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PubMed1997

Intrathecal urokinase as a treatment for intraventricular hemorrhage in the preterm infant.

Despite improvements in the care of preterm infants, intraventricular hemorrhage (IVH) and posthemorrhagic hydrocephalus (PHH) continue to be frequent occurrences in this patient population. Shunt procedures in these children are frequently complicated by obstruction and/or infection. As the hydrocephalus is usually caused by an obliterative arachnoiditis due to contact of the blood with the basilar meninges, it was postulated that infusion of urokinase into the ventricles of infants who have sustained an IVH would clear the blood, mitigate the arachnoiditis, and prevent the progression of PHH. Accordingly, 18 preterm infants who had sustained IVH and subsequently developed PHH were treated with intraventricular urokinase instilled via a surgically implanted subcutaneous reservoir. There were no complications associated with the urokinase. Infants were divided into two dosage groups: low dose (110,000-140,000 IU total) and high dose (280,000 IU total). One infant in the low-dose group died at 1 month of life of respiratory complications. In the low-dose group, 3 of 8 (37%) infants required shunt placement; in the high-dose group, all 9 required shunt placement. For the total group, the shunt rate was 71%. This compares to a historical control group shunt rate of 92%. While the difference between the treatment group as a whole and control group approaches, but does not reach, statistical significance (p = 0.068), there was a significant reduction in the shunt rate when the low-dose group was considered separately (p < 0.002). For those infants that required shunt placement, there were fewer shunt revisions performed in the treatment group than in the control group during the first 24 months following shunt placement: 0.67 versus 1.5 shunt revisions/shunted child. Initial experience with intraventricular urokinase following IVH and PHH in preterm infants suggests a beneficial effect in reducing the shunt revision rate in both high- and low-dose groups. Reduction in shunt placement rate is seen only in the low-dose group.

Animals↗
PubMed1985

Catecholamine involvement in preovulatory LH release: reassessment of the role of epinephrine.

Adult female rats were implanted with permanent cannulae in the third ventricle of the brain and allowed to recover regular 4-day estrous cycles. They received intrajugular cannulae on the morning of proestrus and later between 12.00-13.00 h catecholamines - norepinephrine (NE; 5.3 or 15.9 micrograms), dopamine (DA; 5.3 micrograms), epinephrine (E; 5.3 or 15.9 micrograms) or vehicle (artificial CSF) - were administered intraventricularly. Plasma LH levels were measured in blood samples obtained prior to and 10, 20, 30 or 60 min after catecholamine injections. While NE or DA failed to alter basal plasma LH levels, E evoked a significant 2-fold rise in plasma LH levels. Quite unexpectedly, however, infusion of E (18.5 micrograms) over a 30-min period during the critical period failed to either reverse the pentobarbital-blockade of ovulation or stimulate LH release. Prior suppression of E levels selectively with LY 78335 blocked the preovulatory LH surge and ovulation. However, intraventricular E failed to evoke LH release in these LY 78335-blocked proestrous rats, an observation suggestive of some alpha 1-adrenoreceptor blocking action of the drug. In contrast, the alpha 1-adrenoreceptor blocking action was not evident in the estrogen, progesterone-primed ovariectomized rats similarly pretreated with LY 78335. These studies show that (1) E-containing neurons in the hypothalamus may play an important role in the preovulatory LH release; (2) LY 78335 may exert inhibitory effects on preovulatory LH release, in part, by blocking alpha 1-adrenoreceptors, and (3) participation of NE and DA, if any, in evoking preovulatory LH release remains to be ascertained.

Animals↗
PubMed1982

Behavioral effects of intraventricularly administered (-)-nicotine on fixed ratio schedules of food presentation in rats.

The behavioral effects of intraventricularly (IVT) administered (-)-nicotine on food-maintained behavior were studied. Rats responded by pressing a lever under various fixed ratio (FR) schedules. Infusion of 5 microgram of (-)-nicotine suppressed responding under an FR 16 schedule for 11-13 min. The effect was inversely related to the ratio size (16, 32, 64 responses per food delivery), but it was directly related to the infused (-)-nicotine dose (0.312, 0.624, 1.25, 2.5, 5.0, 10.0 microgram) when ratio size was held constant. Responses rates following the (-)-nicotine-induced suppression were similar to those obtained prior to infusion. The behavioral effects of (-)-nicotine were blocked, in a dose-related manner, by the centrally acting nicotinic-cholinergic antagonist, mecamylamine (0.05-3.0 mg/kg) but not by ther peripherally acting antagonist, hexamethonium (0.5-3.0 mg/kg), suggesting that the behavioral effects of IVT infusions of (-)-nicotine are mediated by central nicotine-cholinergic receptors.

Animals↗
PubMed1990

Effects of antibodies to dynorphin A and beta-endorphin on lateral hypothalamic self-stimulation in ad libitum fed and food-deprived rats.

Many laboratories have reported that systemically administered naloxone has little or no effect on lateral hypothalamic self-stimulation (LH ICSS). In the present study, lateral ventricular infusion of beta-endorphin antiserum and a high dose of naloxone (100 micrograms) produced small but significant increases in stimulation frequency threshold for LH ICSS. beta-Endorphin activity, mediated by a non-mu (e.g. delta or epsilon) receptor, may therefore be involved in the reinforcement of self-stimulation behavior. When rats are deprived of food for 24 h, LH ICSS thresholds decline. Under this condition, systemic naloxone elevates the LH ICSS threshold, often returning it to the pre-deprivation level. In the present study, lateral ventricular infusion of dynorphin A(1-13) antiserum similarly reversed the threshold-lowering effect of food deprivation. The effects of systemic naloxone and intraventricular dynorphin A antiserum on LH ICSS, which are specific to food-deprived animals, may be related to previous findings that these two treatments elevate LH stimulation threshold for eliciting feeding behavior. Results of the ICSS and stimulation-induced feeding studies suggest a model for the mediation of incentive stimuli by dynorphin A activity that is afferent to LH 'reward' neurons and positively gated by 'hunger'. An hypothesized role for 'hunger'-gated dynorphin A release in potentiating the hedonic response to alimentary stimuli and drugs of abuse is discussed.

Animals↗
PubMed1991

[Effects of Diprivan on cerebral blood flow, intracranial pressure and cerebral metabolism in head injured patients].

The effects of propofol on cerebral blood flow, intracranial pressure (ICP) and cerebral oxygen consumption (CMRO2) were assessed in ten severely head-injured patients undergoing surgery for limb fractures. The patients, aged between 15 and 40 years, were in deep coma, scored 6-7 on the Glasgow coma score. They were mechanically ventilated and sedated with 1 mg.h-1 phenoperidine. Anaesthesia was carried out with a 2 mg.kg-1 intravenous bolus of propofol, immediately followed by a 150 micrograms.kg-1.min-1 infusion, which lasted for a mean time of 41.4 +/- 7.3 min. Data were collected 5 min before any propofol was given, 15 min after the start of the infusion, and 15 min after its end. A radial artery cannula, a 7.5 Fr thermodilution flow-directed pulmonary arterial catheter, a cerebral intraventricular catheter and a catheter in the jugular venous bulb were used for this purpose. Carotid arterial injection of 133Xenon was used to determine regional cerebral blood flow (rCBF). Anaesthetic blood concentrations of propofol (3 to 5 micrograms.ml-1) were associated with a decrease in all the parameters studied: cerebral perfusion pressure, from 82 +/- 14 mmHg to 59 +/- 7 mmHg (p less than 0.001); rCBF, from 35 +/- 6 ml.100 g-1.min-1 to 26 +/- 5 ml.100 g-1.min-1 (p less than 0.01); ICP from 11.3 +/- 2.6 mmHg to 9.2 +/- 2.5 mmHg (p less than 0.001); CMRO2 from 1.63 +/- 0.38 mlO2 +/- 100 g-1.min-1 to 1.18 +/- 0.38 mlO2.100 g-1.min-1 (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Galaninergic mechanisms are involved in the regulation of corticotropin and thyrotropin secretion in the rat.

Galanin (GAL), a 29-amino acid peptide, affects the secretion of several anterior pituitary hormones, including PRL and GH. Since GAL coexists with vasopressin and CRH in the hypothalamic paraventricular nucleus (PVN), we have studied the pharmacological and physiological actions of GAL on ACTH and TSH secretion in freely moving male rats. Cannulae were surgically implanted in the right atria and brain, intraventricular or adjacent to the PVN, of adult Sprague-Dawley rats. Seven days later, GAL (500 or 1000 ng) or saline was infused into the PVN, and serial blood samples were obtained 5, 10, 20, and 40 min after the infusion. Some animals were also stressed by the inhalation of ether vapors for 2 min after the PVN infusion. Basal ACTH concentrations were increased 2-fold in saline-treated rats; however, plasma ACTH levels were unchanged after GAL infusion. The exposure of rats to ether vapors for 2 min after the infusion of saline into the PVN increased plasma ACTH concentrations from 22.8 +/- 6.0 to 596.6 +/- 59.9 pg/ml 10 min later. However, the infusion of GAL into the PVN attenuated stress-induced ACTH secretion. After GAL infusion, peak ACTH levels (332.7 +/- 84.0 pg/ml) were attained 5 min after ether exposure, followed by a rapid decline at 10 min (P less than 0.001) and 20 min (P less than 0.05). Plasma TSH concentrations were unchanged by GAL or saline infusion and were not affected by ether vapor inhalation. To determine the physiological significance of GAL in the control of ACTH and TSH secretion, endogenous GAL was immunoneutralized by the infusion of 3 microliters GAL antiserum (GAL-AS) into the third cerebral ventricle 25 and 1 h before withdrawing blood samples every 15 min for 6 h. Animals treated with normal rabbit serum (NRS) served as controls. Plasma ACTH concentrations were unchanged by NRS during the 6-h period. However, infusion of GAL-AS raised plasma ACTH concentrations to over 400 pg/ml 75 min after infusion in some animals. In general, plasma ACTH concentrations were increased 4 h of the 6-h sampling period compared to levels in NRS-treated controls. In contrast, GAL-AS reduced TSH concentrations by 50% compared to control values. In contrast to these marked actions of centrally administered GAL, ACTH secretion from dispersed anterior pituitary cells in vitro was unaffected by GAL in concentrations up to 10(-6) M. Furthermore, GAL did not alter CRH (1 nM)-induced ACTH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed1984

Central depletion of catecholamines--importance of hypertension and anesthesia.

The importance of the brain noradrenergic sympathetic nervous system in blood pressure control during anesthesia with halothane and enflurane was investigated in normotensive and hypertensive rats. Central noradrenergic neurons were destroyed by instillation of 6-hydroxydopamine (6-OHDA) into the cerebral ventricle of both normotensive Wistar rats and spontaneously hypertensive rats (SHR). One week later, arterial and venous lines were placed in the rats under anesthesia; the rats were allowed to recover; and blood pressure and plasma renin activity were measured while the rats were awake. Anesthesia then was induced with 1.3 vol% halothane (Wistar n = 8, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6) or 2.2 vol% enflurane (Wistar n = 6, Wistar 6-OHDA n = 10, SHR n = 8, SHR 6-OHDA n = 6). A control group (Wistar n = 10, Wistar 6-OHDA n = 6, SHR n = 8, SHR 6-OHDA n = 6) was treated identically, but remained unanesthetized throughout the experiment. The untreated normotensive and hypertensive rats received no intraventricular injections. After 1 hr of stable anesthesia, plasma renin activity was measured again, and saralasin, a competitive inhibitor of angiotensin II, was infused to determine the importance of the renin--angiotensin system in blood pressure control. Treatment with 6-OHDA resulted in a 60-90% depletion of norepinephrine in the medulla and hypothalamus. Normotensive Wistar rats treated with 6-OHDA responded to halothane and enflurane anesthesia in a manner similar to untreated normotensive rats. In contrast, hypertensive animals treated with 6-OHDA and then anesthetized with halothane had a significantly greater decrease in blood pressure than untreated hypertensive rats (100 +/- 4 mm Hg vs 125 +/- 4 mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Vasoactive intestinal peptide inhibits luteinizing hormone secretion: the inhibition is not mediated by dopamine.

Vasoactive intestinal peptide (VIP) is a neuropeptide that is present in the hypothalamus and is probably a neuroendocrine regulator. The effect of VIP on pulsatile LH secretion in the long-term ovariectomized rat was re-examined in the light of earlier conflicting reports. VIP or saline was infused into the third ventricle at the rat of 15 microliters/h and blood was sampled frequently before and during the infusion. VIP at 3.5 nmol/h significantly depressed mean LH levels (p less than 0.05) and lowered pulse frequency (p less than 0.05), but had no effect on LH pulse amplitude (p greater than 0.05). VIP at lower levels was not consistently effective, and intraventricular saline was without influence. We examined indirectly whether the site of action of VIP (3.5 nmol/h) was the brain or pituitary by injecting various doses of gonadotropin-releasing hormone (GnRH; 0.5-4.0 ng/100 g BW i.v.) during VIP-induced inhibition of LH secretion and in saline-infused controls. VIP did not alter the response of the pituitary to GnRH or the slope of the GnRH-LH dose-response curve (p greater than 0.05). We conclude that the inhibitory action of VIP on pulsatile LH secretion is probably exerted in the hypothalamus. To test the hypothesis that dopamine mediates the inhibitory effects of VIP (3.5 nmol/h), animals were pretreated with the dopamine receptor blocking agent pimozide (1.26 mg/kg) in an attempt to block the actions of VIP. Pimozide did not affect the response of LH to VIP infusion (p greater than 0.05). We conclude that dopamine is not a likely mediator of the action of VIP.

Animals↗
PubMed1995

Hypotension during dobutamine stress echocardiography: is it related to dynamic intraventricular obstruction?

Although it has been shown that a hypotensive response during dobutamine stress echocardiography is not a marker of coronary artery disease, the mechanism of this response remains unclear. We hypothesize that hypotension during dobutamine stress echocardiography is not related to the development of dynamic intraventricular obstruction. The development of left ventricular outflow obstruction was defined as a late-peaking Doppler velocity profile that exceeded baseline outflow velocity by at least 1 m/sec in 104 consecutive patients undergoing dobutamine stress echocardiography. Left ventricular outflow obstruction was seen in 13% of 15 patients with a hypotensive response (group 1) and in 13% of 89 patients without a hypotensive response (group 2). The mean baseline systolic blood pressure was 157 +/- 21 mm Hg in group 1 compared to 139 +/- 25 mm Hg in group 2 (p = 0.008). An ischemic response to dobutamine infusion as manifested by the development of new or worsening wall motion abnormalities was seen in 40% of group 1 patients and 34% of group 2 patients (p = 0.77). These data demonstrate that a hypotensive response is not related to the development of dynamic intraventricular obstruction during dobutamine stress echocardiography. Rather, there is a significant association between a higher baseline systolic blood pressure and a hypotensive response during dobutamine infusion.

Adult↗
PubMed2002

Changes of propofol concentration in cerebrospinal fluid during continuous infusion.

UNLABELLED: We studied the changes in the propofol concentration in the cerebrospinal fluid (CSF) in 14 patients, undergoing elective intracranial procedures, who were anesthetized with propofol administered by target-controlled infusion. During anesthesia, fentanyl and cisatracurium were administered as required. After intubation of the trachea, the lungs of the patients were ventilated to normocapnia with an oxygen-air mixture (FIO(2) = 0.33). Arterial blood and CSF samples (from an intraventricular drain) were collected between 90-180 min after the induction of anesthesia. Blood propofol concentrations were stable, between 5.0 +/- 1.89 and 4.5 +/- 1.7 microg/mL (mean +/- SD). There was a significant decrease in the CSF propofol concentration, from 52.2 +/- 35.01 ng/mL at 90 min to 28.6 +/- 21.9 ng/mL at 150 min (P < 0.05). The CSF propofol concentration at 180 min (21.4 +/- 14.0 ng/mL) was not significantly different from the concentration at 150 min. Some possible reasons for this decrease after commencing continuous intraventricular drainage are discussed. IMPLICATIONS: Propofol concentrations in the cerebrospinal fluid in neurosurgical patients Propofol concentration in cerebrospinal fluid of investigated patients decreased significantly after starting intraventricular drainage, despite relatively steady blood propofol concentrations. These results supplement the limited information about propofol pharmacokinetics in the human central nervous system.

Adult↗
PubMed1992

Effect of gallopamil on electrophysiologic abnormalities and ventricular arrhythmias associated with left ventricular hypertrophy in the feline heart.

Left ventricular hypertrophy increases vulnerability to ventricular fibrillation. To determine whether calcium channel blockade protects against ventricular arrhythmia in left ventricular hypertrophy, we studied the effects of gallopamil, a potent and specific calcium channel antagonist, in 37 cats undergoing aortic banding (group 1, n = 28) or a sham procedure (group 2, n = 9). Each cat underwent serial echocardiography and was studied after the development of left ventricular hypertrophy, defined as an increase of at least 30% in left ventricular posterior wall thickness. After baseline electrophysiologic testing, animals received gallopamil (70 micrograms/kg loading dose followed by 2.5 micrograms/kg/min infusion) (n = 19) or a control infusion of saline solution (n = 18), and testing was repeated. There was no significant difference between groups 1 and 2 in baseline excitability thresholds intraventricular conduction times, ventricular effective refractory periods, or monophasic action potential durations. Thresholds for induction of ventricular fibrillation were lower in group 1 than in group 2, and only in group 1 was ventricular fibrillation inducible during programmed stimulation. This altered vulnerability was associated with a significantly greater dispersion of excitability thresholds, ventricular effective refractory periods, and monophasic action potential durations. Gallopamil did not change baseline measurements except for prolonging sinus cycle length and atrioventricular conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The TRH analogue CG3509 increases in vivo catechol/ascorbate oxidation in the N. accumbens but not in the striatum of the rat.

The effects of injection of the thyrotrophin-releasing hormone (TRH) analogue, orotyl-histidyl-proline amide (CG3509) into the accumbens and striatum, was studied on dopamine metabolism by means of in vivo voltammetry. Forty minutes after infusion of CG3509 (1-5 micrograms) into the n. accumbens there was a significant dose-related increase in the oxidation peak, corresponding to the oxidation of the dopamine metabolite, dihydroxyphenylacetic acid (DOPAC) and ascorbic acid. The size of this peak returned to normal by 80 min after the infusion. There was no change in the indole oxidation peak. Infusion of CG3509 (5 micrograms) had no effect on the size of either the catechol or the indole oxidation peaks recorded in the striatum. Intraventricular injection of CG3509 (10 micrograms) also increased DOPAC/ascorbic acid oxidation peak recorded in the n. accumbens, without altering the indole peak. While the voltammetric technique used in the present experiments is not able fully to separate ascorbic acid and DOPAC in vivo, the results support the view that TRH and its analogues selectively increase dopaminergic activity in the mesolimbic region.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Cardiac effects of amiloride in the dog.

The cardiac effects of amiloride, a potassium-sparing diuretic, were investigated in isolated, blood-perfused atrioventricular (AV) node, sinoatrial (SA) node, and papillary muscle preparations of dogs. In AV node preparations, when infused into the posterior septal artery (which supplies mainly the AV node), amiloride in a blood concentration of 0.2 mumole/ml gradually prolonged the functional refractory period at atrial pacing rates of 100, 150, and 200 stimuli/min. The lower the pacing rate, the greater was the prolongation. AV conduction time was increased only with pacing at 200 stimuli/min. In the same preparation, when infused into the anterior septal artery (which supplies the His-Purkinje-ventricular system), amiloride did not appreciably prolong AV conduction time, indicating that intraventricular conduction was unaffected. The configuration of ventricular bipolar electrograms was also unchanged. In SA node preparations, amiloride had a negative chronotropic action which was not antagonized by atropine. In papillary muscle preparations, amiloride had a positive inotropic action and prolonged the effective refractory period but did not change ventricular automaticity. The positive inotropic action of amiloride was not antagonized by carteolol, a beta-adrenoceptor-blocking agent. These results indicate that amiloride may have antiarrhythmic properties.

Amiloride↗
PubMed1985

Central role for angiotensin in control of adrenal catecholamine secretion.

Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion of catecholamines after hemorrhage in the dog. To test if ANG II acts centrally, experiments were performed under general anesthesia on bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg. Ventriculocisternal perfusion of ANG II or its antagonist saralasin was accomplished via needles inserted in the left lateral cerebral ventricle and cisterna magna. Mean arterial pressure and adrenal secretion of catecholamines were measured before and after hemorrhage. Nephrectomized dogs receiving only artificial cerebrospinal fluid (CSF) by ventriculocisternal perfusion had a very small adrenal response to hemorrhage compared with animals receiving ANG II intraventricularly (IVT) (at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 . min-1) had no effect on adrenal catecholamine secretion. Animals with intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not blunt the response to hemorrhage. Thus ANG II appears to support catecholamine secretion via a central mechanism. This mechanism is physiologically significant because either nephrectomy or functional elimination of ANG II by saralasin greatly attenuates the adrenal medullary response to hemorrhage in vivo.

Adrenal Glands↗
PubMed1981

Disseminated intravascular coagulation as a complication of ventricular catheter placement. Case report.

A child who developed generalized bleeding immediately after placement of a ventriculoperitoneal shunt was found to have evidence of disseminated intravascular coagulation (DIC). Infusion of fresh frozen plasma was followed promptly by improvement in laboratory values and cessation of bleeding. Complications of the acute bleeding episode included intraventricular hemorrhage, loss of 50% of the red cell volume into subcutaneous tissues, and transient peritoneal irritation. Defibrination syndrome (that is, DIC) due to release of tissue thromboplastin is a recognized complication of trauma, particularly with brain injury. Defibrination can be induced in experimental systems with administration of very small amounts of thromboplastin, which is present in high concentration in brain tissue. This has not been described previously with minor neurosurgical procedures. The diagnosis of DIC should be considered if excessive bleeding occurs after any brain insult, since early recognition and restoration of normal hemostasis by replacement of clotting factors should prevent major complications due to ongoing hemorrhage.

Adolescent↗
PubMed1984

Intraventricular hemorrhage in the premature rabbit pup. Limitations of this animal model.

The authors used the premature rabbit model to examine the pathophysiology of intraventricular hemorrhage (IVH). They studied the brains of 167 control animals, of 45 animals after a hypertensive insult, of three animals after a bolus infusion of normal saline, and of 10 animals after both insults. In none of the brains was IVH identified. Limited reproducibility may restrict the use of this animal model.

Animals↗
PubMed1992

Cortical biopsy in Alzheimer's disease: diagnostic accuracy and neurochemical, neuropathological, and cognitive correlations. Intraventricular Bethanecol Study Group.

Neurochemical assessments were performed on biopsy samples taken from the right frontal lobe of patients diagnosed with Alzheimer's disease (AD), before the implantation of a ventricular catheter and pump assembly for the infusion of bethanechol chloride as an experimental therapy. The pathologically diagnosed patients with AD (n = 35; mean age, 67 +/- 1.5 yr) were compared with a group of samples from normal age-equivalent autopsied controls (n = 22; mean age, 68 +/- 2 yr) and autopsied AD brains (n = 11; mean age, 73 +/- 2 yr). Samples were assayed for choline acetyltransferase (ChAT), acetylcholinesterase, binding to [3H]quinuclidinyl benzilate as an index of total muscarinic cholinergic binding, and [3H]pirenzepine binding as an index of M1 cholinergic receptor subtype binding. Mean levels of ChAT activity were decreased in the biopsied patients to 36% of age-matched autopsied controls. The loss of ChAT activity correlated significantly with the Mini-Mental State Examination, an index of global cognitive function. Mean ChAT activity in autopsied AD cortex was further decreased compared with controls, indicating continuous decline through the course of the disease. Acetylcholinesterase followed a similar, less dramatic decline. No differences were found in [3H]quinuclidinyl benzilate binding or [3H]pirenzepine binding between biopsied and autopsied controls. Neuritic plaque counts did not correlate with either the Mini-Mental State Examination or ChAT activity in the biopsy specimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗