Cerebral Blood Flow and Brain Function During Hypotension and Shock

Kovách, A. G. B.; Sándor, Péter

doi:10.1146/annurev.ph.38.030176.003035

Cited by 95 publications

(25 citation statements)

References 60 publications

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“…This is similar to changes seen by others in the late phases of shock (20,32). In the room-air survivors, brain flow remained constant during hemorrhage when they were hypotensive.…”

Section: Resultssupporting

confidence: 89%

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

et al. 1983

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SummaryNineteen newborn lambs, spontaneously breathing room air, were hemorrhaged of 50% of their measured blood volume over a 30-min period. They were then observed for the following 90 min. No fluid or blood was reinfused during the study. Eight of the 19 lambs survived beyond the study period, the other 11 died at the end of the hemorrhage or during the recovery period. All lambs became hypotensive and bradycardic during the hemorrhage. All became tachycardic after the hemorrhage. Blood pressure of the survivors returned towards baseline levels whereas it continued to fall in the non-survivors. All animals became anemic, acidotic, and hypocarbic but remained normoxemic.Myocardial blood flow fell to approximately 50% of baseline levels in both survivors and non-survivors during, and at the end of the hemorrhage. It returned to near baseline levels in the survivors by 90 min posthemorrhage. Cerebral blood flow remained at baseline levels during the hemorrhage in the survivors but cerebral oxygen delivery decreased. Flow rose 10% above baseline levels 90 min after hemorrhage but oxygen delivery remained low. In the non-survivors, cerebral blood flow fell to 60% of baseline and cerebral oxygen delivery was 50% of baseline by the end of the hemorrhage.A group of five lambs was hemorrhaged and studied in the same fashion as the 19, except that they breathed 4.5% CO 2 beginning 15 min before the hemorrhage, during the hemorrhage and 90 min recovery period. Four of these five survived the study period. They remained normocarbic and became more acidotic than the animals that breathed room air. Blood pressure and heart rate fell during hemorrhage but these decreases were less than in either group of room air breathing animals. During recovery they became tachycardic and blood pressure returned to baseline levels. Myocardial blood flow increased 20% above baseline by the end of hemorrhage and 40% above baseline by 90 min posthemorrhage. Cerebral blood flow increased 40% above baseline during the hemorrhage and remained at that level at the end of hemorrhage and 90 min afterwards. The increase in brain blood flow was sufficient to maintain oxygen delivery to the brain at baseline levels throughout the experiment. SpeculationWe speculate that the normal response for the normocarbic lambs is to increase cerebral and myocardial blood flow in response to anemia and hypotension. Spontaneous hyperventilation with hypocarbia tends to interfere with this response both in the brain and in the myocardium. The effect of hypocarbia is greater in the myocardium. The net result is a decrease in oxygen delivery to these tissues. If the same responses were to occur in the human infant it might be important to maintain normocarbia during resuscitation of infants suffering from hemorrhagic shock. 70

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“…This is similar to changes seen by others in the late phases of shock (20,32). In the room-air survivors, brain flow remained constant during hemorrhage when they were hypotensive.…”

Section: Resultssupporting

confidence: 89%

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

et al. 1983

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“…Evidence for this is that the EEG is impaired at arterial pressures of 50-60 mm Hg, and an isoelectric EEG develops after 20-30 min at 30-40 mm Hg in unanesthetized dogs and cats. 10 Further, the degree of EEG impairment seems also to depend on the rate of hemorrhage. Marked loss of EEG activity is seen in anesthetized cats at arterial pressures below 60 mm Hg if blood withdrawal is very rapid," although Yashon et al 12 report no loss of EEG activity in dogs subjected to rapid hemorrhage from 120-30 mm Hg and maintained for up to 2 h. This might have been due to protection of the brain by the barbiturate anesthesia which is known to reduce cerebral metabolic demand, 13 '" and to protect the brain against ischemia.…”

Section: Electroencephalogrammentioning

confidence: 99%

Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

Gregory¹,

McGeorge²,

Fitch³

et al. 1979

Stroke

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SEVERE HYPOTENSION produces a loss of cerebral function, the extent and reversibility of which depends on the degree and duration of the period of hypotension. Recent studies have described the changes in cerebral function over periods of sustained hypotensionThe present study forms part of a systemic investigation which attempts to correlate the changes in cerebral blood flow during graded hemorrhagic hypotension with the subsequent alteration in cerebral functional activity and the development of hypoxic brain damage.This communication reports the changes observed in cerebral functional activity during hypotension and relates these changes to the arterial pressure and to the corresponding alterations in the cerebral circulation. The detailed accounts of the impairment of the cerebral circulation and development of brain damage due to hypotension are given in the accompanying papers. 5 ' 6 It has been suggested 7 that the somatosensory evoked response is a more accurate guide than the EEG to brain damage during hypotension. Therefore, both these parameters were measured in this study. Methods General DescriptionThe effect of graded hemorrhagic hypotension on electrocortical activity was determined in 2 parallel studies in a total of 12 cats, of either sex, weighing between 1.6 and 4.8 kg. Anesthesia and general Reprints: Dr. David I. Graham, the University of Glasgow, Wellcome Surgical Institute, Garscube Estate, Bearsden Road, Bearsden, Glasgow, G61 1QH, Scotland. preparation of the animals were identical to those described previously. Measurement of Somatosensory Evoked ResponseSix cats were used to study the effects of hypotension on the somatosensory evoked response. The cats were placed in a head-holder and the scalp was incised along the midline and reflected. A small craniotomy (approximately 1.5 X 1.0 cm) was made over the sensory cortex, using a saline-cooled dental drill, and a reference silver-electrode was implanted in the neck muscle. A supramaximal stimulus (0.5-2V, 0.2 msec, 1 Hz) was applied via a DISA type 14 E12 time base unit to the contralateral superficial radial nerve. Bipolar silver ball-tipped recording electrodes were then positioned (1 cm apart) on the surface of the dura to obtain maximal potential. Signals from the recording electrodes were amplified with a band width of 2-500 Hz and the average of 16 evoked potentials recorded with a DISA type 14 GO1 digital averager from which the measurements were taken and of which a photographic record was kept.The somatosensory evoked response was recorded for a control period of 30 min and then the animal was subjected to stepwise hypotension induced by controlled hemorrhage.5 Mean arterial pressure was decreased by approximately 10 mm Hg at each step and allowed to stabilize for approximately 10 min at each new level before the potentials were recorded. The effect of this hypotension on the evoked response was assessed in terms of the average peak-to-peak amplitude of the positive/negative sequence of the primary evoked response; 8 and t...

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“…3). This effect is probably due to a hypoxic transmitter release (Meyer et al, 1976;Kovach and Sandor, 1976), which is followed by progressive EEG depression . This symptomatology is fairly characteristic in cerebrovascular insufficiency.…”

Section: Discussionmentioning

confidence: 99%

“…The correlation of neurotransmitter function and cerebral ener gy production (Meyer et al, 1976), recovery of neuronal function after brain ischemia (Hossmann, 1971;Hossmann and Hossmann, 1973), metabolic changes of the brain tissue due to hypoxia (Siesjd and Nilsson, 1971;Siesjd and Plum, 1973;Ljunggren et al, 1974) and corre lation of cerebral blood flow and brain function (Gygax et al, 1975a, c;Kovach and Sandor, 1976) were some of the most important topics in this field. Meyer et al (1976) have shown that energy deprivation as characteristic of cerebral vascular insufficiency is accompanied by a transmitter release.…”

mentioning

confidence: 99%

Pharmacological Aspects of Dihydrogenated Ergot Alkaloids in Experimental Brain Research

Meier‐Ruge¹,

Emmenegger²,

Enz³

et al. 1978

Pharmacology

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In three different experimental series with 22 experimental and 21 control cats it is demonstrated that DH-ergotoxine mesylate (Hydergine®) improves EEG energy, disturbed by temporary ischemia, in the isolated perfused cat head. It could be shown that improvement of EEG energy and lowering of arteriovenous lactate difference can be directly correlated. DH-ergonine improves experimentally induced metabolic decline as does DH-ergotoxine, but at one tenth of the dosage.

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Cerebral Blood Flow and Brain Function During Hypotension and Shock

Cited by 95 publications

References 60 publications

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

Effects of Arterial Carbon Dioxide Tension on the Newborn Lamb's Cardiovascular Responses to Rapid Hemorrhage

Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

Pharmacological Aspects of Dihydrogenated Ergot Alkaloids in Experimental Brain Research

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