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K Todd

Publications and source records attributed to K Todd.

At least 37 records · Page 2Linked to original sources
PubMed1992

Prospective analysis of mental status progression in ethanol-intoxicated patients.

Distinguishing patients with uncomplicated ethanol intoxication from intoxicated patients with other causes of mental status depression is a common clinical dilemma. The authors serially tested mental status in a group of ethanol-intoxicated patients to determine the interval over which mental status changes could be attributed to uncomplicated intoxication. Study patients were identified by (1) admission breath ethanol greater than or equal to 100 mg/dL; (2) ethanol-related impairment necessitating further observation or treatment; and (3) not critically ill or exhibiting focal neurologic signs. Mental status scores (sums of specific indices of alertness, orientation, and agitation) were determined initially, 1 hour after arrival, then every 2 hours. Causes of mental status depression other than acute intoxication were diagnosed in 16 patients, while another 18 failed to completely normalize mental status by the time of emergency department discharge or hospital admission. The remaining 71 with uncomplicated ethanol intoxication required (mean +/- SD) 3.2 +/- 3.6 hours to normalize mental status scores. A large proportion, however, took considerably longer to normalize mental status: 15 (21%) took 7 or more hours, and three (4%) took as long as 11 hours. Although patients with ethanol-associated depression of mental status lasting 3 hours after emergency department admission should be carefully evaluated for other causes of mental status abnormalities, the authors' observations indicate considerable individual variation in the duration of mental status depression caused by uncomplicated ethanol intoxication.

Alcoholic Intoxication↗
PubMed1992

Effect of body locale and addition of epinephrine on the duration of action of a local anesthetic agent.

STUDY OBJECTIVE: Little information exists relating body locale to the duration of action of local anesthetics. We tested the duration of action of a local anesthetic with and without epinephrine at different body locales. PARTICIPANTS: Twenty healthy volunteers aged 27 to 48 years (mean, 32.0 years). INTERVENTIONS: In the first of two experiments (L), 20 subjects had 1 mL buffered 1% lidocaine injected intradermally on the forehead, hand, forearm, and calf. In the second experiment (LE), ten subjects were injected at the same sites with lidocaine containing epinephrine. METHODS: Subjects ranked anesthesia by reaction to pinprick from 0 (complete) to 20 (none) on a scale with testing done every 15 (L) or 30 (LE) minutes and continued until no anesthetic effect was present. Duration of effective and of any anesthesia were times until score of more than 5 and of more than 19, respectively. Mean duration of anesthesia was compared by analysis of variance (between body areas) and paired two-tailed t-test (L vs LE). Significance was taken as P less than or equal to .05. RESULTS: Anesthesia was significantly briefer for the face than for all other body locales by both indexes of duration and for both plain lidocaine and lidocaine with epinephrine (P less than .001 to P less than .05). Anesthesia with epinephrine lasted significantly longer than with lidocaine alone at all body locales and for duration of both effective or any anesthesia (P = .0001 to P = .001). Based on 95% confidence interval limits, the duration of anesthesia at other body locales is predicted to be 1.3- to 3.2-fold that on the face. Confidence interval analysis indicated that addition of epinephrine to lidocaine increases the duration of anesthetic action by 1.3- to 13.0-fold that of lidocaine alone. CONCLUSION: The duration of action of local anesthesia is considerably shorter for the face than for other body areas. Epinephrine significantly increases the duration of action of lidocaine at all body locales.

Adult↗
PubMed1991

Incidence of cocaine-associated rhabdomyolysis.

STUDY HYPOTHESIS: Rhabdomyolysis is a common complication of cocaine use, and muscle symptoms fail to predict its development. STUDY POPULATION: A prospective, convenience sample of patients presenting to the emergency department of a large inner-city hospital with complaints related to cocaine use were eligible for inclusion. Patients were excluded if they had other potential causes of elevated creatine kinase (CK) levels or rhabdomyolysis. A control group comprised patients who were not cocaine users and satisfied the exclusion criteria. Sixty-eight patients were studied. METHODS: Initial evaluation included determination of the presence of muscle pain or swelling and total CK levels. Patients with a CK level of more than 800 U/L had additional tests, including a urine myoglobin, urine drug screen, and serum phosphorus. Rhabdomyolysis was defined by a serum CK level of more than 1,000 U/L (more than fivefold that of normal). CK levels were compared by two-tailed Student's t test. Muscle symptoms were compared with the development of rhabdomyolysis by Fisher's exact test. RESULTS: The CK level in the cocaine group was 931 +/- 1,785 U/L (mean +/- 1 SD). The CK level in the control group was 242 +/- 168 U/L (P = .028). Of the cocaine users, 24% (eight of 34) had rhabdomyolysis; one developed multiorgan failure and died. No patient in the control group had a CK level of more than 1,000 U/L. Only one cocaine user who developed rhabdomyolysis had muscle symptoms. Three cocaine users had muscle symptoms but did not develop rhabdomyolysis. No patient in the control group had muscle symptoms or developed rhabdomyolysis. Muscle symptoms did not predict the CK level (P = .55). CONCLUSION: This study revealed that 24% of the cocaine users had rhabdomyolysis. Many of the cases of rhabdomyolysis were not predictable from history or physical examination, making laboratory evaluation essential.

Adult↗
PubMed1991

PVD: nurse--patient interventions.

The intervention program described began with teaching patients in simple terms about PVD, associated risk factors, and why change is important. Teaching aids such as posters and booklets were used to supplement discussion. Positive reinforcement was emphasized. Phone calls, follow-up visits, encouragement and praise were frequent. Newsletters focusing on different aspects of the various risk factors were developed and mailed monthly. Patients were encouraged and helped to develop an individualized program of change based on discussions and practicality. They were encouraged to start slowly and increase gradually. Emphasis was placed on reinforcement, self-help, and praise for efforts. Patients were encouraged to keep a brief daily log of progress and thoughts. Regularly scheduled physical assessments provided a tool to assess change and provide tangible evidence of their ability to set a goal, follow through, and make life-style change.

Aged↗
PubMed1989

Osmotic regulation of hypothalamo-neurointermediate lobe corticotrophin-releasing factor-41 in the rat.

We have detected significant amounts of corticotrophin-releasing factor-41 (CRF-41) in the rat hypothalamo-neurointermediate lobe system using a radioimmunoassay and reversed-phase high-performance liquid chromatography. Total amounts of CRF-41 in extracts of median eminence (ME), supraoptic nucleus (SON), paraventricular nucleus (PVN) and neurointermediate lobe (NIL) from control animals were 1076 +/- 132, 196 +/- 44, 22 +/- 7 and 147 +/- 50 fmol respectively (means +/- S.E.M., n = 6). In animals given 340 mmol NaCl/l instead of tap water to drink for 12 days, no significant changes occurred in the CRF-41 content of the ME, SON or PVN, but CRF-41 content increased more than twofold in the NIL (362 +/- 58 fmol). Plasma concentrations of CRF-41 and ACTH in control animals were 23 +/- 6 and 51 +/- 8 pmol/l respectively. After saline treatment no significant change in plasma CRF-41 was detected (20 +/- 8 pmol/l) but concentrations of circulating ACTH were decreased (15 +/- 2 pmol/l). The CRF-41 content of both the ME and the NIL was significantly depleted after intracerebroventricular injection of colchicine (414 +/- 81 and 34 +/- 7 fmol respectively). These data suggest that NIL CRF-41 is of hypothalamic origin and can be regulated by an osmotic stimulus.

Adrenocorticotropic Hormone↗
PubMed1988

Differential effects of hypothalamic catecholamine depletion on the release of arginine vasopressin and CRF-41 into hypothalamo-hypophyseal portal blood.

The effects of 6-hydroxydopamine lesions of the ventral noradrenergic bundle (VNAB) and of intracerebroventricular 6-hydroxydopamine on hypothalamo-hypophyseal portal blood (HPB) concentrations of arginine vasopressin (AVP), corticotrophin releasing factor (CRF-41), and noradrenaline have been investigated. VNAB lesions and intracerebroventricular 6-hydroxydopamine caused a reduction of HPB CRF-41 concentration, while AVP remained unchanged. HPB noradrenaline concentration was reduced in animals treated with lateral ventricular 6-hydroxydopamine, but was unchanged in VNAB lesioned animals. Our results suggest differential effects of noradrenaline on the release of AVP and CRF-41 into HPB.

Adrenergic Fibers↗
PubMed1988

Immunoreactive vasopressin and oxytocin in hypothalamo-hypophysial portal blood of the Brattleboro and Long-Evans rat: effect of adrenalectomy and dexamethasone.

Immunoreactive vasopressin and oxytocin were measured in the hypothalamo-hypophysial portal blood of both Long-Evans and homozygous Brattleboro rats. Adrenalectomy caused an increase in vasopressin immunoreactivity in portal blood in the Long-Evans strain, whilst administration of dexamethasone to these adrenalectomized animals resulted in a reduction in portal vasopressin immunoreactivity to levels below those seen in sham-operated animals. This vasopressin immunoreactivity co-eluted with synthetic vasopressin on high-pressure liquid chromatography (HPLC), and diluted in parallel in radio-immunoassay. In Brattleboro rats, however, although vasopressin-like immunoreactivity was detected, the portal concentration did not vary with the adrenal status of the animal, nor did it show the characteristics of standard vasopressin on HPLC or in immunoassay. Oxytocin was present in the portal blood of both Long-Evans and Brattleboro rats at similar very high concentrations, but did not vary in response to adrenalectomy. These results are consistent with a role for vasopressin, but not oxytocin, in the hypothalamic response to adrenalectomy and glucocorticoid feedback. Neither vasopressin immunoreactivity nor oxytocin appear to subserve this role in the homozygous Brattleboro rat.

Adrenalectomy↗
PubMed1987

Oxytocin in the central nervous system and sexual behaviour in male rats.

Concentrations of oxytocin (OT) and vasopressin (AVP) were measured in cerebrospinal fluid (CSF) obtained from the cisterna magna of freely moving rats. Basal levels of OT and AVP were approximately 9 fmol/ml in both male and female. In the male rats this increased to approximately 18 fmol/ml 5 min after ejaculation, and 27 fmol/ml 20 min after ejaculation. No increase from basal levels occurred when males were placed with unreceptive females, or alone in the test environment. AVP levels were unchanged in any condition. Preliminary investigations indicate that discrete electrolytic lesions to the lateral and posterior parvocellular hypothalamic paraventricular nucleus (PVN) abolished this ejaculation-associated increase in CSF OT, prolonged mount and intromission latencies and reduced the absolute postejaculatory interval (PEI). We conclude that intracerebrally projecting OT systems may be activated during coitus and may contribute to the mechanisms underlying postejaculatory refractoriness.

Animals↗
PubMed1987

Vasopressin activation of phosphatidylinositol metabolism in rat anterior pituitary in vitro and its modification by changes in the hypothalamo-pituitary-adrenal axis.

The ability of vasopressin to stimulate the accumulation of 3H-labelled inositol phosphates was studied in vitro using prelabelled rat anterior pituitary quarters. [8-Arginine] vasopressin activates inositol lipid breakdown in this system in a time- and dose-dependent manner; vasopressin (3 X 10(-7) M) resulted in a 1.8-fold stimulation of inositol phosphate accumulation over control accumulation after 10 min. This response to vasopressin is inhibited by the specific V1 antagonist (CH2)5Tyr(Me)AVP. Both oxytocin and the selective V2 agonist DDAVP also show some agonist activity, but are considerably less potent than arginine vasopressin. Corticotrophin-releasing factor alone had no effect on inositol phosphate production, whilst a high dose given in conjunction with vasopressin resulted in a diminution of the response below that found with the same concentration of vasopressin alone. Anterior pituitaries from vasopressin-deficient Brattleboro rats also show a phosphatidylinositol response to vasopressin. Pituitaries from rats that had been adrenalectomized 4 days earlier showed no increase in inositol phosphate accumulation in response to vasopressin. Daily administration of dexamethasone (40 micrograms/day) reversed this effect of adrenalectomy. This reversal was not seen when dexamethasone (40 micrograms/ml) was added to the incubation medium of adrenalectomized rat pituitary quarters. These results confirm that the rat anterior pituitary contains functional vasopressin receptors capable of activating inositol phospholipid metabolism and that this biochemical response is modified by changes in the hypothalamo-pituitary-adrenal axis.

Adrenalectomy↗
PubMed1986

Oxytocin release during coitus in male and female rabbits: effect of opiate receptor blockade with naloxone.

Blood was collected from freely moving rabbits pretreated with saline or naloxone both before and after coitus. In the males, ejaculation was associated with a marked increase in plasma oxytocin concentrations. In the females, oxytocin release was an all-or-nothing phenomenon-either there was no change in oxytocin or it rose to levels very similar to that found post-ejaculation in the males. Naloxone did not alter the proportion of occasions in which females showed an oxytocin response, nor did it have a significant effect on the levels of oxytocin achieved during coitus in either the male or the female rabbits.

Animals↗
PubMed1985

Oxytocin and sexual behaviour in the male rat and rabbit.

In male New Zealand white rabbits, it was shown that oxytocin but not vasopressin concentrations in plasma were markedly raised after ejaculation. In male Wistar rats, oxytocin infused into the internal carotid artery reduced the number of intromissions made before ejaculation but had no other significant effect. Infusion of oxytocin into the third ventricle increased the latencies to the first mount and intromission and lengthened post-ejaculatory refractory periods. It is suggested that oxytocin released into the periphery during coitus, while not essentially involved in ejaculation, may exert effects on the genital periphery. Behavioural effects of centrally administered oxytocin suggest that it may play a role in the neural mechanisms underlying post-ejaculatory refractoriness.

Animals↗
PubMed1984

Ascending noradrenergic projections from the brainstem: evidence for a major role in the regulation of blood pressure and vasopressin secretion.

The role of projections from the lateral tegmental (A1, A2) and coeruleal (A6) noradrenergic cell groups in the control of arginine vasopressin (AVP) secretion was studied following lesions to the ventral (VNAB) and dorsal (DNAB) noradrenergic bundles by 6-hydroxydopamine. These lesions were associated with the expected, large reductions in cortical (DNAB) and hypothalamic (VNAB) noradrenaline concentrations. Vehicle injected, control animals and VNAB lesioned animals showed a similar AVP secretory response to haemorrhage, whilst the DNAB group showed a markedly diminished release of AVP in response to this challenge. Following Clonidine injection, both controls and VNAB animals showed major reductions in plasma AVP concentrations, but again the DNAB group behaved in a different manner, with a marked attenuation of the inhibitory effect of Clonidine on AVP secretion. In addition, the DNAB group had a significantly lower basal blood pressure, a greater initial agonist response to Clonidine and a loss of the hypotensive response to Clonidine in comparison to sham and VNAB lesioned groups. All three groups showed a similar AVP response to intravenous nicotine. These data suggest that noradrenergic projections originating in the locus coeruleus, or in the lateral tegmental NA groups but which ascend together with coeruleal axons in the DNAB, modulate the vasopressin response to visceral stimuli and to Clonidine, and that they also play an important role in mediating the hypotensive effect of Clonidine.

Afferent Pathways↗
PubMed1984

Ascending brain-stem noradrenergic pathways modulate the renin response to haemorrhage.

Ventral noradrenergic projections (VNAB) from lateral tegmental (A1, A2) and dorsal noradrenergic projections (DNAB) from the coeruleal (A6) as well as A1 cell groups in the brain-stem of the rat were lesioned by intracerebral injection of 6-hydroxydopamine. A marked increase in plasma renin activity and adrenaline concentrations followed haemorrhage (0.5 ml/100 g body weight) in the sham-operated rats. VNAB-lesioned rats showed a similar response to the sham-operated controls, but in DNAB-lesioned animals the rise of plasma renin was markedly attenuated.

Animals↗
PubMed1984

Localization and actions of cholecystokinin in the rat pituitary neurointermediate lobe.

Rat pituitary neural lobe contained high concentrations of cholecystokinin-like immunoreactivity (CCK-LI). Section of the pituitary stalk resulted in loss of CCK-LI, and both lactation and replacement of drinking water with 2% saline resulted in marked depletion of CCK-LI. Rats with congenital diabetes insipidus (Brattleboro strain) had a 73% reduction in CCK-LI below the levels of hooded Long-Evans controls, where as levels in the brain were unchanged. Release of CCK-LI, labeled dopamine, and gamma-amino butyric acid in response to potassium depolarization was studied. There was a low fractional release of CCK-LI. Addition of sulfated CCK-8 (CCK-8s) to the medium enhanced the calcium-dependent potassium-stimulated release of dopamine, but basal release was unaffected. gamma-Amino butyric acid release was only poorly calcium dependent and not effected by extracellular CCK-8s. Vasopressin and oxytocin release were stimulated by electrical stimulation of the pituitary stalk, and were unaffected by the addition of CCK-8s to the medium. In vivo, however, the injection of 5 micrograms CCK-8s into the third ventricle resulted in increased plasma vasopressin concentrations.

Animals↗
PubMed1983

Role for lateral tegmental noradrenergic neurons in the vasopressin response to hypertonic saline.

Lesions to the dorsal and ventral noradrenergic pathways were achieved by injecting 6-hydroxydopamine in the periaqueductal midbrain or lateral pons, respectively. Four to 6 weeks after surgery the rats were anaesthetized with pentobarbitone, and hypertonic saline was administered into the peritoneum. Rats with lesions of the ventral noradrenergic pathways showed a significant reduction in the saline-induced rise in plasma vasopressin concentrations, while lesions to the dorsal pathway or control injections were without effect.

Animals↗