before, during and after intracarotid infusion of 10 mg/kg of fusaric acid, a potent DBH inhibitor. The effects of 5% CO2 inhalation and hyperventilation were measured before and after the inhibition of DBH. Following the intracarotid infusion of fusaric acid, cerebrocortical PO2 and cerebrocortical blood flow increased significantly. After the inhibition of DBH, the degree of the increase in cerebrocortical PO2 during 5% CO2 inhalation was enhanced while the degree of the decrease in cerebrocortical PO2 during hyperventilation did not show any significant change. The cerebral vasodilatation caused by fusaric acid suggests that the sympathetic nervous system takes part in the resting tone of cerebral blood vessels. The increase in the cerebrovascular CO2 reactivity produced by the inhibition of DBH suggests that the sympathetic nervous system modifies cerebrovascular CO2 reactivity.
Thirty-one cats were divided by age into 3 groups, young (Y), middle (M) and old (O). Continuous recordings of local cerebral blood volume (CBV) and frequent measurements of mean transit time of blood (t) were made from the Sylvian opercula after ischemia was produced by transorbital clipping of the middle cerebral artery at its origin (MCA occlusion). Control recordings were made simultaneously from the corresponding area of the contralateral cerebral hemisphere. MCA occlusion temporarily stopped cerebral blood flow (CBF) in the area supplied by the ipsilateral MCA, as indicated by a rapidly decreasing CBV and complete disappearance of hemodilution curves. Within 30 sec, CBF resumed with a dilatation of the vascular bed and reappearance of hemodilution curves through newly developed collateral channels. Despite a low CBF, below half the control, CBV recovered, overshooting the control level. The appearance of hyperemia in the ischemic area was statistically significant. Such "low perfusion hyperemia" was slower in appearance and of more diverse magnitude in group O than in group Y. This suggested that aging may lead to a decrease in rapidity of the vascular response to ischemia and impair the integrity of collateral vessels.
The retinal arterial diameter and its response to changes in perfusion pressure were measured by means of a fundus camera in 65 normal subjects. A reduction of effective MABP was induced by a postural change from a recumbent to an erect position. A small but significant increase in retinal arterial diameter was observed by reduction of the perfusion pressure in all subjects. The reduction of retinal arterial reactivity in response to blood pressure changes (-% change in diameter/delta effective MABP) was significantly correlated with advancing age (p less than 0.01). No significant correlations were observed between the retinal arterial reactivity, magnitude of the retinal arterial diameter (range: 60-140 mu), and systemic blood pressure (range of MABP: 75-110 mmHg). These results indicate that the retinal artery has an autoregulatory mechanism which is influenced by aging.
The steal phenomenon due to a vasodilator was investigated in 6 cats in which cerebral ischemia had been produced by left middle cerebral artery (MCA) occlusion. The photoelectric method was employed for continuous recording of the cerebral blood volume together with frequent determinations of the cerebral blood flow (CBF) through the ischemic cerebral tissue at the following four stages: before MCA occlusion, 2 hours after MCA occlusion before the injection of papaverine, after the injection of papaverine, and when the systemic arterial blood pressure (SABP) was adjusted non-pharmacologically to the control level using a "vasculator". The administration of the vasodilator produced conflicting results for the CBF changes in the ischemic area with a decrease in SABP as reported previously in the literature. However, when the SABP was corrected to the control level, the CBF in the ischemic region became increased in all 6 cases to above the control ischemic flow values. It is concluded that the decreased CBF in the ischemic tissue after vasodilator administration was not due to the steal phenomenon, but simply to a fall in SABP.
Due to methodologic difficulties, few investigations have been made on the blood flow velocity in the cerebral microcirculation. Using a newly developed video camera method, we simultaneously measured the blood flow velocity and diameter of pial arteries during hemorrhagic hypotension, after blood pressure recovery, and during CO2 inhalation in cats. When the mean arterial blood pressure was lowered from 129.7 +/- 6.6 to 71.5 +/- 4.1 mm Hg, the blood flow velocity inevitably decreased from 36.6 +/- 5.3 to 27.0 +/- 3.9 mm/sec (p less than 0.001). The calculated blood flow rate [pi X (diameter/2)2 X flow velocity] was preserved in cases with concomitant vasodilation. Conversely, the blood flow velocity increased from 25.3 +/- 5.1 to 31.0 +/- 5.4 mm/sec (p less than 0.001) after mean arterial blood pressure recovery from 67.1 +/- 3.7 to 129.8 +/- 5.8 mm Hg. The blood flow rate was again preserved in vessels with a vasoconstrictive response. Each pial artery apparently dilated or constricted in proportion to the decrease or increase in flow velocity during blood pressure changes, maintaining a constant cerebral blood flow. This indicated the importance of the pial arteries in the mechanisms of cerebral blood flow autoregulation. During 5% CO2 inhalation, the blood flow velocity increased markedly from 25.4 +/- 4.6 to 37.2 +/- 10.0 mm/sec (p less than 0.05), while the pial artery diameter (85.0 +/- 13.7 microns) increased by 9.6 +/- 1.5% (p less than 0.01). The increased flow velocity might be attributable to preferential dilatation of small arterioles or intraparenchymal vessels during hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
A newly developed photoelectric method was used in 5 rhesus monkeys to measure the mean transit time of blood through the carotid and vertebral arteries, together with measurement of the blood flow through the tissues of the fronto-parietal area supplied by the carotid artery and of the cerebellar tonsil supplied by the vertebral artery. Following intravenous administration of betahistine mesylate, a histamine analog, the mean transit times of blood through the 2 arteries were equally shortened by 10%, despite a 20% decrease in the mean arterial blood pressure (P less than 0.05). The cerebral tissue and cerebellar tissue blood flow was increased by betahistine, from 70.4 to 81.4 ml/100g/min and from 73.2 to 84.0 ml/100g/min, respectively. Since histamine has been reported to produce a decrease in cardiac output, the increase in cerebral blood flow confirmed that betahistine is a selective cerebral vasodilating agent. However, by comparing the hemodynamic data for the two cerebral arterial systems, it can be concluded that the responses of the carotid and vertebral arterial systems to the vasodilating action of betahistine were essentially the same in extent.
Cerebrovascular autoregulation and CO2 reactivity were measured repeatedly in 3 patients with the multiple system atrophy type of autonomic insufficiency (Shy-Drager syndrome) by means of the 133Xe injection method. The degree of cerebral blood flow (CBF) dysautoregulation showed day-to-day variations in 2 of the 3 patients. The CO2 reactivity was normal or supernormal in the supine position in patients with impaired autoregulation. In the head-up position the response to CO2 was slightly suppressed in 2 of the patients, suggesting that chemical control may have tended to compensate for CBF dysautoregulation. It is concluded that the mechanism of chemical control of the cerebrovasculature is different from that which controls autoregulation and may have partially compensated for CBF dysautoregulation.
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