Somatosensory evoked potentials in hepatic encephalopathy

Median nerve somatosensory evoked potentials were recorded from 33 patients with various degrees of hepatic failure and from 10 age-matched controls. Within 20 ms poststimulation, one negative peak (N13) could be recorded from the middle of the back of the patient's neck at the C2 vertebral level. Within 150 ms, three negative and three positive peaks, sequentially designated as N1, P1, N2, P2, N3, and P3, could be recorded from the scalp over the contralateral sensory cortex. There was a progressive prolongation of peaks and interpeak latencies correlating with the severity of hepatic encephalopathy. In 10 patients with hepatic failure but no clinical evidence of hepatic encephalopathy, latencies of peak N3 and P3 were delayed and N1-N3 interpeak latencies were prolonged. Thirteen patients with grade 1 or 2 hepatic encephalopathy showed further delayed latencies of peaks P2, N3, and P3, further prolonged N1-N3, N1-P2 interpeak latencies, and distortion of waveforms. Peaks N2, P2, N3, and P3 were further delayed, and even disappeared in 10 patients with grade 3 or 4 hepatic encephalopathy. However, central conduction time (N13-N1 interpeak latency) was not prolonged in all stages of hepatic failure. In addition, serial somatosensory evoked potential studies correlated well with the clinical course. The present data suggest that somatosensory evoked potential recording is a reliable objective method in the early assessment and monitoring of hepatic encephalopathy.     

Subcortical somatosensory evoked potentials in patients with hepatic encephalopathy caused by severe acute hepatitis

We studied the median nerve stimulated somatosensory evoked potentials (SEP) of 23 patients with hepatic encephalopathy (HE) resulting from severe acute hepatitis and 22 healthy volunteers. Ten patients who improved and survived more than 60 days were classified as Group 1 and the remaining 13 patients who died shortly after the SEP studies were classified as Group 2. The mean N9-N13 interpeak latencies (IPL) were not different among control and two patient groups. The mean N13-N20 IPL of Group 2 was significantly prolonged when compared with normal controls (P < 0.001) and Group 1 (P < 0.001). Five of the six patients with abnormal N13-N20 IPL died of hepatic failure within 24 h after SEP testing. The occurrence of abnormal subcortical conduction together with cortical dysfunction suggested that brain damage in terminal hepatic encephalopathy was diffuse. The presentation of abnormal prolongation of N13–N20 IPL of SEP during the course of severe acute hepatitis indicated a poor prognosis. Peripheral somatosensory conduction is unaffected even in terminal HE.     

Role of zinc in subclinical hepatic encephalopathy: comparison with somatosensory-evoked potentials

BACKGROUND AND AIM: The purpose of the present paper was to determine the role of zinc in subclinical portosystemic encephalopathy (SPSE). METHODS: The serum zinc levels were studied for 10 cirrhotic patients who did not suffer SPSE and for 10 patients who did, and the results compared with those deriving from 10 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, and transferrin levels, body mass index (BMI), mid-arm muscle circumference (MAMC), and tricep skin-fold (TSF). The occurrence of SPSE was defined as a situation when the N20-N65 interpeak latencies of median nerve-stimulated somatosensory-evoked potentials (SEP) exceeded 2.5 SD of the control mean value. RESULTS: Cirrhotic patients suffering SPSE (57.5 +/- 10.5 microg/dL) had lower serum zinc levels than those not experiencing SPSE (69.5 +/- 16.6 microg/dL, P = 0.03) and controls (77.7 +/- 6.8 microg/dL, P < 0.001). Four of the non-SPSE and nine SPSE patients had zinc levels less than the lower normal limit. Cirrhotic patients suffering SPSE had lower levels of albumin (2.8 +/- 0.4 g/dL vs 3.8 +/- 0.4 g/dL, P < 0.001), prealbumin (9.0 +/- 4.3 mg/dL vs 14.3 +/- 6.0 mg/dL, P = 0.02), and transferrin (158 +/- 56 g/L vs 218 +/- 50 g/L, P = 0.01), but a greater total bilirubin level (1.2 +/- 1.5 mg/dL vs 0.9 +/- 0.4 mg/dL, P = 0.005) than those not suffering SPSE. The serum zinc levels correlated with N20-N65 interpeak latencies (P = 0.03), serum albumin (P = 0.006), prealbumin (P < 0.001), and total bilirubin (P = 0.02) levels. CONCLUSIONS: The data show that zinc deficiency is common in cases of non-alcoholic cirrhosis with SPSE. The early assessment of malnutrition and zinc deficiency are important.     

Age-related interrelation of vibration perception thresholds and somatosensory evoked potentials in normal subjects

In order to establish the age-related changes of vibration perception thresholds (VPTs) and somatosensory evoked potentials (SEPs), which are known to share a common afferent pathway in the central nervous system, 119 normal subjects ranging in age from the 20s to the 90s were studied. The VPTs of the index fingertip were measured at 63 Hz, 125 Hz and 250 Hz by a Rion vibrometer, nd the latencies of the SEPs to the median nerve stimulation (N9, N13 and N20) were simultaneously evaluated. The VPT, tended to elevate from the 40s, became increased towards higher frequencies (63 Hz less than 125 HZ less than 250 Hz) in the 80s to the 90s, whereas the VPT in younger ages showed just an opposite pattern (63 Hz greater than 125 Hz greater than 250 Hz). None of the height-corrected latencies of N9, N13, N20 and central conduction time (N20-N13) revealed a significant correlation between the VPTs at any frequencies. The age-related decline of vibration sense, therefore, could not be explained solely by the degenerative changes of he posterior column and/or the delay of the peripheral nerve conduction velocity. This phenomenon was rather thought to be compatible with an age-associated characteristics of Pacinian corpuscles.     

Somatosensory and visual evoked potentials in insulin-dependent diabetics with mild peripheral neuropathy

Using somatosensory and visual evoked potential techniques we have looked for evidence of central neuropathy in a group of insulin-dependent diabetics with mild peripheral neuropathy. The N9, N13, and N20 components of the somatosensory evoked potential were significantly (P less than 0.001) delayed in the diabetic group compared with the control subjects. There was a small but non-significant increase in the interpeak N13-9 and N20-13 latencies in the diabetic group. The visual evoked potential (P100) showed a small but insignificant delay. The delay in cerebral evoked potentials was mostly attributable to peripheral neuropathic damage and no firm evidence was obtained in favour of central diabetic neuropathy.     

Changes in central and peripheral nervous system function during hypoglycemia in man: an electro-physiological quantification.

We measured somatosensory evoked potentials (SEP) in normal subjects during acute (group A) and moderately prolonged (group B) hypoglycemia. We considered the following parameters: peripheral conduction velocity (wrist-Erb CV), conduction time (CT) between brachial plexus and the cervical cord (Erb-N13) and central CT from the cervical cord/lower brainstem lemniscal pathway to the cortex (N13-N20). In group A, the electrophysiological parameters did not change significantly throughout the study. In group B, mean N13-N20 CT increased from a basal values of 5.82 +/- 0.11 to 6.22 +/- 0.11 msec at 105 min (p less than 0.02) and 6.33 +/- 0.11 msec at 120 min (p less than 0.05). This study indicates that neither acute nor moderately prolonged hypoglycemia influence the peripheral nerve function in normal subjects and provides evidence that hypoglycemia as low as 2.4 mmol/L, lasting more than 60 min, can significantly increase the conduction time of central somatosensory pathways.     

Effect of meal temperature on gastric emptying of liquids in man.

Serial studies were carried out on six healthy volunteers (19-24 years) to investigate the effect of meal temperature [either 4 degrees C (cold), 37 degrees C (control) or 50 degrees C (warm)] on the rate of gastric emptying of a radiolabelled isosmotic drink of orange juice. The mean maximum intragastric temperature occurred 60 seconds after the onset of ingestion of the warm drink and reached 43.0 degrees C (0.4) mean (SD) while the mean minimum intragastric temperature occurred 45 seconds after the onset of ingestion of the cold drink and reached 21.2 degrees C (1.9). Intragastric temperature then returned to body temperature within 20-30 minutes of ingestion of the warm and cold drinks. Warm and cold drinks appeared to empty from the stomach more slowly than the control drink. The initial rate of gastric emptying of the cold drink was significantly slower than the control drink (p less than 0.05) and the difference in emptying rates between cold and control drinks were significantly correlated with the differences in intragastric temperatures (p less than 0.01). The difference in the initial emptying rates between warm and control drinks were not statistically significant.     

Relationship between bronchial response to respiratory heat exchange and nonspecific airways reactivity in asthmatic patients

In this study we have examined the relationship between the bronchial response to inhaled histamine and the bronchial response to breathing cold air at rest in nine control subjects and nine patients with asthma. Dried warm air (mean temp: +/- 1SD: 25.4 +/- 1.6 degrees C) and cold air (-19.7 +/- 2.6 degrees C) were breathed for 10 minutes each during quiet breathing at rest prior to as well as during both measurements of forced expired spirograms and the phase 3 slope of the single-breath oxygen test (delta N2/L). Subjects were also challenged with inhaled aerosolized histamine to determine the concentration required to reduce the forced expired volume in one second (FEV1) by 20 percent (PC20). Both asthmatic and control subjects had significantly greater respiratory heat exchange breathing cold as compared to warm air (p less than 0.01 in both cases). Control subjects did not change FEV1 or delta N2/L breathing cold air. Asthmatic patients increased delta N2/L from a mean warm air value of 2.41 +/- 1.31% N2/L to a mean cold air value of 5.39 +/- 4.55% N2/L (p less than 0.05). There was a significant linear correlation between the percent increase in delta N2/L from warm to cold air and 1/log10PC20 (r = -0.97, p less than 0.001) and also the percent decrease in FEV1 and log PC20 (r = -0.76, p less than 0.03) in the asthmatic patients. We conclude that cold air-induced alterations in ventilation/distribution and expired flow rates in asthmatic patients are related to pre-existing nonspecific airways reactivity.     

非糜烂性胃食管反流病患者大脑皮质诱发电位的研究

目的通过比较食管扩张刺激-脑诱发电位(OD-CEP)的改变,探讨非糜烂性胃食管反流病(NERD)患者食管内脏高敏感性的发生机制,旨在进一步获得NERD患者食管-中枢内脏感觉传导通路失调的客观依据。方法10例正常健康自愿者和21例NERD患者参与试验;采用Synectics内脏刺激器/电子气压泵和带有低顺应性气囊的导管给食管以时相性扩张刺激;利用食管气囊扩张术检测受试者食管最大耐受痛阈,用75%最大疼痛耐受容积作为诱发刺激的强度(刺激频率为12次/分,连续64次);采用OD-CEP系列技术记录并分析NERD患者和正常人CEP的变化。结果食管气囊扩张刺激能诱发出可识别、可重复的、多峰的CEP波形,以NP型为主。与正常对照者比较,NERD患者CEP波形变异性大,其N1、P1、N2波潜伏期明显缩短(P值分别为0·016,0·003,0·031),且NERD患者CEP的P1-N2峰间波幅明显增加(P=0·03)。结论NERD患者经食管时相性扩张后产生的特征性CEP改变证实其食管内脏高敏感性及食管-中枢内脏感觉传导通路的失调。     

Twenty four hour intragastric acidity and plasma gastrin concentration in healthy volunteers taking nizatidine 150 mg, nizatidine 300 mg, ranitidine 300 mg, or placebo at 21:00 h.

Nine healthy volunteers were studied on the seventh day of dosing at 21:00 h with nizatidine 150 mg (N 150), nizatidine 300 mg (N 300), ranitidine 300 mg (R 300), or placebo, given in a predetermined random order. The double-blind 24 hour studies, using the Royal Free Hospital standard protocol, simultaneously measured intragastric acidity and plasma gastrin concentration. Compared with placebo, subjects responded to dosing with each H2-antagonist by a significant decrease of 24 hour intragastric acidity (N 150-45%; N 300-49% R 300-56%; p less than 0.01) and a significant rise of plasma gastrin concentration (N 150 + 20%; N 300 + 27%; R 300 + 58%; p less than 0.01). All three drug regimens caused similar significant decreases of nocturnal acidity (N 150-72%; N 300-79%; R 300-85%; p less than 0.01) and increases of nocturnal plasma gastrin concentration (N 150 + 41%; N300 + 52%; R 300 + 80%; p less than 0.01). Dosing with ranitidine 300 mg at 21:00 h also caused a simultaneous significant decrease of morning acidity (-32%; p less than 0.05) with a significant increase of plasma gastrin concentration (+36%; p less than 0.05), but the antisecretory effects of nizatidine 150 or 300 mg at 21:00 h were only observed during the night, with no effect during the morning. No drug regimen had any effect on acidity or plasma gastrin in the afternoon or early evening.     

Nutritional status in non-alcoholic sub-clinical porto-systemic encephalopathy

AIM To understand the role of nutritional status in cirrhotic patients without clinical porto-systemic encephalopathy (PSE).METHODS Fifty-one non-alcoholic patients with cirrhosis without PSE were studied prospectively and compared with 20 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, transferrin, body mass index (BMI), mid-arm muscle circumference (MAMC), and grip power. The occurrence of subclinical PSE (SPSE) was defined when N20-N65 inter-peak latencies of median nerve-stimulated somatosensory evoked potentials were ＞2.5 standard deviations of control means. Blood chemistries were tested within 12h of somatosensory evoked potentials test and nutritional evaluation.RESULTS Twenty-five, 17 and 9 cirrhotic patients were graded as Child-Pugh class A, B, and C, respectively. Twenty-four (47.1%) patients developed SPSE. Cirrhotic patients with SPSE had lower serum albumin (2.8g/dL±0.5g/dL vs 3.1g/dL±0.7g/dL, P＜0.001) levels than those without SPSE. Prealbumin (10.6mg/dL±5.7mg/dL vs 12.5mg/dL±5.8mg/dL), transferrin (164mg/dL±46mg/dL vs 178mg/dL±58mg/dL), BMI (23.7kg/m2±2.7kg/m2 vs 25.3kg/m2±3.6kg/m2), MAMC (22.2cm±2.6cm vs 22.7cm±3.5cm), and grip power (26.3kg±6.4kg vs 26.9kg±6.8kg) were not different between cirrhotic patients with and without SPSE. N20-N65 inter-peak latencies were correlated with serum albumin levels (P=0.01) but not with prealbumin, transferrin, BMI, MAMC, or grip power. Serum albumin, prealbumin and transferrin levels were different among cirrhotic patients with Child-Pugh classes A, B, and C (P＜0.05). BMI, MAMC, and grip power were not different among Child-Pugh classes A, B and C.CONCLUSION Our data suggest that serum albumin level is a simple test in the evaluation of nutritional status in patients with cirrhosis.     

Digital pressure and flow measurement upon local cooling in Raynaud's disease. Effect of naftidrofuryl

Two local cold provocation tests were carried out in 25 healthy volunteers and in 14 patients with Raynaud's disease, using finger systolic pressure (FSP) and digital blood flow measurements. Mean FSP was significantly lower in Raynaud's patients compared to healthy volunteers at 15 degrees C and 10 degrees C (cuff temperature). Maximal digital flow (at skin temperature of 38 degrees C) was slightly though not significantly lower in Raynaud's patients as compared to normals (27 +/- 3 versus 36 +/- 4 ml/100 ml/min). Upon cooling, statistical significance was reached starting from finger skin temperature of 24 degrees C. Overlap between the two groups was considerable but only 1 out of 13 patients with Raynaud's disease had both tests normal. Ten of the patients participated in a double-blind cross-over trial with naftidrofuryl (200 mg t.i.d.) versus placebo. Significant (p less than 0.05) subjective improvement was noted after 6 weeks with naftidrofuryl but this was not necessarily substantiated by an increased digital flow or pressure in the test situation.     

The effect of ambient temperature on glucose tolerance.

Standard (75 g) oral glucose tolerance tests were performed at two different ambient temperatures (23 and 33 degrees C) in random order in 16 (eight obese) diabetic and 16 (eight obese) non-diabetic Nigerian subjects. Consistently higher plasma glucose values were found 120 min post-glucose ingestion at 33 degrees C, with mean differences of 0.5 (SE 0.3) and 4.5 (SE 1.5) mmol l-1 in the non-diabetic and diabetic subjects, respectively. This caused reclassification of two of the non-diabetic subjects as Impaired Glucose Tolerance at 33 degrees C, applying the WHO criteria. The difference was consistently greater (p less than 0.01) in the non-obese subjects (non-diabetic 0.8 (0.4), diabetic 6.9 (2.8) mmol l-1) than in the obese (non-diabetic 0.2 (0.4), diabetic 2.1 (0.9) mmol l-1). In the diabetic subjects, a negative correlation (r = -0.50, p less than 0.01) was established between the difference and the body mass index. This variability in responses to ambient temperature between the obese and non-obese subjects could be due to a variable influence of heat on arm blood flow consequent on differences in amounts of subcutaneous fat. The ambient temperature for the conduct of the oral glucose tolerance test is important.     

Effects of cold exposure on submaximal exercise performance and adrenergic activation in patients with congestive heart failure and the effects of beta-adrenergic blockade (carvedilol or metoprolol)

Patients with congestive heart failure (CHF) exhibit a decrease in maximal exercise capacity in response to a cold environment. The aim of this study was to further investigate the impact of cold exposure on submaximal exercise capacity, systemic adrenergic drive, and the effects of long-term beta-adrenergic blockade on these parameters. Thirty-three patients with CHF, with exercise limited by dyspnea and left ventricular ejection fraction of 26 +/- 4%, were randomized to receive metoprolol or carvedilol for 6 months. The observations were compared with 12 age-matched healthy volunteers. Maximal exercise performance with gas exchange analyses were assessed using a ramp protocol, and endurance capacity was measured using 2 constant-load exercise tests performed randomly at 20 degrees C and -8 degrees C. Healthy volunteers increased their submaximal exercise time by 20% (1,353 +/- 455 [20 degrees C] vs 1,635 +/- 475 seconds [-8 degrees C]; p <0.05), whereas patients with CHF exhibited a 21% decrease in exercise time (1,182 +/- 549 [20 degrees C] vs 931 +/- 524 seconds [-8 degrees C]; p <0.05) at -8 degrees C. Beta blockers increased submaximal exercise duration at 20 degrees C (+261 +/- 617 seconds; p <0.05) and -8 degrees C (+374 +/- 729 seconds; p <0.05). Norepinephrine increased to a greater extent at 4 minutes and at the time of exhaustion (at -8 degrees C) only in patients with CHF. Beta-adrenergic blockade caused no significant decrease in plasma norepinephrine levels. Patients with symptomatic CHF exhibited a significant decrease in submaximal exercise time in response to moderate cold exposure. Beta-blocker therapy with either metoprolol or carvedilol significantly increases submaximal exercise time and attenuates the impact of cold exposure on functional capacity.     

Nifedipine and the conditioning response

The effect of nifedipine (N) on conditioning was studied in 14 healthy sedentary men, aged 20 to 34 years. Subjects were ranked according to maximal oxygen consumption (VO2 max), paired, and 1 of each pair randomly assigned to take N, 20 mg, or placebo (C) 3 times daily. Exercise conditioning was 5 times/week for 6 weeks at greater than 85% of maximal heart rate for both groups. Adherence to exercise was 81% for the N and 82% for the C group. After training, the N group improved VO2 max from 41.4 +/- 1.4 to 51.6 +/- 2.0 ml/kg/min (p less than 0.05) and exercise time from 22 +/- 1 to 28 +/- 1 minutes (p less than 0.05). Heart rate (HR) at rest and the product of heart rate and systolic blood pressure both decreased (p less than 0.05): 70 +/- 6 to 55 +/- 4 beats/min; 9,300 +/- 900 to 6,800 +/- 700 beats/min X mm Hg. In the C group, VO2 max increased from 43.2 +/- 2.5 to 49.9 +/- 2.5 ml/kg/min (p less than 0.05); exercise duration improved from 24 +/- 2 to 29 +/- 2 minutes (p less than 0.05), and the rate-pressure product at rest decreased from 8,000 +/- 400 to 6,700 +/- 400 (p less than 0.05). Differences between N and C were not significant. Thus, N, unlike propranolol, does not inhibit the response to exercise conditioning.     

Thermosensitivity, a possible new locus involved in genetic hypertension

Spontaneously hypertensive mice have been characterized as more sensitive to environmental heat than normotensive mice. A breeding program was therefore initiated to examine the possible genetic link between thermosensitivity and hypertension. Crossbreeding of spontaneously hypertensive mice with randomly bred normotensive mice produced F1 hybrids, which were then intercrossed to create a F2 population. Thermosensitivity was measured with a noninvasive method. The rate of body temperature increase was significantly (p less than 0.001) higher in the hypertensive mice (1.74 +/- 0.04 degrees C/min) compared with normal controls (1.13 +/- 0.03 degrees C/min). The frequency distribution of the rate of body temperature increase among the progenies was consistent with the hypothesis that a single gene locus determines the observed difference in thermosensitivity between normal and hypertensive mice. The allele that determines the rate of body temperature increase in normal mice was dominant in relation to the allele contributed by hypertensive mice. In the F2 population, a bimodal distribution determined two phenotypes: less than 1.40 degrees C/min and greater than 1.40 degrees C/min. A significant difference (p less than 0.01) in blood pressure of 11 mm Hg was observed between these two phenotypes. In addition, a positive correlation (p less than 0.01) was noted between the rate of body temperature increase and blood pressure in the F2 progeny. We conclude that there is possibly a single locus controlling thermosensitivity, which exhibits additive-dominance inheritance. Alleles of this particular trait segregate in part with an increment in blood pressure. The results support the possibility that the increased thermosensitivity seen in hypertensive mice is associated with one of the genes that contributes to their high blood pressure.     

Lymphocytotoxic antibodies in systemic lupus erythematosus: studies of their temperature dependence, binding characteristics, and specificity in vitro.

The lymphocytotoxicity of 33 lupus sera was tested against purified helper/inducer (OKT4) and cytotoxic/suppressor (OKT8) subsets of T lymphocytes at 15 degrees C and 37 degrees C in vitro. There was significantly less killing of both OKT4 and OKT8 cells at 37 degrees C (p less than 0.001 and p less than 0.01) and the ratio of OKT4/OKT8 cell killing at 15 degrees C (1.39 (0.73); mean (SD] was different from that observed at 37 degrees C (0.79 (0.42)) (p less than 0.001). OKT4 killing was greater than OKT8 killing in 21 out of 33 sera at 15 degrees C, while 22 of these sera showed predominantly OKT8 cytotoxicity at 37 degrees C. The relation between the OKT4/OKT8 cell ratio and OKT4/OKT8 serum killing was examined in 22 patients at both temperatures: a significant inverse correlation was observed at 37 degrees C (r = -0.53; p = 0.015) but not at 15 degrees C (p greater than 0.05). The addition of metabolic and cytoskeletal inhibitors increased cytotoxicity at 37 degrees C, but not IgM surface binding. A Scatchard binding analysis of the reaction at 15 degrees C showed that large numbers of antibody molecules were bound to both subsets, with a low average dissociation constant of less than or equal to 6 x 10(-8) mol/l, and electrophoretic blotting indicated that the target surface antigens varied in type and number among individual lymphocytotoxic sera. The demonstration of temperature dependent, tight binding between lymphocytotoxic antibody and variable antigens on the T cell surface emphasises the potential for this phenomenon to affect lymphocyte function in vivo in patients with systemic lupus erythematosus.     

Development of acute tolerance during steady-state arterial alcohol concentrations: a study of auditory event-related potentials in rats

BACKGROUND: The blood alcohol clamp is a method whereby alcohol is infused intravenously to maintain a predetermined arterial alcohol concentration (AAC) for an indefinite period of time. The objective of this study was to use the clamp to examine the effects of alcohol on event-related potentials (ERPs) in rats and to assess the development of tolerance during a single alcohol exposure. METHODS: Adult male Wistar rats that had a chronic implant of EEG electrodes overlying the frontal cortex and were equipped with cannulae in the jugular vein, were clamped at 75 or 150 mg/dl via an intravenous infusion of 20% (v/v) alcohol. Auditory ERPs were recorded before the alcohol infusion (baseline) and at 5, 15, 120, 135, or 195 min after steady-state AAC was achieved. In a separate group of rats, test-retest reliability was examined by acquiring ERPs two to three times in the same rat at 60-min intervals. Dependent variables were calculated as changes from baseline for each time point for P1-N1 amplitude and P1 and N1 latencies. RESULTS: In the test-retest study, there were no differences in any of the dependent variables over time, indicating that the measures were stable and repeatable. Estimated AACs of 75 and 150 mg/dl significantly (p = 0.0001) decreased P1-N1 amplitude in a dose-related manner. During both clamps, the alcohol effect peaked at 120 min (p < 0.03) and decreased thereafter. Alcohol had no effect on P1 or N1 latencies. CONCLUSIONS: Pharmacologically relevant AACs significantly decreased the amplitude but not the latencies of the long-latency components of the rat auditory ERP. Acute tolerance developed because the amplitude of the ERP component recovered as AACs were held relatively constant.     

Arrhythmic breathing in torpid pipistrelle bats, Pipistrellus pipistrellus

The arrhythmic breathing pattern of torpid female pipistrelle bats (Pipistrellus pipistrellus) was monitored using Doppler radar. A total of 98 h of radar measurements were made on 11 individuals over 17 experiments, during which time 974 apneic intervals were monitored, over ambient temperatures (Ta, degrees C) ranging from -1 to 14 degrees C, and body masses ranging from 4.6 to 7.4 g. As Ta declined, a greater proportion of all breaths occurred in discrete breathing bouts. Apneic intervals lengthened at lower Ta, but were not related to body mass. Mean apneic length, averaged over 1 degree C intervals, was best described by the least squares fit regression equation: ln (apneic length in s) = 7.07-0.811 ln (Ta + 1), (r2 = 0.96, P less than 0.01). Ventilation frequency (breaths.min-1), averaged over a breathing bout and the subsequent apnea, increased as Ta increased, and was not related to body mass. Mean ventilation frequency (f), averaged over 1 degree C intervals, was best described by the least squares fit regression equation: f = 0.812 + 0.499 Ta (r2 = 0.92, P less than 0.01). Using previously published values for O2 consumption (VO2) in torpid pipistrelles, and tidal volume and O2 extraction efficiency at 4 degrees C in torpid bats of the same mean size (6.2 g), we calculated that at 4 degrees C ventilation would, on average, supply only 14.2-21.3% of VO2. This suggests that in torpid pipistrelles the glottis may remain open during apnea, allowing a significant diffusive influx of O2 into the lungs.     

Treating hypertension in non-insulin-dependent diabetes: a comparison of atenolol, nifedipine, and captopril combined with bendrofluazide

Twenty-five of thirty NIDDS who remained hypertensive (diastolic greater than 95 mmHg supine) after 4 weeks on bendrofluazide 2.5 mg daily (B), completed a single-blind, observer-blind randomized crossover study, in which the additional use of atenolol (50 mg daily) (A), slow-release nifedipine (20 mg twice daily) (N), and captopril (25 mg twice daily) (C) was compared. Patients took each drug for 8 weeks with dose doubling at 4 weeks if supine diastolic remained greater than 90 mmHg. All three combinations were more effective than bendrofluazide alone (p less than 0.01). In nine patients studied 2 h after tablets at the end of each treatment period nifedipine was more effective than the other two drugs (B:174/104 mmHg, A:162/95 mmHg, -8%, N:141/88 mmHg, -17%, C:157/94 mmHg, -10%, supine), whereas in 16 patients studied 15 h after their evening dose there was no significant difference. Fasting insulin and HbA1 levels were not significantly different between groups. No drug had a significant adverse effect on creatinine, glomerular filtration rate, overnight urinary albumin excretion or foot transcutaneous oxygen levels (43 degrees C). All three drugs studied were effective without deleterious effects on renal function or peripheral blood flow.