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Biomedical subjects

R M Lehman

Publications and source records attributed to R M Lehman.

At least 19 recordsLinked to original sources
PubMed1992

Use of the callosal grid system for the preoperative identification of the central sulcus.

The callosal grid system based on modern imaging techniques facilitates the identification of the central sulcus by its relationship to the midcallosal plane. Imaging with or without the stereotactic frame allows precise localization of various anatomic sites, which can be compartmentalized within subdivisions of the grid system. The information gained permits accurate preoperative planning and intraoperative recognition of the central sulcus and adjacent neurovascular structures.

Brain↗
PubMed1991

Mechanism of enlargement of major cerebral collateral arteries in rabbits.

Major cerebral collateral arteries enlarge following bilateral ligation of the common and internal carotid arteries. The purpose of this investigation was to determine the relative contribution of cellular hypertrophy versus cellular hyperplasia to this vessel change in a morphometric analysis as well as the functional properties of remodeled vessels in an in vitro study. We assessed cell number and vessel dimensions by morphometric analysis of 16 perfusion-fixed rabbit basilar arteries. Results demonstrated significant increases in luminal diameter from 761 to 946 microns (p less than 0.01), medial cross-sectional area from 5.1 x 10(4) to 7.6 x 10(4) micron2 (p less than 0.005), smooth muscle cell volume from 9.19 x 10(5) to 1.44 x 10(6) micron3 (p less than 0.0005), and overall arterial length from 17.41 to 20.36 mm (p less than 0.005) in basilar arteries from the eight ligated rabbits compared with the eight sham-operated controls. Smooth muscle cell volume fraction and cell numerical density were unchanged whereas the number of cells per unit length of artery was increased significantly from 21.5 to 31.0 cells/micron (p less than 0.05). These data indicate that smooth muscle cell hyperplasia rather than hypertrophy contributes to increases in vessel mass. Functional properties of the basilar arteries from 10 ligated and 10 normal control rabbits were analyzed in vitro. Results showed increased contraction to potassium chloride (approximately 74%) (p less than 0.01) and increased sensitivity of smooth muscle to acetylcholine (p less than 0.05) while maximal relaxation was the same as control in the ligated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Etiology of the disruption in blood-arterial wall barrier following experimental subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage is associated with a sudden rise in intracranial pressure, acute arterial hypertension, and subarachnoid blood. The role that each of these factors may play in the development of the acute barrier disruption of the major cerebral arteries following subarachnoid hemorrhage was investigated in 42 rabbits. Horseradish peroxidase was given intravenously to assess the integrity of the barrier by transmission electron microscopy. Permeation of the tracer into the vessel was noted only in animals with increased intracranial pressure. A sudden rise in intracranial pressure is suggested to trigger acute barrier disruption following subarachnoid hemorrhage.

Animals↗
PubMed1990

Computer-assisted detection and intervention in adolescent high-risk health behaviors.

Because adolescents avoid bringing sensitive issues, such as substance abuse, suicide, and sexual activity, to pediatricians, and may fail to realize that they need health education or services, a computer program was designed to facilitate reporting of high-risk psychosocial and health behaviors and to provide specific health advice and referral for timely professional intervention. Computer printouts done anonymously by a random sample of 265 adolescents after a physical examination were compared with those of a matched group of 294 who were predirected to share the printout with the clinician at their examinations. The former elicited more positive responses to sensitive health problems, but both computer groups responded significantly more often about most high-risk issues than a matched written questionnaire group of 251. Almost all adolescents said that they reported true information to the computer and read all the information it printed. Experience with 3327 teenagers demonstrated that 89% preferred the computer over a questionnaire or personal interview, but nearly all were willing to share the printout with the pediatrician, which should facilitate clinical evaluation. The nonjudgmental computer can identify problem areas and deliver automated medical advice and referral. Automated health assessment and education may become a useful adjunct for addressing adolescent health issues.

Adolescent↗
PubMed1989

Time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage.

The time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage (SAH) was studied in 24 rabbits. Animals with SAH received two successive blood injections through the cisterna magna. Horseradish peroxidase (HRP) was given intravenously 30 minutes before sacrifice to assess the integrity of the barrier. In the basilar arteries taken from animals that were sacrificed 4 days after the first SAH, HRP-reaction products were diffusely observed in the subendothelial space. Three weeks following the first SAH, permeation of HRP was still observed in half of the animals. However, in animals sacrificed 7 weeks after the first SAH, no permeation of HRP into the subendothelial space was noted. Opening of the interendothelial space seemed to be the major mechanism for HRP permeation into the subendothelial space rather than transendothelial vesicular transport. Disruption of the blood-arterial wall barrier in the major cerebral arteries following SAH may play a role in the pathogenesis of vasospasm.

Animals↗
PubMed1989

Blood-arterial wall barrier disruption to various sized tracers following subarachnoid haemorrhage.

Disruption of the blood-arterial wall barrier in the major cerebral arteries occurs following subarachnoid haemorrhage (SAH) and may be related to the pathogenesis of cerebral vasospasm. Using FITC dextrans of various sizes, the present study was undertaken to determine if the barrier disruption shortly after SAH occurs equally to various sized tracers. Forty-two Sprague-Dawley rats were divided into 5 groups. Four groups were injected with FITC-dextrans of differing molecular weights (MW): FD4 (MW = 4,080), FD 40 (MW = 40,500), FD 70 (MW = 71,400), and FD 150 (MW = 156,900). One group was injected with horseradish peroxidase (HRP: MW = 40,000). Each group was further divided into two subgroups: with or without SAH. SAH was induced by injecting arterial blood into the cisterna magna. To assess the integrity of the blood-arterial wall barrier by transmission electron microscope, the tracers were intravenously injected prior to sacrificing the animals. The groups without SAH showed no permeability of tracers into the subendothelial spaces of the basilar arteries. In contrast, with the exception of FD 150, FITC-dextrans (FD 4, FD 40, FD 70) were noticed in the subendothelial spaces. The distribution of FITC-dextrans in the elastic lamina was similar to that of HRP. These results suggest that barrier disruption occurs with a wide range of molecular sizes of FITC-dextrans, although there seems to be some limitation to the permeation of the larger molecules. The present study suggests that the mechanism of barrier disruption of the major cerebral arteries in the acute stage following SAH may be vesicular rather than by separation of tight junctions.

Animals↗
PubMed1989

Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries.

An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteries in vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in the in vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0 U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10(-6)M prostaglandin F2 alpha. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.

Animals↗
PubMed1989

Effect of intracisternal antithrombin III on subarachnoid hemorrhage-induced arterial narrowing.

The ability of antithrombin III, an endogenous plasma glycoprotein, to reverse the arterial narrowing in a rabbit model of cerebral vasospasm was evaluated. The vasodilator activity of antithrombin III on rabbit arteries was first assessed in vitro using a myograph-arterial ring preparation. Antithrombin III (10 IU/ml) induced a 55.4% +/- 2.66% (mean +/- standard error of the mean) relaxation in basilar artery precontracted with serotonin (5-HT) in five specimens as compared with a 9.8% +/- 1.6% relaxation of common carotid artery in six specimens. For in vivo analysis, 21 New Zealand White male rabbits were separated into three groups: Group 1 served as normal controls; Group 2 received a subarachnoid blood injection (SAH) and were sacrificed on Day 3 thereafter; and Group 3 animals were subjected to SAH, then received a 2-hour intracisternal infusion of antithrombin III (100 IU) in saline prior to sacrifice on Day 3. Basilar artery caliber was determined using a morphometric method to analyze perfusion-fixed arterial segments. Control basilar artery diameter in Group 1 was 0.64 +/- 0.02 mm. In Group 2 a 27% reduction in arterial caliber to 0.47 +/- 0.03 mm was observed by Day 3 post SAH (p less than 0.0001). Group 3 animals had a mean basilar artery diameter of 0.68 +/- 0.02 mm. This was significantly larger than the untreated SAH rabbits in Group 2 (p less than 0.0001), but not different from control artery diameters in Group 1. The findings demonstrate that antithrombin III in saline has a significant ability to reverse delayed narrowing of the rabbit basilar artery after SAH.

Animals↗
PubMed1988

Computed-tomography-directed stereotaxis for movement disorder with postoperative magnetic resonance imaging confirmation.

Movement disorders may respond dramatically to properly placed lesions in thalamic and subthalamic areas. Proper location of lesions may be verified postoperatively by magnetic resonance imaging (MRI). Herein is reported a case of stereotactically placed bilateral lesions under computed tomography control using the Leksell apparatus, with successful clinical outcome, and the verification of lesion placement by subsequent MRI images.

Demyelinating Diseases↗
PubMed1988

Comparison of intraluminal and extraluminal inhibitory effects of hemoglobin on endothelium-dependent relaxation of rabbit basilar artery.

To determine whether extraluminal or intraluminal hemoglobin inhibits endothelium-dependent relaxation, we measured the vascular responsiveness of rabbit basilar artery in an in vitro perfusion system and we performed immunohistochemical staining for hemoglobin. In the in vitro study, we applied agents from either the intraluminal or the extraluminal side of excised basilar arteries. KCl-induced contraction was the same with either application. Acetylcholine-induced maximal relaxations were 57.6 +/- 8.5% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 3.3 +/- 0.3% for intraluminal, and 34.9 +/- 8.6% for extraluminal applications. Adenosine triphosphate-induced maximal relaxations were 64.2 +/- 4.1% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 26.9 +/- 3.8% for intraluminal, and 42.2 +/- 6.0% for extraluminal applications. Hemoglobin's inhibition of acetylcholine- and adenosine triphosphate-induced relaxation was significantly greater with intraluminal than with extraluminal application (p less than 0.05). The immunohistochemical study revealed hemoglobin in the outer layer of the smooth muscle and in the adventitia when 10(-5) M hemoglobin was applied extraluminally for 5 minutes, whereas hemoglobin was observed on the surface of the endothelial cells after intraluminal application. Our findings suggest that hemoglobin inhibits acetylcholine- or adenosine triphosphate-induced relaxation by binding to endothelium-derived relaxing factor (EDRF) and by inhibiting production of EDRF. Hemoglobin's inhibitory effect on endothelium-dependent relaxation may be important in the pathogenesis of vasospasm after subarachnoid hemorrhage.

Acetylcholine↗
PubMed1988

Metabolic alterations in rabbit cerebral arteries caused by subarachnoid hemorrhage.

The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.02 mumol/g wet wt in control rabbit basilar arteries (n = 6). The ATP content decreased significantly to 0.17 +/- 0.02 mumol/g wet wt 2 days after experimental subarachnoid hemorrhage (n = 6), although only a slight decrease was detected in the basilar arteries 2 days after cisternal injection of the same amount of artificial cerebrospinal fluid. Hypoxia significantly decreased ATP content in the control basilar arteries to 0.26 +/- 0.04 mumol/g wet wt (n = 6). The same degree of hypoxia did not decrease ATP content in the basilar arteries after subarachnoid hemorrhage. Release of L-lactate was significantly higher from the arteries after subarachnoid hemorrhage than from the control arteries under both aerobic and hypoxic conditions. Our results indicate that subarachnoid hemorrhage induced an alteration of metabolic rates in rabbit cerebral arteries. The oxygen-requiring pathways to synthesize ATP may be important in control cerebral arteries; however, after experimental subarachnoid hemorrhage, the main pathway in the cerebral arteries may shift from oxygen-requiring pathways to an anaerobic glycolytic pathway.

Adenosine Triphosphate↗
PubMed1988

Effect of removal of the endothelium on vasocontraction in canine and rabbit basilar arteries.

The effect of endothelium removal on the contractile responses to KCl, hemoglobin, serotonin (5-HT), norepinephrine (NE), prostaglandin (PG)F2 alpha, PGD2, and PGE2 was investigated in canine and rabbit basilar arteries by an isometric tension-recording method. In canine basilar arteries, endothelium removal elevated the dose-response curves to 5-HT, PGF2 alpha, and PGD2, and PGE2, but not to KCl, hemoglobin, or NE. In rabbit basilar arteries, on the other hand, removal of the endothelium elevated the dose-response curves to 5-HT, NE, PGF2 alpha, and PGD2, but not to KCl or hemoglobin. Neither contractile nor inhibitory response was elicited by PGE2 in rabbit basilar arteries. Contraction induced by 5-HT and NE following endothelium removal had a much more pronounced effect in rabbit basilar arteries than in canine basilar arteries. These results suggest that, following endothelium removal, abolition of the spontaneous release of endothelium-derived relaxing factor is the most probable mechanism of the enhanced vasocontraction. Since endothelial damage results from subarachnoid hemorrhage, the aforementioned mechanism of vasocontraction enhancement may play a role in the pathogenesis of cerebral vasospasm.

Animals↗
PubMed1988

Subarachnoid hemorrhage inhibition of endothelium-derived relaxing factor in rabbit basilar artery.

Vascular contractions in response to KCl and serotonin (5-hydroxytryptamine, 5-HT) in rabbit basilar artery were studied in vitro using an isometric tension-measurement technique. Hemoglobin (10(-5)M) markedly augmented contractions induced by 5-HT (10(-9) to 10(-6)M) and slightly augmented those induced by KCl (20 to 80 mM) in arteries with intact endothelium. On the other hand, the augmentation induced by hemoglobin was almost abolished in arteries that were chemically denuded of endothelial cells by pretreatment with saponin. Since hemoglobin is known to be a selective inhibitor of endothelium-derived relaxing factor (EDRF), it is possible that the augmentation of contraction by hemoglobin in endothelium-intact arteries was mediated via an inhibition of spontaneously released EDRF. The effect of subarachnoid hemorrhage (SAH) on spontaneously released EDRF was investigated by injecting 5 ml of blood into the cisterna magna and sacrificing the rabbits 2 days later. Arteries after SAH showed a significant reduction in hemoglobin-induced augmentation compared to that seen in control arteries with intact endothelium. This result suggests that spontaneously released EDRF is significantly reduced after SAH. It is concluded that EDRF is released spontaneously in the rabbit basilar artery and that inhibition of its release might be involved in pathogenesis of cerebral vasospasm.

Acetylcholine↗
PubMed1988

Pharmacological comparison of endothelium-dependent relaxation in isolated cerebral and extracerebral arteries.

Endothelium-dependent relaxation was induced by acetylcholine (ACh), adenosine triphosphate (ATP), and thrombin in isolated cerebral and extracerebral arteries obtained from rabbits and dogs. Using an isometric tension-recording method, the authors then examined the difference in the extent of relaxation between the cerebral and extracerebral arteries. In rabbits, the dose-response curve of the basilar artery for ACh was significantly different (p less than 0.05) from curves of the femoral and common carotid arteries. The IC50 value (the concentration inducing a one-half inhibition of the initial contractile tone) for the basilar artery in ACh-induced relaxation was significantly higher (p less than 0.05) than for the common carotid artery, although the mean maximum relaxation of the basilar artery to ACh was not significantly different from that seen in extracerebral arteries. The relaxing effect of ACh in dogs was much less in the middle cerebral and basilar arteries than in the common carotid, vertebral, and femoral arteries. On the other hand, both ATP (in rabbits and dogs) and thrombin (in dogs) induced significantly more (p less than 0.05) relaxation in the cerebral arteries than in the extracerebral arteries. Endothelium-dependent relaxation induced by ACh or ATP has been demonstrated in a wide range of arteries from a variety of animals. The present results suggest that ATP has a more important role than ACh in the regulation of the vascular tone of the major cerebral arteries in these two species.

Acetylcholine↗
PubMed1987

Immunohistochemical demonstration of increase in prostaglandin F2-alpha after recirculation in global ischemic rat brains.

Immunohistochemical localization of prostaglandin F2 alpha (PG F2 alpha) was studied in 24 rats. In 21 rats, global brain ischemia was produced for 5 min by Pulsinelli's method. Prior to decapitation, 13 were recirculated for 5 min, while the remaining eight were not. Three recirculated rats were pretreated with indomethacin before the occlusion. Hypotension was induced during the occlusion to 40-50 mm Hg of mean arterial blood pressure in 11 rats including those unrecirculated, recirculated and pretreated with indomethacin. Three normal rats without occlusion of arteries served as control. The brains were snap frozen and 10-microns cryostat sections were incubated in rabbit anti-PG F2 alpha serum and stained by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2 alpha was noted mainly in pial vessels in normal and ischemic rats both with and without hypotension. The rats recirculated without hypotensive ischemia revealed a positive reaction in the walls of pial and parenchymal vessels. All rats recirculated after the hypotensive occlusion showed positive staining in blood vessels, in the cytoplasm of neurons (especially in hippocampi) and in the interfascicular oligodendrocytes. The above results indicate that recirculation after ischemia results in an increase in PG F2 alpha in parenchymal vessels, neurons and oligodendrocytes.

Animals↗
PubMed1987

Barrier disruption in the major cerebral arteries after experimental subarachnoid hemorrhage in spontaneously hypertensive and normotensive rats.

The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the major cerebral arteries were studied in 24 spontaneously hypertensive rats (SHR) and 13 Sprague-Dawley rats (SDR). Horseradish peroxidase (HRP) was given intravenously before killing the animals to assess the integrity of the barrier. In the acute experimental group, transient elevation of intracranial pressure (ICP) and systemic arterial pressure produced by cisternal injection of whole blood, saline solution, or Elliott's B solution resulted in extensive disturbance of the blood-arterial wall barrier. In the chronic group, only the cisternal injection of whole blood in SHR brought about an extensive and marked disturbance of the arterial permeability. These results suggest that: (a) early breakdown of the blood-arterial wall barrier seems to be due to a sudden rise in the ICP or arterial pressure; (b) in the chronic experiments, the subarachnoid clot is the most important factor responsible for the permeability changes; and (c) in the chronic SAH experiments, the blood-arterial wall barrier seems to be more vulnerable in SHR than in Sprague-Dawley rats. Due to the well-known similarities between SHRs and hypertensive human beings, patients with chronic hypertension should be considered at high risk after SAH for extensive blood-arterial wall barrier disturbances.

Animals↗