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Simultaneous recordings of several cortical neurons were obtained before, during and after transient 15 min occlusion of the middle cerebral artery in cats. With the use of a multiple electrode array consisting of 4-7 platinum/iridium microelectrodes, the cortical pericellular blood flow was concurrently measured by means of the hydrogen clearance technique. Hydrogen clearance measurements revealed a homogeneous blood flow distribution throughout all phases of the experiment in the area covered by the different microelectrodes. Considering only the results of experiments with low residual blood flow during ischemia (less than 0.1 ml/g/min), single unit activity ceased immediately after occlusion and remained so during the ischemic period. The recovery time of action potentials after reperfusion ranged from 10 min to 3 hours depending on the examined neuron. Lower values for discharge rates of the individual cells were generally observed after reoccurrence, although some units exhibited temporarily an even higher spike frequency. Furthermore, the spike form usually changed in that the hyperpolarizing afterpotentials were enlarged after recirculation. However, some cells with a nearly unchanged spike form were found as well. The results indicate that the recovery of cell function largely depends on the individual neuron which supports the idea of a selective functional vulnerability of cortical neurons in response to ischemia.
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PMID:Selective functional vulnerability of cortical neurons following transient MCA-occlusion in the cat. 394 88

Nimodipine and its solvent containing ethanol were tested in a randomized in vivo study by local administration to the outer vessel wall surface of pial arteries and veins in 15 anesthetized cats. Reactions were studied through a cranial window. Diameter variations of 90 arterial and 78 venous vessel segments were continuously analyzed using a multichannel videoangiometer. The solvent alone caused minor though statistically significant (p less than 0.001) 7.6% dilatation, 8% in small and 7% in large arteries, which returned to their resting state after stopping treatment. 2.4 X 10(-5) M nimodipine plus solvent induced a 21% pial arterial dilatation (p less than 0.001), 26% in small and 17% in large arteries; dilatation induced by nimodipine plus solvent was significantly greater than dilatation by the solvent alone (p less than 0.001). After ceasing topical administration, arteries remained dilated by some 5%. Pial veins exhibited only minor reaction, i.e. a 6% (statistical n.s.) dilatation of large veins during nimodipine, and an 8% dilatation of small veins 20 minutes after stopping nimodipine. During solvent-administration rCBF, as estimated with the hydrogen clearance technique, remained unchanged. It is concluded that the dilatatory effect of the investigated compound on pial arteries is predominantly due to nimodipine.
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PMID:Effect of topical nimodipine versus its ethanol-containing vehicle on cat pial arteries. 396 31

The present study was designed to clarify the effect of blood glucose level on cerebral blood flow and metabolism during and after acute cerebral ischemia induced by bilateral carotid ligation (BCL) in spontaneously hypertensive rats (SHR). Blood glucose levels were varied by intraperitoneal infusion of 50% of glucose (hyperglycemia), insulin with hypertonic saline (hypoglycemia) or hypertonic saline (normoglycemia). Cerebral blood flow (CBF) in the parietal cortex and thalamus was measured by hydrogen clearance technique, and the supratentorial metabolites of the brain frozen in situ were determined by the enzymatic method. In non-ischemic animals, blood glucose levels had no influence on the supratentorial lactate, pyruvate or adenosine triphosphate (ATP) concentrations. In ischemic animals, however, cortical CBF was reduced to less than 1% of the resting value at 3 hours after BCL. However, there were no substantial differences of CBF during and after ischemia among 3 glycemic groups. Cerebral lactate in the ischemic brain greatly increased in hyperglycemia (34.97 +/- 1.29 mmol/kg), moderately in normoglycemia (23.43 +/- 3.13 mmol/kg) and less in hypoglycemia (7.20 +/- 1.54 mmol/kg). In contrast, cerebral ATP decreased in hyperglycemia (0.93 +/- 0.19 mmol/kg) as much as it did in normoglycemia (1.04 +/- 0.25 mmol/kg), while ATP reduction was much greater in hypoglycemia (0.45 +/- 0.05 mmol/kg). At 1-hour recirculation after 3-hour ischemia, ATP tended to increase in all groups of animals, indicating the recovery of energy metabolism. Such metabolic recovery after recirculation was good in hypo- and normoglycemia, and was also evident in hyperglycemia. Our results suggest that hyperglycemia is not necessarily an unfavorable condition in acute incomplete cerebral ischemia.
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PMID:Cerebral blood flow and tissue metabolism in experimental cerebral ischemia of spontaneously hypertensive rats with hyper-, normo-, and hypoglycemia. 396 37

A reproducible model of thromboembolism in the rat was developed and the temporal relationship between hydrogen clearance, regional cerebral blood flow (rCBF) and power spectral-analyzed electroencephalographic (EEG) activity explored for up to four hours postinsult. Sixteen rats were subjected to right internal carotid artery homologous blood embolization after electrocautery of the pterygopalatine artery. Four rats were subjected to sham operation. Cerebral angiography before and for up to four hours postinsult was used to verify the distal migration and fragmentation of the emboli. Preembolic mean rCBF was 62 +/- 9 ml . 100g-1 . min-1 and 65 +/- 12 ml . 100g-1 . min-1 in the embolized and contralateral sides, respectively. Based upon the distribution of the emboli at sacrifice, the experimental group of 12 rats fell into three subgroups: unilateral proximal embolism, n = 8; unilateral peripheral embolism, n = 3; and bilateral proximal embolism, n = 1. In unilateral proximal embolism the mean rCBF in the embolized hemisphere ranged between 10 and 20 ml . 100g-1 . min-1 and correlated well with changes in EEG power spectra. In unilateral peripheral embolism, the mean rCBF in the embolized hemisphere fell significantly 30 min postembolism. It returned progressively towards preembolic values as the embolic clots migrated distally and fragmented. Despite the restoration of rCBF, recovery of EEG activity appeared to be delayed. Our results did not show luxury perfusion after embolic insults. The time course for the reopening of the embolized artery and the delay in recovery of neuronal function (i.e., EEG activity) relative to the restoration of rCBF are discussed.
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PMID:Cerebral infarction in rats using homologous blood emboli: development of a new experimental model. 396 71

The upper limit of cerebral autoregulation was studied in pre- or early established hypertension in spontaneously hypertensive rats (SHR). Cerebral blood flow (CBF) was measured with the hydrogen clearance method, and wall/lumen ratio of cerebral arteries was morphometrically measured with the freeze-substitution technique. To test autoregulation, phenylephrine was intravenously infused to cause stepwise increments of blood pressure. Unilateral superior cervical ganglionectomy was carried out to examine the effects of sympathetic denervation on CBF autoregulation and thickness of vascular wall. Resting blood pressure at 4 weeks, 3 months and 6 months of age were 89 +/- 3 mm Hg (mean +/- SEM), 140 +/- 6 and 165 +/- 6, respectively. Baseline CBF was slightly diminished with age; 50.6 +/- 9.2 ml/100 g/min at 4 weeks, 49.8 +/- 8.1 at 3 months and 44.1 +/- 5.6 at 6 months. The upper limit of autoregulation was markedly raised with age; 118 +/- 5 mm Hg at 4 weeks, 180 +/- 7 at 3 months and 208 +/- 10 at 6 months. Acute sympathetic denervation lowered the upper limits to 105 +/- 2, 162 +/- 4 and 185 +/- 7 mm Hg, respectively. On the other hand, in chronic denervation which was made at 4 weeks of age, the upper limit of autoregulation in the denervated hemisphere was slightly lower than that in innervated hemisphere at 2 months (165 +/- 5 and 178 +/- 6 mm Hg), and at 5 months (202 +/- 8 and 215 +/- 8 mm Hg) after ganglionectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Upper limit of cerebral autoregulation during development of hypertension in spontaneously hypertensive rats--effect of sympathetic denervation. 400 63

A model for studying changes in local CBF and evoked potentials in selective thalamic ischaemia has been developed. The arterial supply to the posterior thalamus (mainly from the posterior choroidal arteries) was occluded in the baboon using a transorbital approach to the region of prepontine and ambient cisterns. Local CBF was measured by the hydrogen clearance method using electrodes introduced into the nucleus ventralis posterior lateralis of thalamus as well as cortex on both sides. The production of focal ischaemia was demonstrated by a significant decrease in thalamic CBF and confirmed by examination of the brain perfused with carbon particles.
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PMID:A model of selective experimental ischaemia in the primate thalamus. 400 65

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia]. 609 92

The effect of perfusion of the cerebral ventricles with artificial cerebrospinal fluid containing carbachol on the blood flow in the caudate nucleus of the cat and the possibility to inhibit this effect by anticholinergic drugs was studied by means of the hydrogen clearance technique. After a control period during which both lateral ventricles were perfused with artificial CSF of identical composition, the drug under study was added on one side (experimental side) while the other side continued to be perfused with the control artificial CSF (control side). The blood flow on the experimental side and on the control side were compared. A dose dependent response to carbachol was observed. Lower concentrations of carbachol (10(-6) up to 10(-4)M) caused vasodilatation whereas high concentrations (10(-3)M) caused local vasoconstriction. The increase in the local blood flow caused by the low carbachol concentrations was reduced by both atropine (10(-5)M) and hexamethonium (10(-3)M). The fall in CBF observed with the high carbachol concentration was prevented by atropine (10(-5)M). It may be concluded that low, physiologically more meaningful, carbachol concentrations cause a local vasodilatation due to interaction with both muscarinic and nicotinic receptors.
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PMID:Response of local blood flow in the caudate nucleus of the cat to intraventricular administration of carbachol. 614 38

Proton nuclear magnetic resonance (NMR) images depict the distribution and concentration of mobile protons modified by the relaxation times T1 and T2. Using the steady-state-free-precession (SSFP) technique, serial coronal images were obtained sequentially over time in laboratory animals with experimental ischemic infarction. Image changes were evident as early as 2 hours after carotid artery ligation, and corresponded to areas of ischemic infarction noted pathologically. Resulting SSFP images in experimental stroke are contrasted to inversion-recovery NMR images in an illustrative patient with established cerebral infarction. Bulk T1 and T2 measurements were made in vitro in three groups of gerbils: normal, those with clinical evidence of infarction, and those clinically normal after carotid ligature. Infarcted hemispheres had significantly prolonged T1 and T2 (1.47 +/- .12 sec, 76.0 +/- 9.0 msec, respectively) when compared to the contralateral hemisphere (T1 = 1.28 +/- .05 sec, T2 = 58.7 +/- 3.9 msec) or to the other two groups. These data suggest that changes in NMR parameters occur and can be detected by NMR imaging as early as two hours after carotid artery ligation.
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PMID:Proton NMR imaging in experimental ischemic infarction. 630 Nov 12

Eicosapentaenoic acid prevents platelet aggregation and inhibits arachidonate conversion into thromboxane A2 and prostaglandins. Consequently eicosapentaenoic acid might protect the brain from the ischemia that follows cerebral arterial occlusion. We studied the effect of eicosapentaenoic acid on cerebral ischemia in anesthetized gerbils. Ischemia was produced by bilateral carotid occlusion for 10 min, followed by reperfusion for 60 min, in gerbils fed either a standard diet (control) or a diet supplemented with menhaden fish oil for 2 months. The menhaden fish oil contained 17 mole % eicosapentaenoic acid. Regional cerebral blood flow was measured by the hydrogen clearance method and brain water by the specific gravity technique. In control animals cerebral blood flow was decreased 30 and 60 min after reperfusion (p less than .001) and brain water was increased (p less than .001). In the experimental group cerebral blood flow did not fall during reperfusion and edema did not appear. Brain prostaglandins and thromboxane were measured by radioimmunoassay. PGF2 alpha, PGE2, 6-keto PGF1 alpha and TXB2 increased after severe ischemia and reperfusion. The synthesis of brain diene prostaglandins was not altered by eicosapentaenoic acid. Our study indicates that eicosapentaenoic acid prevented post-ischemic cerebral edema and hypoperfusion, without affecting the levels of brain diene prostaglandin and thromboxane.
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PMID:Eicosapentaenoic acid: effect on brain prostaglandins, cerebral blood flow and edema in ischemic gerbils. 632 May 4


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