Cerebrospinal fluid creatine kinase-BB activity: a perspective.
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Publications and source records attributed to R D Bell.
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Dural sinus thrombosis is a rare, potentially fatal complication of a radical neck dissection. The prognosis can vary from complete recovery to rapid death. Magnetic resonance venography provides an effective, noninvasive diagnosis. The goals of therapy are to decrease intracranial pressure and to lyse the thrombus. Systemic anticoagulation and systemic thrombolytics are controversial therapies. The direct intrasinus infusion of thrombolytic agents is under investigation.
The effect of rigid blood pressure control on renal function is an unsettled issue. This study describes a retrospective analysis on the relationships between blood pressure control, hematocrit levels, and renal function in 97 treated hypertensive patients. Data analysis was done on systolic and diastolic blood pressure, hematocrit levels, renal function assessed by serum urea nitrogen (SUN), serum creatinine (Scr), and hydrochlorothiazide (HCTZ) dose at entry and at four anniversary dates thereafter. The patients were divided into two groups: group I and group II on the basis of HCTZ dose. Group I received an average of 100 mg HCTZ daily, whereas group II received an average of 50 mg HCTZ daily. In group I, the decrement in both systolic and diastolic blood pressure over time was highly significant (P < .0001); however, no change in renal function was noted. In group II, systolic blood pressure decreased significantly (P < .01) from entry to year 1, then leveled off. In year 4, systolic blood pressure was not different from that of entry. Conversely, the difference between entry and year 4 diastolic blood pressure was highly significant (P < .0001). In group II, significant decreases were noted between entry and year 4, SUN (16.5 +/- 5.7 versus 14.9 +/- 4.1 mg/dL; P < .0012) and Scr (1.29 +/- .23 versus 1.24 +/- .19 mg/dL; P < .0192). Hematocrit showed diverse responses; in group I, hematocrit significantly increased from entry to year 4 (44.8 +/- 2.5 versus 47.2 +/- 3.9%; P < .01); whereas, in group II, hematocrit significantly decreased (47.7 +/- 3.8 versus 44.9 +/- 3.4%; P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)
Heparin given over a long term by a subcutaneous route consistently lowers blood pressure in the hypertensive rat models. The decrease in blood pressure is accompanied by a parallel decrease in hematocrit suggesting a causal relationship between hematocrit and blood pressure. The aim of this study was to define the relationships between acute and chronic hematocrit changes and blood pressure in the normotensive and hypertensive states. Normotensive Wistar (NWR) and spontaneously hypertensive (SHR) rats were used. Hematocrit was decreased acutely by blood-letting, and chronically by treatment with either heparin (H) or phenylhydrazine (P) for 4 weeks. Acute and chronic hematocrit increase was accomplished by packed cells transfusion. Systolic blood pressure was measured weekly; and at the end of the experimental period, plasma volume, cardiac output, and mean arterial pressure were obtained. Acute hematocrit decrease or increase (hematocrit ranging from 25 to 65%) did not affect blood pressure in either strain of rats; whereas chronic hematocrit changes (hematocrit ranging from 35 to 61%) significantly affected blood pressure only in SHR. Thus, chronic hematocrit decrease induced by H or P resulted in a significant fall in blood pressure compared to control (201 +/- 3 v 175 +/- 4, 167 +/- 4 mm Hg, respectively; P < .05). Conversely, a chronic hematocrit increase resulted in a significant rise in blood pressure (201 +/- 3 v 219 +/- 4 mm Hg; P < .05). Similar hematocrit changes produced in NWR, as in SHR, did not affect blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
There is no accepted efficacious treatment for ischemic cerebral edema. We show in a cat model of focal cerebral ischemia that infarct volume can be reduced (p less than 0.05) by ventriculocisternal perfusion with an oxygenated fluorochemical emulsion (bis-perfluorobutylethylene). An accompanying effect of such ventriculocisternal perfusion is a reduction in intracranial pressure. At 18 hours following the start of the perfusion, there was a significant (p less than 0.05) difference in intracranial pressure between nonperfused controls (mean 11.4 [range 2.3-23.0] torr, n = 6) and cats perfused with an oxygenated nutrient solution not containing fluorochemical (mean 11.3 [range 3.0-29.0] torr, n = 8) or animals perfused with the oxygenated fluorochemical emulsion (mean 2.21 [range 0-3.5] torr, n = 7). Perfusion with this oxygenated fluorochemical emulsion warrants further study as a treatment for elevated intracranial pressure.
We studied renal function, urinary enzymes, urinary sediment, and renal histopathology in Fischer 344 rats that were treated with one dose of mercuric chloride (HgCl2) alone, HgCl2 followed by gentamicin, gentamicin alone, or gentamicin, followed by HgCl2. HgCl2 was administered intraperitoneally at 1 mg/kg body weight. Gentamicin was injected subcutaneously at 40 mg/kg body weight. Renal function was assessed by creatinine clearance. Urinary sediment was examined using transmission electron microscopy; particular attention was given to the numbers by myeloid bodies in the urinary sediment. Renal tissue was assessed using light microscopy for acute tubular necrosis (ATN). In either HgCl2- or saline-treated rats urinary sediment showed no myeloid bodies, and renal morphology was essentially normal. The rats given HgCl2 48 h prior to initiation of gentamicin therapy showed significant decrease of myeloid bodies excretion. This was accompanied by significantly less impairment of renal function, mild renal lesion, and no necrotic tubule cells in urinary sediment. The rats treated with either gentamicin alone or gentamicin followed by HgCl2 developed significant impairment of renal function in association with marked elevation of the urinary enzymes, and variable extent of ATN. In both of these groups, urinary sediment showed a profusion of free myeloid bodies and many necrotic renal tubule cells. The urinary sediment findings, however, did not aid in distinguishing between these two treatment groups. From these data we conclude that (1) a tentative relationship exists between the concentration of the urinary myeloid bodies and severity of gentamicin nephrotoxicity; (2) prior treatment with compound(s) analogous to HgCl2 which could minimize urinary excretion of the myeloid bodies might be useful in the mitigation of gentamicin nephrotoxicity.
Bilateral renal artery occlusion (RAO) for 120 minutes in dogs results in acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion with rapidly deteriorating renal function. We have shown that prior splenectomy minimizes RAO-induced renal functional and histopathologic changes. The purpose of this study was to examine whether this renal protection is due to prevention of red blood cell echinocyte formation and resultant renal PTC congestion. Echinocytes (burr cells) are poorly deformable, impart high viscosity to the blood, and may hinder reperfusion by increasing resistance to renal capillary blood flow. Splenectomized (SPLX) or sham-SPLX dogs were treated with bilateral RAO for 120 minutes. After RAO, renal function and renal blood flow were monitored, and peripheral blood red blood cells were examined at 1 hour and at 24-hour intervals for 96 hours. Renal biopsies were taken 1 hour after RAO and the kidneys removed 96 hours after RAO. The RBCs and renal tissues were studied using scanning electron microscopy. Renal function was assessed by endogenous creatinine clearance. Sham-SPLX animals showed a marked and sustained decrease in creatinine clearance, consistently elevated serum creatinine levels and fractional excretion of sodium, and diffuse ATN and PTC congestion with echinocytes. These animals had a peak in circulating echinocytes 1 hour after RAO (p less than 0.05), which showed an excellent negative correlation with creatinine clearance (r = -0.999; p less than 0.001). On the contrary, SPLX animals had essentially no change in serum creatinine or fractional excretion of sodium, minimal tubular changes, no PTC congestion, and no rise in circulating echinocytes during the 96-hour observation. In vitro treatment of the postischemic red blood cells from sham animals with adenosine-inosine or fresh postischemic plasma from the SPLX animals showed almost complete reversal to discocytes (normal red blood cells), whereas in vitro treatment of postischemic red blood cells from the SPLX animals with fresh postischemic plasma from the sham animals resulted in a marked echinocytic response. We conclude that 1) a marked echinocyte response in the immediate postischemic period is an important mechanism in initiating ischemic ATN, 2) an echinocyte inducing factor may reside in the plasma of spleen-intact animals, and 3) mitigation of ATN and PTC congestion by splenectomy is, at least in part, consequential to attenuated echinocytic response in the immediate postischemic period.
In summary the advantages of providing custom-fitted mouthguards for athletes, especially those involved in contact sports, has been discussed along with the methodology of construction. Because of the apparent lack of negative effects on physical performance and the superior protective characteristics of custom-fitted mouthguards, it seems logical to recommend their use in the competitive sports arena.
In order to analyse the relationship between maximal aerobic power (VO2max) and height, body mass and lean body mass a multi-longitudinal survey was conducted on three different age groups of randomly selected children from a small Czech community. Beginning at the initial ages of 8, 12 and 16 years subjects were subsequently retested three times at 2-year intervals. At overlapping ages there were no differences in the various age groups between height and VO2max. By utilizing mean values for the various parameters at specific calendar ages a growth curve was constructed for each sex for the age range 8-20 years. The values were compared with longitudinal studies in various countries and no substantial differences were found. When VO2max was then compared to height, body mass and lean body mass it was apparent that the almost linear relationship with height was the most precise. In addition the children remained, generally speaking, in their same rank order for VO2max for the three different age groupings.
The local cerebral metabolic rate for glucose (LCMRg) was measured in cats subjected to global cerebral ischemia (GCI). Control (nonperfused) cats showed decreased LCMRg (P less than 0.01) in the frontal, temporal, parietal, and occipital cortex 9.5 hours after a 10-minute exposure to GCI. Cats perfused ventriculocisternally with oxygenated nutrient solution (ONS) for 8 hours showed significant increases in the LCMRg (p less than 0.05) at 9.5 hours postischemia in the parietal and occipital areas over the levels found in untreated ischemic cats. Supplementing the ONS perfusion medium with fluorocarbon (OFNS) increased the LCMRg (P less than 0.05) in the frontal, as well as the parietal and occipital areas, over that seen in untreated ischemic brains. The increase of LCMRg in three (rather than only two) cortical areas may be a result of the ability of the fluorocarbon in OFNS to deliver greater quantities of oxygen to the brain than ONS without fluorocarbon. Perfusion with OFNS without glucose, or with low (50 mg%) glucose, was more effective than OFNS with high (200 mg%) glucose in restoring LCMRg to normal in all four cortical areas affected by GCI. In five brain areas not affected by GCI, perfusion with OFNS having no glucose significantly increased LCMRg as compared to normal animals. This study demonstrates that OFNS perfused by the ventriculocisternal route can restore toward normal the LCMRg following GCI and that different concentrations of glucose in the perfusing fluid will have variable effects on LCMRg in certain brain areas.
Experiments were conducted to assess the effects of chronic haloperidol (CHAL) administration on gamma-aminobutyric acid (GABA) receptor binding within the rat globus pallidus (GP) and on the responsiveness of individual pallidal neurons to microiontophoretically applied GABA and glycine. Rats were administered haloperidol in their food for 30 days in increasing concentrations and the experiments were conducted 2 days after termination of the haloperidol treatment. GABA receptor binding and neuronal responsiveness to GABA were significantly increased within the GP following CHAL treatment. The mean EC50 value for GABA was significantly decreased in the CHAL-treated rats, but there was no change in the EC50 for glycine. Scatchard analysis of [3H]muscimol binding demonstrated a single high-affinity binding site (Kd = 5 nM) within both control and CHAL-treated rats. The binding capacity (Bmax) of this high-affinity site was significantly increased in CHAL-treated rats without any change in the dissociation constant (Kd) for this site. These results suggest that CHAL administration may lead to a decrease in GABA release by striatopallidal efferents. The results of this study, combined with those of our previous study on SNR neurons, have demonstrated that blockade of striatally mediated dopamine (DA) neurotransmission leads to similar changes in GABAergic mechanisms at the level of the GP and SNR and suggest that DA regulation of the striatopallidal and striatonigral GABAergic pathways need not be differentially organized as has previously been postulated.
Splenectomy (SPLX) prevents ischemic acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion. This study attempts to reverse the protective effect of splenectomy in the ischemic model of ATN by increasing hematocrit before inducing ATN. Sham-SPLX, SPLX, and SPLX dogs given packed red cells to elevate hematocrit by 30% (SPLX-high hematocrit) received bilateral renal artery obstruction (RAO) for 120 minutes. Renal function was tested for 6 days post-RAO. Hematocrit in the SPLX-high hematocrit group was greater (p less than .05) than the SPLX-RAO group but did not differ from the non-SPLX group. All groups had different (p less than .05) serum creatinine levels for 48 hours post-RAO, and untreated animals differed from all the others at 144 hours. Serum creatinine was highest in untreated, lowest in SPLX-high hematocrit, and intermediate in noninfused SPLX animals. The same pattern was observed in blood urea nitrogen, creatinine clearance and renal histopathology. Fractional excretion of sodium in the SPLX groups was six times that in the intact animals (p less than .05), irrespective of hematocrit level. We conclude that increased hematocrit is protective in ischemic ATN, and does not promote PTC congestion or ATN in the SPLX animal. In addition, the protective effect of splenectomy may be mediated, in part, by mechanism(s) that alter sodium transport or osmolar excretion.
The effects of intramuscular glycerol on ischemic acute renal failure was investigated in dogs. Anesthetized dogs received a bilateral 120-min renal artery obstruction (RAO) alone, RAO plus 5 ml/kg of 50% glycerol or RAO plus 5 ml/kg of 75% glycerol. Control groups received the glycerol injection, but not RAO. Renal histopathology was minimal in dogs receiving glycerol alone. In RAO dogs, those receiving 50% glycerol showed diffuse acute tubular necrosis (ATN), while those receiving 75% glycerol had severe ATN with extreme mortality. Changes in serum creatinine, creatinine clearance, and fractional excretion of sodium were consistent with the histopathologic changes. We conclude that myoglobinuria, of a degree insufficient to cause renal failure itself, can interact with renal ischemia to significantly exacerbate the renal damage produced.
The reliability and objectivity of two curl-up protocols in assessing abdominal muscle endurance were evaluated in 262 adults (18-69 + years of age). The two protocols consisted of the Canada Fitness Award procedure (Type I) and a partial curl-up described by Fitness Canada (Type II). The relationship of these protocols, body mass, trunk flexion, body mass index and waist/hip ratio to the incidence and degree of low back pain also was investigated. Based on the results, Fitness Canada recommended that a modified Type II partial curl-up be considered for adoption into the Canadian Standardized Test of Fitness (CSTF) procedure.
The effects of a single morphine pellet (75 mg) implanted in developing male rats at 27 days of age on reproductive endocrine parameters were compared to those found in adult (65-day-old) animals after the same treatment. The pellets were left in place to provide the release of morphine during critical phases of puberty and sexual maturation and to prevent an abrupt withdrawal syndrome upon pellet removal which would confound our results. Developing rats were sacrificed at representative intervals after pellet insertion to assess the development of key indices of reproductive endocrinology; adult rats were sacrificed at the same time intervals to permit an evaluation of age-related differences in the sensitivity to opiate-induced endocrine disturbances. Our results showed that morphine markedly influenced a number of endocrine parameters associated with the maturation of the hypothalamic-pituitary-gonadal axis in developing rats for prolonged periods of time, whereas the effects of the opiate in the adult rat were relatively modest and transient. In the developing rat, serum luteinizing hormone (LH), testosterone, the wet tissue weights of the seminal vesicles and testes and hypothalamic LH-releasing hormone (LHRH) levels were substantially depressed immediately after pellet implantation and these effects persisted for up to 4 weeks when compared to placebo-implanted, age-matched controls. In contrast to these results, adult rats showed only transient effects (less than 1 week) of morphine on certain reproductive endocrine parameters (e.g., serum LH, testosterone and the weights of the seminal vesicles) and no effects on others (e.g., testes weights and hypothalamic LHRH).(ABSTRACT TRUNCATED AT 250 WORDS)
It has been previously reported that the excitatory amino acid, N-methyl-D-aspartic acid (NMDA), elicits prompt increases in serum luteinizing hormone (LH) levels in young male rats. The present studies were carried out to determine whether the effects of NMDA on LH were mediated by the release of LHRH from the hypothalamus. We also examined whether NMDA-sensitive neuronal pathways interacted with the endogenous opioid system regulating LHRH release and the ontogeny of NMDA-evoked increases in serum LH. We found that the age-response curve for NMDA-induced increases in LH was an inverted U; at early ages (10 and 15 days) the amino acid was marginally effective in increasing LH levels, it became maximally effective from post-natal days 20-40 and thereafter rapidly lost its efficacy such that it was virtually inactive in adult animals. Dose-response curves revealed that adult animals were more than 10-fold less sensitive to NMDA than their younger counterparts. Our studies also demonstrated that NMDA increased LH via a direct effect on the hypothalamic release of LHRH since a potent LHRH antagonist competitively inhibited the effects of NMDA. Finally, we observed that morphine competitively inhibited the effects of NMDA on LH release, suggesting a relationship between NMDA-sensitive neuronal pathways and those endogenous opioid-containing systems which are known to regulate LH release.
It has been shown in developing male rats that morphine maximally depresses serum luteinizing hormone (LH) levels as early as postnatal day 15. In contrast, naloxone fails to increase serum LH in the prepubescent male rat but, coincident with the onset of puberty (30-35 days of age), the antagonist becomes increasingly more effective until adult appropriate responses are achieved at sexual maturation. The purpose of the present studies was to examine and characterize further the dichotomous response to naloxone and morphine in the prepubescent male rat. We found that the inability of naloxone to affect a release in LH-releasing hormone (LHRH) was not related to pharmacokinetic factors as the dose and time-response characteristics were identical in young and adult animals. In addition, our results indicated that the release of LHRH and its actions on the pituitary to promote LH release were equivalent in prepubescent and adult rats, indicating that if naloxone was capable of releasing LHRH then robust increases in LH should have occurred. Our results indicate further that the ineffectiveness of naloxone in prepubescent animals was not unique to this compound inasmuch as kappa antagonists also were devoid of activity in young animals but were highly effective in adults; delta opiate antagonists failed to increase LH either in young or adult animals. In contrast to these data, we observed that mu and kappa agonists were equipotent in depressing serum LH levels in both young and adult animals.(ABSTRACT TRUNCATED AT 250 WORDS)
This article reviews neurologic problems that have been categorized into two groups: parenchymal and vascular disease. Each disease has a brief summary of key clinical points, followed by recommended management strategies. The neurologic diseases most frequently encountered by the medical consultant are presented.