Biomedical subjects

R M Bryan

Publications and source records attributed to R M Bryan.

At least 37 records · Page 2Linked to original sources

PubMed1998

Calcium-dependent and ATP-sensitive potassium channels and the 'permissive' function of cyclic GMP in hypercapnia-induced pial arteriolar relaxation.

The conclusion that cyclic 3'-5 guanosine monophosphate (cGMP) functions in a 'permissive' manner in promoting cerebrovasodilation during hypercapnia was based on findings showing that the nitric oxide synthase (NOS) inhibitor-induced repression of the CO2 response could be reversed upon addition of exogenous cGMP. We hypothesized that the action of cGMP revealed in those studies does not define its normal role in hypercapnic cerebral vasodilation, but rather is a unique function of the artificial situation of NOS inhibition coupled with cGMP repletion. Thus, although CO2 reactivity may be the same in normal versus cGMP-repleted animals, the factors contributing to that response may differ. To test that possibility, the effects of calcium-dependent (KCa) or ATP-sensitive (KATP) potassium channel blockers on pial arteriolar CO2 reactivity, in vivo, were evaluated in the presence and absence of NOS inhibition plus administration of a cGMP analogue. Pial arteriolar diameter changes in hypercapnia were measured in three principal groups of anesthetized rats: (I) KCa channel-inhibited (via iberiotoxin); (II) KATP channel-inhibited (via glibenclamide); and (III) controls. Group I and II rats were further divided into: (a) those treated with the neuronal NOS (nNOS) inhibitor, 7-nitroindazole (7-NI), followed by successive suffusions of the cGMP analogue, 8-bromo-cGMP (8Br-cGMP) and 8Br-cGMP+K-channel blocker; and (b) rats where 7-NI and 8Br-cGMP applications were omitted. Group III rats were divided into time and 8Br-cGMP controls. Hypercapnia (PCO2 congruent with60 mmHg, 3 min)-induced dilations were reduced by 70-80% following 7-NI and restored by 8Br-cGMP. That restoration was reversed by both K-channel blockers. In the absence of 7-NI and exogenous cGMP, CO2 reactivity was unaffected by K-channel inhibition. These findings confirmed that nNOS-derived NO is critically important to the hypercapnic reactivity of cerebral arterioles, and that cGMP repletion, following NOS inhibition, could restore CO2 reactivity. The observation that KCa and KATP channel blockade did not alter CO2 reactivity under baseline conditions, but attenuated CO2 reactivity only in the presence nNOS inhibition (and cGMP repletion), suggests that multiple, redundant, and interactive mechanisms participate in CO2-induced vasodilation. These results also imply that current strategies for revealing permissive actions of cGMP (or NO) may need to be re-evaluated.

Adenosine Triphosphate↗

PubMed1998

Comparison of the myogenic response in rat cerebral arteries of different calibers.

The myogenic response, the characteristic of blood vessels to contract with increasing pressure, was studied at three different locations along the middle cerebral artery (MCA) vascular tree. We hypothesized that smaller caliber vessels would have a more pronounced myogenic response at lower pressures than larger diameter arteries, corresponding to pressures normally experienced in vivo. Cerebral vessels (MCAs, branches of the MCA, and penetrating arterioles) were isolated from male rats, cannulated with glass micropipettes, and pressurized. Changes in diameter were measured as the transmural pressure was increased from 20-100 mmHg. The MCAs, which had a resting diameter of 202 +/- 10 micron (n = 9) at 50 mmHg, showed its greatest myogenic response between 60-100 mmHg (8+/-2% constriction, n = 9, p < 0.001). The penetrating arterioles [58 +/- 4 micron (n = 8) at 50 mmHg], on the other hand, showed its greatest myogenic response between 20-60 mmHg (10 +/- 4% constriction, n = 8, p < 0.05). Branches of the MCA [118 +/- 14 micron (n = 8) at 50 mmHg] showed a slight constriction over the entire pressure range (5 +/- 9% constriction between 20-100 mmHg, p=ns). Our results suggest that the myogenic response appears to be best developed in the range of pressures found during physiological conditions for a given vessel in the MCA territory. This characteristic is fundamental in the overall control of cerebrovascular resistance.

Animals↗

PubMed1998

Endothelial-mediated dilations following severe controlled cortical impact injury in the rat middle cerebral artery.

The mechanisms associated with dysfunction of the cerebral vasculature following head trauma have not yet been fully elucidated. In an attempt to shed more light on the matter, we investigated the endothelial-mediated dilations in the rat middle cerebral artery (MCA) following severe traumatic brain injury (TBI). Rats were subjected to severe controlled cortical impact injury (CCI; 5 m/s, 130 ms duration, 3 mm deformation) over the right parietal cortex. At 24 h postinjury, ipsilateral segments of MCA and corresponding contralateral segments were isolated, mounted in a vessel chamber, and pressurized. The responses to 2 methylthio-ATP (2MeSATP), a selective agonist for the P2Y1 purinoceptors, N(omega)-nitro-L-arginine (L-NAME), an NO synthase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), an exogenous NO donor, were determined. 2MeSATP elicited concentration dependent dilations in all MCAs studied. Ipsilateral MCAs harvested following TBI or sham-TBI, showed similar maximum dilations to 2MeSATP [70 +/- 4% (n = 17) and 72 +/- 6% (n = 13), respectively]. However, TBI reduced the concentration of 2MeSATP necessary to elicit one-half of the maximum dilation (EC50) from 15 to 9 nM (p < 0.05). Inhibition of NO synthase with 10(-5) M L-NAME abolished the dilation to 2MeSATP in both TBI and sham-TBI MCAs. The constriction to L-NAME was significantly reduced in TBI MCAs compared to sham vessels. Dilations to SNAP, an NO donor, were not altered by TBI indicating that the mechanisms of dilation involving NO in the vascular smooth muscle were not affected. Unlike other pathological conditions which often diminish endothelial-mediated responses, severe TBI enhanced the sensitivity to 2MeSATP without altering the maximum response.

Adenosine Triphosphate↗

PubMed1998

Temporal effect of severe controlled cortical impact injury in the rat on the myogenic response of the middle cerebral artery.

The present study examined the effect of severe traumatic brain injury (TBI) on the myogenic response in the rat middle cerebral artery (MCA). Rats were subjected to severe controlled cortical impact (CCI; 5 m/sec, 130-msec duration, 3-mm deformation) injury over the right parietal cortex. At 2, 24, and 120 h postinjury, ipsilateral and contralateral segments of MCAs were isolated, mounted in a vessel chamber, and pressurized. After equilibration, the myogenic tone, the difference in vessel diameter in the presence and absence of calcium for a given pressure, and the myogenic response (the active contractile response elicited by a vessel to increasing pressure), were measured. At 24 h postsurgery, there was a significant interaction between myogenic tone and pressure in the ipsilateral and contralateral MCAs when TBI was compared to shams. However, this was not apparent, at the 2- and 120-h time points. At 2- and 24-h postsurgery, there was a significant interaction between myogenic response and pressure in the ipsilateral MCAs when TBI was compared to shams. While the response of the vascular smooth muscle was altered following injury, it was still functioning, suggesting that these vessels compensate, perhaps through alternate mechanisms or by relying on those remaining intact mechanisms.

Animals↗

PubMed1998

Effect of decreased glucose concentration on cerebrovascular tone in vitro.

We studied the effect of decreased glucose concentration on cerebrovascular tone in vitro. Segments of rat middle cerebral arteries (MCA) were isolated, cannulated at both ends with glass micropipettes, and pressurized to 85 mm Hg. Decreasing the glucose in the extraluminal bath and luminal perfusate from 5.5 mmol/L to 1.0 or 0.5 mmol/L for 1.5 hours each had no significant effect on the diameter of the arteries. When all the glucose was removed from the extraluminal bath and luminal perfusate for 1.5 hours, the MCA dilated by 23% [252 +/- 24 (SD) microns to 311 +/- 7 microns (P < .5, n = 7)]. This dilation was 80% of the maximum dilation produced by removal of Ca+2 from the bathing solutions. Neither removal of the endothelium nor inhibition of the ATP-sensitive K channels with 10(-5) mol/L glibenclamide altered the response of the isolated MCA to the removal of glucose. We conclude that rat MCA are relatively more resistant to substrate limitation compared to the brain as a whole.

ATP-Binding Cassette Transporters↗

PubMed1998

Inward rectifier potassium channels in the rat middle cerebral artery.

Inward rectifier K+ channels (Kirs) were studied in the isolated perfused rat middle cerebral artery (MCA). The addition of 15 mM K+ (KCl) to the extraluminal bath dilated the MCAs. These dilations were blocked by selective inhibitors for the Kirs (40 microM BaCl2 or 40 mM CsCl) but not selective inhibitors for other K+ channels (glibenclamide, tetraethylammonium, or 4-aminopyridine). Neither removal of the endothelium nor treatment with the nitric oxide synthase inhibitor (NG-nitro-L-arginine methyl ester, 10 microM) affected the K(+)-induced dilation. The addition of BaCl2 to resting MCAs produced a dose-dependent constriction of 8-12%, indicating that, during resting conditions, Kirs aid in setting or determining the resting tone. The magnitude of the dilations produced by the addition of K+ or constrictions produced by BaCl2 were independent of pressure over a range of 40-100 mmHg. We conclude that Kirs, which produce a dilation when activated, exist on the vascular smooth muscle of the rat MCA. These Kirs aid in determining the resting tone of the vessel, and their function is independent of pressure over physiological pressure ranges.

Animals↗

PubMed1998

Altered function of inward rectifier potassium channels in cerebrovascular smooth muscle after ischemia/reperfusion.

BACKGROUND AND PURPOSE: Several recent studies have demonstrated that inward rectifier potassium channels (K(ir)s) are located on vascular smooth muscle of cerebral arteries in the rat. Activation of the K(ir)s dilates the arteries by relaxing the vascular smooth muscle. We tested the following hypothesis in the present study: function of inward rectifier potassium channels is altered after ischemia/reperfusion (I/R). METHODS: Temporary (2-hour) focal ischemia was induced in male Long-Evans rats (3% isoflurane anesthesia) by the intraluminal filament model. After 24 hours of reperfusion, ipsilateral and contralateral middle cerebral arteries (MCAs) were harvested and mounted on micropipettes, pressurized to 85 mm Hg, and luminally perfused. RESULTS: Resting diameters for contralateral (control) and ipsilateral (I/R) MCAs were not significantly different (215+/-4 microm and 211+/-5 microm [n = 6 and n = 7], respectively). Activation of the K(ir)s by abluminal administration of 15 mmol/L KCl to the control MCAs dilated the MCA by 34+/-4% (n = 8). Activation of the K(ir)s in I/R MCAs produced a dilation of only 11+/-3% (n = 8; P<0.001 compared with control). BaCl2 (75 micromol/L), a concentration-selective inhibitor of the K(ir)s, significantly attenuated the dilation produced by 15 mmol/L KCl in control MCAs but not in the I/R MCAs. Endothelial-mediated dilations elicited by the luminal administration of uridine triphosphate (10 micromol/L) produced similar dilations in both groups (32+/-5% for sham [n = 4] and 33+/-2% for I/R [n = 4]), indicating that dilator function in general was not altered in I/R vessels. CONCLUSIONS: We conclude that Kir function is altered after I/R. The Kir altered function is likely to exacerbate the brain injury occurring after I/R.

Animals↗

PubMed1997

Endothelial-mediated dilations of rat middle cerebral arteries by ATP and ADP.

The hypothesis that ATP and ADP produce dilations of rat middle cerebral arteries (MCAs) by different mechanisms was tested. Vessel diameters were measured from pressurized, perfused MCAs after application of different agonists. The luminal administration of ATP and ADP elicited concentration-dependent dilations (35% maximum). Removal of endothelium abolished the dilation to intraluminal ATP and attenuated the dilation to intraluminal ADP. The dilations to ATP were abolished with N omega-nitro-L-arginine methyl ester (L-NAME; 10 microM), a nitric oxide synthase inhibitor, at ATP concentrations of 1 microM and below. However, at concentrations of 10 microM ATP and above, L-NAME had no effect on the response. The dilations to ADP were attenuated by L-NAME to the same degree as removal of endothelium. The mechanism for dilation by ATP was identical to that of UTP, a selective P2u purinoceptor agonist. The mechanism of dilation by ADP was similar to that of 2-methylthioadenosine 5'-triphosphate, a selective P2y purinoceptor agonist. We conclude that ATP and ADP elicit dilations of rat MCA by different mechanisms. ATP and ADP likely stimulate P2u and P2y purinoceptors, respectively.

Adenine Nucleotides↗

PubMed1997

Nitric oxide-synthesizing perivascular nerves in the rat middle cerebral artery.

Although perivascular nerves containing nitric oxide synthase (NOS) have been anatomically described for rat cerebral arteries, a dilator function for these nerves has eluded investigators when using isolated vessels. Rat middle cerebral arteries (MCAs) were isolated, pressurized, and electrically stimulated. The resting diameter of the MCAs after pressurization was 233 +/- 4 microns (n = 17) in one study. The MCAs showed a frequency-dependent dilation when stimulated. Maximum dilation (25-30% increase in diameter) occurred at a frequency of 8-16 Hz. Removal of endothelium or glibenclamide (10(-5) M), a blocker of ATP-sensitive potassium channels, had no effect on the dilations. The dilations were completely blocked with NG-nitro-L-arginine methyl ester (L-NAME) (10(-5) M), a general NOS inhibitor, and cold storage (24 h). The inhibition by L-NAME could be reversed by the addition of 10(-8) M L-arginine, the active precursor of NOS. Furthermore, 7-nitroindazole (10(-4) M), an inhibitor specific for the neuronal isoform of NOS, reduced the dilations by 43% (P < 0.05). Transections of nerve bundles originating from the sphenopalatine ganglia at the ethmoidal foramen blocked the dilations produced by electrical stimulations. We conclude that rat cerebral arteries have functionally intact perivascular nerves that dilate by releasing nitric oxide.

Animals↗

PubMed1996

The in vitro action of polyamines on rat basilar and femoral artery contractile activity.

This study was performed to assess the role of exogenously administered polyamines on rat basilar and femoral artery contractile activity in vitro. With the endothelium removed, rings of tissue were set up in organ chambers to measure isometric tension. The polyamines (0.1-3 mM), putrescine, spermidine, and spermine, were added to the tissue baths; after 30 min of incubation a cumulative concentration response curve (CRC) was obtained with either KCl or serotonin (5-HT). Additional CRCs were run with Ca(2+) in high K+ Krebs (60 mM). In both tissues, the CRCs to KCl were shifted to the right in a dose-dependent manner for spermidine and spermine (1 & 3 mM) but not putrescine. Spermine (3 mM) depressed the KCl maxima by 18.6% and 10.1% in the basilar and femoral artery respectively. For 5-HT CRCs, only spermine (3 mM) slightly inhibited the maximal response in both tissues. The most potent action of spermine was on inhibition of Ca(2+) responses in high K+ where the EC50S were shifted 3.5 and 10 fold over control values in the basilar and femoral respectively. We conclude spermidine and spermine, but not putrescine, attenuate vascular smooth muscle contractions on the basilar and femoral arteries in vitro. The exact nature of the inhibition remains to be fully explored, but blockade of calcium entry through voltage operated Ca channels may play a role. Thus, certain polyamines may affect cerebral perfusion by inhibition of vascular contractility.

Animals↗

PubMed1996

Stimulation of alpha 2 adrenoceptors dilates the rat middle cerebral artery.

BACKGROUND: Because alpha 2 adrenoceptor agonists are used as adjuncts to anesthetics, their effects on the cerebrovascular circulation are of prime importance. We studied changes in the diameter of rat middle cerebral arteries after stimulation of alpha 2 adrenoceptors with UK14,304. METHODS: Rat middle cerebral arteries were isolated, cannulated at each end with a glass micropipette, and pressurized to 85 mmHg. The middle cerebral arteries were immersed in a bath (37 degrees C) containing physiologic saline solution, and luminally perfused with physiologic saline solution (100 microliters/ min). Changes in vessel diameter were measured after magnification with a microscope. RESULTS: Resting diameter of the middle cerebral arteries was 239 +/- 13 microns (n = 8) for the first study. A dose-dependent dilation was produced by addition of UK14,304 to the extraluminal bath; a 10-15% increase in diameter occurred at a concentration of 10(-4)M. The dilations produced by UK14,304 were blocked with selective alpha 2-antagonists, idazoxan and rauwolscine, but not by the selective alpha 1-antagonist, prazosin. The dilations could be blocked by removal of the endothelium, or the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (10(-5) M). The inhibitory effects of N-nitro-L-arginine methyl ester were reversed with the addition of 10(-3) M L-arginine, but not 10(-3) M D-arginine. Furthermore the dilation produced by UK14,304 was completely abolished with pertussis toxin (100 ng/ml). CONCLUSIONS: It was concluded that the stimulation of alpha 2 adrenoceptors with UK14,304 produced a dilation in the rat middle cerebral artery that (1) was dependent on intact endothelium, (2) involved nitric oxide, and (3) acted via a pertussis toxin-sensitive G protein.

Animals↗

PubMed1995

Regional cerebral blood flow after controlled cortical impact injury in rats.

Regional cerebral blood flow (rCBF) and laser-Doppler perfusion were measured in rats after controlled cortical impact injury (CCII), a model of traumatic brain injury. Male Long-Evans rats were anesthetized with isoflurane and surgically prepared with arterial and venous cannulae. CCII was induced after a craniectomy by deforming the right parietal cortex to a depth of 2 mm with a metal cylinder traveling at a velocity of 5.2 m/s. Laser-Doppler perfusion was monitored from the surface of the left frontal cortex. rCBF, using 14C-isopropyliodoamphetamine, and laser-Doppler perfusion were measured in three groups of rats consisting of a sham group (n = 6), a group 30 min after CCII (n = 6), and a group 4 h after CCII (n = 5). CCII was characterized by cortical ischemia (rCBF < 20 mL.100 g-1.min-1) surrounding the site of impact. The occipital cortex, a cortical region distant from the impact site, was also ischemic in some, but not all, injured rats. In the 30-min group, the ischemic zone showed very sharp boundaries with cortical areas of hyperperfusion surrounding the ischemic zone. In the 4-h group, the ischemic boundaries were not as sharp and the hyperperfusion surrounding the ischemic zone was no longer present. The caudate-putamen, hippocampus, and thalamus showed significant reductions in rCBF ranging from 50% to 30% of control 30 min and 4 h postinjury, respectively. We conclude that complex changes in rCBF occur shortly after CCII and persist for at least 4 h. During this time several brain regions, especially the cortical areas, may suffer damage due to the ischemia.

Animals↗

PubMed1995

Radial columns in autoradiographs generated from tracer methods for measuring cerebral cortical blood flow.

Radial columns in the cerebral cortex, sometimes seen in autoradiographic methods for measuring cerebral blood flow, were studied. Radioactively labeled tracers were injected into the internal carotid artery in pentobarbital sodium-anesthetized rats. The cortical patterns of tracer uptake were determined using autoradiography. When tracers for measuring cerebral blood flow were administered, cortical columns were apparent in the autoradiograph. The darker columns (higher tracer concentration) in the image aligned with penetrating arterioles, suggesting that the tracer was being removed from the penetrating arterioles. In another experiment, [14C]glucose was used as a qualitative blood flow tracer. Modeling of glucose uptake predicts that 26-29% more glucose should be extracted in the dark columns than the light columns if the columns represent capillary blood flow. [14C]glucose did not produce the cortical columns consistent with the model prediction. We conclude that capillary blood flow in the cortex is not organized in radial columns of higher and lower flow. The results support the idea that the flow tracers are removed from blood primarily in the penetrating arterioles.

Amphetamines↗

PubMed1995

Permissive role of NO in alpha 2-adrenoceptor-mediated dilations in rat cerebral arteries.

Dilations produced with UK-14304, a selective alpha 2-adrenoceptor agonist, in rat middle cerebral arteries (MCAs) were blocked after removal of the endothelium or inhibition of nitric oxide synthase (NOS). After endothelium removal or inhibition of NOS, the addition of subthreshold doses of an exogenous nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine, restored the dilations produced by UK-14304. In a similar manner the guanosine 3',5'-cyclic monophosphate (cGMP) analogues 8-bromoguanosine 3',5'-cyclic monophosphate and N2,2'-O-dibutyrylguanosine 3',5'-cyclic monophosphate restored the dilations of MCAs after endothelial removal. Because NO cannot be synthesized and released in MCAs after inhibition of NOS, it cannot be directly responsible for the dilation. The basal release of NO from the endothelium acts permissively in the vasodilation by maintaining adequate levels of cGMP. Removal of this basal release of NO by removal of endothelium or inhibition of NOS abolishes the alpha 2-adrenoceptor-mediated dilation.

Adrenergic alpha-Agonists↗

PubMed1994

Lateral cortical impact injury in rats: cerebrovascular effects of varying depth of cortical deformation and impact velocity.

Intracranial pressure (ICP), blood pressure (BP), cerebral perfusion pressure (CPP), and cortical perfusion (LDF) of the contralateral parietal cortex were measured after cortical impact injury in 36 rats. Changes in these physiologic parameters were compared using analysis of variance to a group of 11 rats who received a sham impact. In one series of experiments, the velocity and duration of the impact injury were kept constant, and the severity of the injury was determined by varying the depth of cortical deformation from 2 to 3 mm. The peak pressure inside the skull was directly related to the depth of cortical deformation, and was 93 +/- 16, 182 +/- 18, and 268 +/- 57 mm Hg with the 2, 2.5, and 3 mm deformation, respectively, when the impact velocity was 5 m/sec. With the 2 mm depth injury, there was a transient decrease in BP (p < 0.05) and a 12% decrease in LDF after the impact. With the 2.5 mm depth injury, a small transient increase in ICP and decrease in BP and a 30% decrease in LDF occurred (p < 0.05). ICP then gradually increased throughout the 8 h experiment, becoming significantly greater than the sham-injured animals by 5 h after the impact. LDF gradually returned toward normal throughout the experiment. With the 3 mm depth injury, a marked transient increase in ICP (p < 0.05) and BP (p < 0.05) occurred immediately after the impact. The increase in BP lasted < 5 min, and subsequently the BP decreased to approximately 50 mm Hg for the rest of the experiment. The initial marked increase in ICP lasted 15 min and then remained 5-10 mm Hg higher (p < 0.05) than in the sham-injured animals for the rest of the experiment. LDF decreased by an average of 50% (p < 0.05) immediately after the impact and remained lower than that of the sham-injured animals for the rest of the experiment. In another series of experiments, the depth of cortical deformation was kept constant at 2.5 mm, and the severity of the injury was determined by varying the velocity from 1 to 5 m/sec. The peak ICP was significantly related to the impact velocity, averaging 45 +/- 12, 66 +/- 9, and 182 +/- 18 mm Hg with the 1, 3, and 5 m/sec impact injuries, respectively. The 1 m/sec impact had no effect on ICP and only a transient decrease in BP.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗

PubMed1994

Lateral cortical impact injury in rats: pathologic effects of varying cortical compression and impact velocity.

Direct lateral cortical impact through the intact leptomeninges using a pneumatically driven piston produces increasingly severe pathophysiologic derangements with increasing cortical deformation. We studied the histopathologic correlates of cortical impact injury produced by 2 mm, 2.5 mm, and 3 mm deformation in the rat at 5 m/sec. Additionally, the effect of impact velocity at a 2.5 mm deformation was assessed at 1 m/sec, 3 m/sec, and 5 m/sec. The brains were examined 14 days after injury. Cortical contusion maximum cross-sectional area, volume, and the percentage CA1 and CA3 hippocampal neuronal loss correlate with cortical deformation and impactor velocity. Contusion volume increased with increasing cortical deformation. Deformations of 2, 2.5, and 3 mm at 5 m/sec produced contusion volumes of 4.59, 8.9, and 21.68 mm3, respectively. At a fixed cortical deformation of 2.5 mm, contusion volume increased with increasing impact velocity. Impact velocities of 1, 3, and 5 m/sec produced contusion volumes of 5.79, 7.42, and 8.9 mm3, respectively. Hippocampal CA3 neuronal loss increased with increasing cortical deformation. Deformations of 2, 2.5, and 3 mm at 5 m/sec produced neuronal loss of 29%, 48.3%, and 79.5%, respectively. At a fixed cortical deformation of 2.5 mm, hippocampal CA3 neuronal loss increased with increasing impact velocity. Impact velocities of 1, 3, and 5 m/sec produced neuronal loss of 18.25%, 33.75%, and 48.3%, respectively. Hippocampal CA1 neuronal loss was also seen and paralleled cortical deformation and impact velocity. Cortical deformation and impact velocity are critical parameters in producing cortical contusion and must be considered when comparing results using this model.

Animals↗

PubMed1994

Cerebral blood flow, plasma catecholamines, and electroencephalogram during hypoglycemia and recovery after glucose infusion.

Regional cerebral blood flow (rCBF) and plasma catecholamines were measured in separate experiments during the onset of insulin-induced hypoglycemia and during recovery. The purpose of these experiments was twofold: first, to study the relationship between plasma catecholamines and rCBF to determine if increased concentrations of plasma catecholamines were responsible for the increase in rCBF observed during insulin-induced hypoglycemia, and second, to study changes in rCBF after recovery from hypoglycemia. Male Long-Evans rats were fasted overnight, surgically prepared under isoflurane anesthesia, restrained, and allowed to awake from anesthesia. In the first series of experiments, plasma catecholamines, arterial blood pressure, arterial blood gases, and electroencephalogram (EEG) were measured during the onset of hypoglycemia produced by i.v. insulin and the recovery after i.v. glucose. The EEG showed a characteristic high-amplitude, slow-wave pattern during hypoglycemia (plasma glucose, 38 +/- 2 mg/dl; n = 3). Plasma epinephrine in the normoglycemic control rats was 529 +/- 122 pg/ml (n = 5) and increased 4.5 times as plasma glucose reached 50 +/- 3 mg/dl. After the initial increase, plasma epinephrine steadily decreased toward baseline over the next 90 min as the hypoglycemia became more severe. Plasma norepinephrine significantly increased by 60% when plasma glucose was 40 +/- 2 mg/dl and remained increased during much of the recovery period. In other studies, rCBF was measured in four groups of rats, one group with normoglycemia (control), one with hypoglycemia, one at 5 min of recovery, and one at 30 min of recovery. Regional CBF increased during hypoglycemia (plasma glucose, 39 +/- 1 mg/dl; n = 6) in most regions studied and ranged from 28 to 99% above control. After 5 min of the recovery (plasma glucose, 269 +/- 15 mg/dl), rCBF returned to or decreased below baseline. In a previous study, we determined that rCBF did not increase during hypoglycemia until plasma glucose decreased to 40 mg/dl. In the present study, the peak increase in plasma epinephrine occurred when plasma glucose was 50 mg/dl. At plasma glucose concentrations which rCBF began to increase, plasma epinephrine was decreasing from its peak level. Regional CBF and plasma norepinephrine increased in parallel during the onset of hypoglycemia; however, during the recovery period, plasma norepinephrine remained increased while rCBF decreased to or below baseline. The dissociation of rCBF and plasma catecholamines casts doubt on the hypothesis that plasma catecholamines are responsible for increases in rCBF.

Animals↗

PubMed1994

Regional cerebral blood flow during submergence asphyxia in Pekin duck.

The cerebrovascular response to submergence asphyxia was studied in the Pekin duck (Anas platyrhynchos var.) by use of the cerebral blood flow (CBF) tracer [14C]isopropyliodoamphetamine and quantitative autoradiography. Blood flow of the whole brain was 158 +/- 14 (SE) ml.min-1 x 100 g-1 (n = 7) in control animals. There was a doubling of flow to 320 +/- 61 ml.min-1 x 100 g-1 (n = 6) during submergence asphyxia. The hypothesis that CBF is redistributed within the brain during asphyxia was not supported. There were no regional reductions in CBF during submergence asphyxia. Mean arterial blood pressure was similar (approximately 140 mmHg), but heart rate, arterial blood gas tensions, and arterial pH were significantly different in control and submerged ducks at the time CBF was measured. The differences in CBF among submerged animals correlated strongly with arterial PCO2 and mean arterial blood pressure. The smallest proportional difference in regional CBF between control and submerged ducks occurred in the ectostriatum (+141%) and the largest in the locus ceruleus (+241%). The largest absolute difference in regional CBF was in the nucleus ruber (+322 ml.min-1 x 100 g-1). These are the first measurements of blood flow in discrete nuclei and regions of the avian brain.

Amphetamines↗