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L H Pitts

Publications and source records attributed to L H Pitts.

122 records · Page 7Linked to original sources
PubMed1978

Carotid-cavernous fistula. Demonstration of asymptomatic vascular "steal".

Abnormal distribution of cerebral vascular flow was studied in a patient who had a traumatic carotid-cavernous sinus fistula. Serial studies were performed using a method for determining relative cerebral vascular flow:99mtechnetium-diethylenetriamine pentaacetic acid (99mTc-DTPA) was injected intravenously and flow data were processed by a digital computer. Serial studies documented the occurrence of a vascular "steal" during temporary carotid occlusion; postoperative studies showed disappearance of the steal and obliteration of thiling arterial structures and capillary filling in the brain, and in demonstrating alteration in the cerebral circulation.

Adult↗
PubMed1975

Pneumocephalus following ventriculoperitoneal shunt. Case report.

The authors describe a case of massive pneumocephalus following ventriculoperitoneal shunting for hydrocephalus. After multiple diagnostic and surgical procedures, congenital defects in the tegmen tympani of both temporal bones were identified as the sources for entry of air. A functioning shunt intermittently established negative intracranial pressure and allowed ingress of air through these abnormalities; when the shunt was occluded, air did not enter the skull, and there was no cerebrospinal fluid leakage. Repair of these middle ear defects prevented further recurrence of pneumocephalus.

Adult↗
PubMedDate not supplied

Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination.

We have examined the incidence and size of infarction after occlusion of different portions of the rat middle cerebral artery (MCA) in order to define the reliability and predictability of this model of brain ischemia. We developed a neurologic examination and have correlated changes in neurologic status with the size and location of areas of infarction. The MCA was surgically occluded at different sites in six groups of normal rats. After 24 hr, rats were evaluated for the extent of neurologic deficits and graded as having severe, moderate, or no deficit using a new examination developed for this model. After rats were sacrificed the incidence of infarction was determined at histologic examination. In a subset of rats, the size of the area of infarction was measured as a percent of the area of a standard coronal section. Focal (1-2 mm) occlusion of the MCA at its origin, at the olfactory tract, or lateral to the inferior cerebral vein produced infarction in 13%, 67%, and 0% of rats, respectively (N = 38) and produced variable neurologic deficits. However, more extensive (3 or 6 mm) occlusion of the MCA beginning proximal to the olfactory tract--thus isolating lenticulostriate end-arteries from the proximal and distal supply--produced infarctions of uniform size, location, and with severe neurologic deficit (Grade 2) in 100% of rats (N = 17). Neurologic deficit correlated significantly with the size of the infarcted area (Grade 2, N = 17, 28 +/- 5% infarction; Grade 1, N = 5, 19 +/- 5%; Grade 0, N = 3, 10 +/- 2%; p less than 0.05). We have characterized precise anatomical sites of the MCA that when surgically occluded reliably produce uniform cerebral infarction in rats, and have developed a neurologic grading system that can be used to evaluate the effects of cerebral ischemia rapidly and accurately. The model will be useful for experimental assessment of new therapies for irreversible cerebral ischemia.

Animals↗
PubMedDate not supplied

Vasomotor effects of dimethyl sulfoxide on cat cerebral arteries in vitro and in vivo.

We studied the direct vascular effects of dimethyl sulfoxide (DMSO) in isolated middle cerebral arteries and on pial arteriolar caliber after subarachnoid perivascular microinjection in chloralose-anesthetized cats, and on brain retraction in cats given DMSO intravenously. DMSO did not constrict isolated cerebral arteries at any of the concentrations studied (10(-10) to 4 X 10(-1) M). In middle cerebral arteries precontracted with potassium, 5-hydroxytryptamine, prostaglandin F2 alpha, or with mechanically raised tone, DMSO at concentrations of 10(-10) to 10(-2) M had no significant effects; at concentrations greater than 10(-2) M, DMSO consistently relaxed the arteries, probably because of the hyperosmolarity of the bathing solution. Microapplication of DMSO (10(-6) to 10(-2) M) around pial arterioles on the cortical surface did not change arteriolar caliber significantly. Higher concentrations of DMSO (1%) increased arteriolar caliber by 56 +/- 4% (p less than 0.001), probably as a consequence of solution hypertonicity. DMSO did not modify in vivo cerebrovascular responses to alterations in perivascular potassium ion concentrations. Intravenous administration of DMSO did cause obvious brain shrinkage. These data provide no support for the view that direct cerebral vascular effects play a major role in the clinical efficacy of DMSO, but are consistent with the hypothesis that DMSO's ability to lower intracranial pressure derives from its osmotic effect on cerebral issue.

Animals↗
PubMedDate not supplied

Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats.

We have evaluated the use of 2,3,5-triphenyltetrazolium chloride (TTC) as an histopathologic stain for identification of infarcted rat brain tissue. The middle cerebral artery (MCA) of 35 normal adult rats was occluded surgically. At various times after surgical occlusion, rats were sacrificed and brain slices were obtained and stained with TTC or hematoxolin and eosin (H & E); the size of the area of infarcted tissue stained by each method was quantified. In rats sacrificed 24 hr after occlusion of the MCA, the size of the area of infarction was 21 +/- 2% of the coronal section for TTC, and 21 +/- 2% for H & E (mean +/- S.D., N = 13). The size of areas of infarction determined by either staining method was not significantly different in area by the paired test, and a significant correlation between sizes determined by each method was found by linear regression analysis (r = 0.91, slope = 0.89, and the y intercept = 4.4%). Staining with TTC is a rapid, convenient, inexpensive, and reliable method for the detection and quantification of cerebral infarction in rats 24 hr after the onset of ischemia.

Animals↗
PubMedDate not supplied

NMR in experimental cerebral edema: value of T1 and T2 calculations.

In an experimental investigation, the efficacy of nuclear magnetic resonance (NMR) relaxation times in measuring brain water was studied. Cerebral edema was induced in four dogs with a freeze lesion, which was produced by contact with a steel cylinder cooled in liquid nitrogen and placed on the exposed dural surface of the brain. NMR proton imaging was performed 2, 3, 6, or 24 hr after production of the lesion, at a field strength of 0.35 T, using multiparametric spin-echo (SE) technique. The animals were sacrificed immediately after imaging, and brain samples were analyzed for water content (wet-to-dry, microgravimetry). Correlation between water content, NMR imaging, and resulting T1, T2 relaxation times and mobile proton density values calculated with SE technique was performed. Brain sample analysis showed elevation of water content in the white matter subjacent to the lesion in all four dogs, rising at least 15% in each of the animals. NMR imaging detected the freeze lesion and subjacent vasogenic edema of the white matter in all animals. The 2 sec pulse interval SE technique was most sensitive in the detection of the abnormality, and provided optimal differentiation of gray and white matter. The second echo sampling (56 msec) was most sensitive to the detection of edema. The T1 and T2 relaxation values, as well as the mobile proton density values, were elevated in the normal gray matter and in the abnormal white matter when compared with normal white matter in any given animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗