Elderly patients have more infectious complications following laparoscopic colorectal cancer surgery.

AIM: Elderly patients may be at higher risk of postoperative complications, particularly infective, than younger patients. METHOD: We prospectively followed 163 consecutive patients undergoing elective laparoscopic resection for cancer. We compared patients < 65, 65-80 and > 80 years of age at the time of surgery. RESULTS: Seventy (42.9%) patients had no complication; 93 (57.1%) had at least one complication following surgery and in 20 (12.3%) this was major. There was no difference in major complications between the groups (P = 0.47). Patients over 65 years of age were more likely to have a complication of any severity [< 65 years, 39.3%; 65-80 years, 69.3%; and > 80 years, 63.0% (P = 0.002)]. The frequency of gastrointestinal complications (30.1%) was similar in the groups (P = 0.29), as was wound infection (25.2%) (P = 0.65). There was an increase in the frequency of infectious complications, especially chest infection, with age, from 14.8% in patients < 65 years, to 22.7% in patients 65-80 years, to 44.4% in patients > 80 years (P = 0.01). Multivariate analysis showed no increase in overall complications in elderly patients, but Stage II or Stage III cancer (OR = 2.59, P = 0.04) and increasing body mass index (BMI) (OR = 1.07 for each unit increase in BMI, P = 0.04) were related to complications. Age remained the only predictor of an infective complication on multivariate analysis. Patients > 80 years of age had 4.21 times the OR of an infective complication (P = 0.03). CONCLUSION: Older patients are more susceptible to infective complications postoperatively, particularly chest complications. Surgeons should alter their practice to reduce morbidity, such as adopting protocols requiring early physiotherapy.

A keyhole approach gives a sound repair for ileal conduit parastomal hernia.

PURPOSE: The purpose of this study was to report and evaluate a laparoscopic surgical technique for the treatment of parastomal hernia (PSH) after ileal conduit urinary diversion aiming to minimize PSH recurrence and perioperative complications. METHODS: We retrospectively evaluated all patients who underwent a PSH (after ileal conduit urinary diversion) repair at Addenbrookes Hospital, Cambridge. As a surgical approach, a laparoscopic repair with mesh was utilized in all cases. Subsequently, we performed a voluntary follow-up of the patients to evaluate long-term recurrence and complication rates. In addition, we conducted a reassessment of the cross-sectional imaging available. RESULTS: Between November 2008 and December 2019, 27 patients underwent hernia repair due to a clinically significant hernia. Out of those patients, one suffered from a post-operative wound infection. In total 23 patients participated in the follow-up with a median follow-up period of 91 months. Follow-up examination revealed two cases of recurrent PSH (8.7% of patients followed up), four patients suffered from minor complications (14.8%). CONCLUSION: Repair of PSH associated with ileal conduit is particularly scarce. Our surgical approach presents the only laparoscopic case series of an effective method for treating a PSH from an ileal conduit with a low complication and recurrence rate.

Motion sickness-induced pica in the rat.

Two experiments investigating the effects of motion sickness on pica (the consumption of non-nutritive substances) are reported. In the first experiment rats subject to rotational stimulation subsequently engaged in geophagia (clay consumption). In the second experiment use of a conditioned aversion paradigm confirmed that the method of rotational stimulation used in the first experiment causes motion sickness in rats. The results of these experiments indicate that simple gastrointestinal malaise in the absence of a deficiency state or acute toxemia will elicit pica. It is suggested that gastrointestinal distress may be a significant factor in the etiology of pica and its relationship to other causes of pica is discussed.

Plasma insulin-like growth factor-1 elevated in mild-to-moderate but not severe heart failure.

BACKGROUND: Insulin-like growth factor 1 (IGF-1) promotes favorable cardiac remodeling in heart failure. However, the relation of plasma IGF-1 in patients with various degrees of heart failure is not known. METHODS: Venous plasma samples were collected from patients with clinically documented heart failure (n = 24) and from control subjects (n = 21) for measurements of IGF-1 levels. In the heart failure group, functional assessment of the physical capacity was determined by means of the New York Heart Association (NYHA) score. Objective determination of ventricular performance was made by transthoracic echocardiographic measurement of left ventricular fractional shortening (FS). RESULTS: IGF-1 levels were higher in patients with heart failure (mean age, 67 +/- 2 years; 17 men) than in control subjects (age, 71 +/- 2 years; 9 men) (20.2 +/- 2 mU/L, 14.1 +/- 2 mU/L, respectively, P <.05). However, the elevated IGF-1 levels were demonstrated only in patients with mild-to-moderate symptoms (NYHA classes I and II) of heart failure (24.7 +/- 3.3 mU/L, n = 12, P =.005 vs control subjects) but not in patients with severe symptoms (NYHA classes III and IV) (15.7 +/- 2.3 mU/L, n = 12). There was a strong positive correlation between IGF-1 levels and left ventricular FS (%) (r = 0.58, P =.003, n = 24). Adjustments for other potential confounders including age, sex, treatment received, and underlying cause of heart failure did not alter the relation between IGF-1 and left ventricular FS (odds ratio, 2.01; 95% confidence interval, 1.26 to 6.24; P =.01). CONCLUSIONS: Plasma levels of IGF-1 show distinct variations with the severity of heart failure and may play a vital role in compensated heart failure.

Cardiovascular interactions between vasopressin, angiotensin and noradrenaline in the Brattleboro rat.

1. The cardiovascular effects of bolus intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in 6-hydroxydopamine pretreated, anaesthetized Brattleboro rats with hereditary diabetes insipidus and normal rats of the parent Long Evans strain. 2. Pretreatment with 6-hydroxydopamine did not significantly affect control values for mean arterial blood pressure, cardiac output or total peripheral resistance in either Brattleboro or Long Evans rats but the pressor response to haemorrhage was reduced in both strains compared to the control animals. 3. The pressor responses of the untreated Brattleboro rats to 250 mu kg-1 vasopressin were significantly greater and more prolonged than in control rats of the Long Evans strain. 4. Pretreatment with 6-hydroxydopamine significantly enhanced the peak pressor response to vasopressin, but not to angiotensin II (1 microgram kg-1), in Brattleboro and Long Evans rats. 5. Pretreatment with 6-hydroxydopamine resulted in an enhanced pressor response to 1 microgram kg-1 noradrenaline in both Brattleboro and Long Evans rats, but the effect was significantly greater in the vasopressin-deficient animals. 6. These results indicate differences in the pressor responsiveness of Brattleboro rats to vasopressin and noradrenaline, but not to angiotensin II, compared with control Long Evans rats and provide evidence for important interactions between the sympathetic nervous system and these pressor hormones.

Potentiation of the response to vasopressin (pitressin) by treatment with a combination of chlorpropamide and chlorothiazide in Brattleboro rats with hereditary hypothalamic diabetes insipidus.

1 The effect of a combination of chloropropamide and chlorothiazide in Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI) treated with low doses of vasopressin (Pitressin tannate in oil) was investigated with particular reference to the time course of response from the initiation of treatment. 2 Analysis of the relationship between water intake and body weight indicated no real correlation and body weight accounted for only 4.4% of the variation in water intake. It was therefore decided to use whole body responses as the index in preference to the response per unit body weight. 3 The daily administration of 5 mg chlorpropamide combined with chlorothiazide in the drinking water (4 mg/1) to Pitressin-treated DI rats potentiated the response to small doses of vasopressin (25 and 50 mu Pitressin/24 hours). Water intake was reduced by the drug combination by an average of 12.35 ml/24 h, but only on the second day of treatment was the decrease of any real magnitude (30 ml/24 h but otherwise 9 ml/24 h or less). Analysis of urine volume measurements gave similar results to those obtained for water intake and the potency ratio measured in terms of free water clearance was 1.26 (agreeing closely with the ratio for water intake which was 1.24). 4 A reduction in the solute excretion was observed only in those DI rats treated with the higher dose of Pitressin (50 mu/24 h) combined with the two drugs. 5 Possible reasons for the discrepancy between the effect of the combination of chlorpropamide and chlorathiazide on water metabolism in the DI rat and the DI patient are discussed.

The effect of chlorpropamide on water balance in pitressin-treated Brattleboro rats.

1 The daily administration of a 5% glucose solution to the heterozygous Brattleboro rat produced an experimental model in a comparable state of polydipsia and polyuria to the homozygous rat with diabetes insipidus (DI).2 The effect of chlorpropamide on water metabolism was then examined in both the homozygous DI rat treated with submaximal doses of pitressin tannate in oil (Pitressin), and in the glucose-hydrated heterozygous rat with and without simultaneous pitressin therapy.3 A dose-response curve for chlorpropamide (5, 10, and 20 mg/24 h) in DI rats treated with Pitressin (25 mu/24 h) indicated that the drug decreased fluid intake further, but only by a maximum of 13.8% (at the 20 mg/24 h dose of chlorpropamide), differing markedly from results obtained in patients with diabetes insipidus. A second experiment in which chlorpropamide (5 mg/24 h) was administered to DI rats treated with Pitressin (either 25 or 50 mu/24 h) confirmed the lack of any significant drug-effect on water metabolism in these animals.4 Chlorpropamide (20 mg/24 h), when administered alone or simultaneously with a submaximal dose of Pitressin (25 mu/24 h), had no obvious effect on the fluid intake of glucose-hydrated heterozygous rats. The absence of any action by chlorpropamide on water metabolism was confirmed in these experimental animals using 5 mg/24 h of the drug together with Pitressin (either 25 or 50 mu/24 hours).5 Indirect evidence for the slower growth-rate in the DI rat being due to an insufficient daily calorific intake was obtained from the study on glucose-hydrated heterozygous rats.

Renal effects of recombinant prolactin in anaesthetized rats.

OBJECTIVE: To re-examine the controversial possibility that prolactin exerts renal effects, using recombinant mouse prolactin (rmP), in the presence and absence of circulating vasopressin. DESIGN: In experiment 1, the renal effects of rmP were examined in anaesthetized Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) lacking circulating vasopressin and normal animals of the parent Long Evans (LE) strain. In experiment 2, salt and water excretion were studied in fluid-loaded normal Sprague-Dawley (SD) rats, some of which received rmP. METHODS: In experiment 1, BDI and LE rats maintained in fluid balance were infused i.v. with each of three concentrations of rmP (10, 20 and 40 microg/ml per h) or maintained on 150 mmol/l NaCl vehicle (controls). In experiment 2, the SD rats were infused with 75 mmol/l NaCl in order to induce a state of diuresis comparable to that of BDI rats, some of them then receiving the rmP i.v. RESULTS: A profound rmP-induced dose-dependent decrease in urine excretion (P<0.005) and a lesser decrease in sodium excretion in the BDI rats was in marked contrast with the small but significant increase in urine excretion in the LE rats compared with controls (P<0.025). The rmP-infused fluid-loaded SD rats also demonstrated a significant (P<0.05) dose-related antidiuresis compared with the control animals, in addition to a decrease in sodium excretion. CONCLUSIONS: These results show that prolactin has a profound antidiuretic effect in the absence of circulating vasopressin. In contrast, when vasopressin is present in the circulation rmP has a small, but opposite, diuretic effect. Thus the use of a recombinant prolactin has provided evidence for renal effects of this hormone which are modified in the presence of the circulating neurohypophysial hormone vasopressin.

Effect of ovariectomy and steroid hormone replacement on the recovery of arterial blood pressure following haemorrhage in anaesthetized Brattleboro rats.

There is increasing evidence that ovarian steroids inhibit vascular responsiveness to the neurohypophysial hormone vasopressin. The present study examined the recovery of the arterial blood pressure following a single (2 ml/100 g body weight) haemorrhage in ovariectomized (OVX) Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) and rats of the parent Long Evans (LE) strain. Some groups of OVX rats received subcutaneous implants of either 17 beta-oestradiol (E2) or progesterone 7 days prior to haemorrhage. The arterial blood pressure recovery immediately following haemorrhage was significantly impaired in both groups of steroid-treated OVX LE rats compared with the OVX controls (both comparisons P < 0.05). The impairment in blood pressure recovery seen in the steroid-replaced OVX LE rats was similar to that seen in pro-oestrous rats (when ovarian steroid levels are raised) compared with male rats of this strain (P < 0.05). In contrast, ovariectomy with or without steroid replacement in BDI rats had no further effect on the already attenuated recovery of arterial blood pressure after haemorrhage in this strain. Heart rate responses to haemorrhage also showed strain differences, which were dependent on steroid treatment. Pro-oestrous female LE rats showed a small decrease in heart rate after haemorrhage, followed by a recovery process, and this initial bradycardia was markedly enhanced in the OVX steroid-treated animals. In contrast, untreated OVX LE rats showed an initial and sustained increase in heart rate which was significantly higher than in the steroid-treated OVX animals (P < 0.05). All BDI rats, irrespective of treatment, consistently showed an increased heart rate after haemorrhage. In conclusion, ovarian steroid replacement in OVX LE, but not vasopressin-deficient BDI, rats was associated with an attenuated pressor recovery after haemorrhage. This provides further evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin. The initial decrease in heart rate observed in pro-oestrous and steroid-treated OVX LE rats after haemorrhage also appears to be related to an ovarian steroid-vasopressin interaction.

Influence of oestrous cycle on the pressor recovery following haemorrhage in anaesthetized Brattleboro rats.

A sexual dimorphism in the pressor responsiveness to the neurohypophysial hormone vasopressin may be associated with a peripheral interaction between ovarian steroids and the neurohypophysial hormone. Indeed, the ovarian steroids may inhibit the vasopressin-dependent component of the pressor response to haemorrhage. The present study examined the recovery of the arterial blood pressure following it single large (2% v/w) haemorrhage in anaesthetized male Long Evans (LE) rats and females of the same strain during either pro-oestrous or di-oestrous phases of the reproductive cycle. In addition the same recovery process was examined in Brattleboro rats with diabetes insipidus (BDI) lacking circulating vasopressin. All BDI rats had an impaired blood pressure recovery following haemorrhage compared with male rats of the parent LE strain, and this was irrespective of sex or stage of the oestrous cycle. While the blood pressure recovery was more impaired in both groups of BDI female rats than in the males of the same strain during the first 20 min after haemorrhage (both comparisons p < 0.001; ANOVA), there was no difference between the recoveries of the female rats in pro-oestrus or di-oestrus. In contrast a significantly impaired blood pressure recovery was observed in female LE rats at pro-oestrus, when circulating ovarian steroid concentrations are raised, compared with male (p < 0.001: ANOVA) and di-oestrous (p < 0.02: ANOVA) rats of the same strain. Heart rate responses to haemorrhage showed strain differences, with LE rats having initial decreased heart rates followed by a recovery process, while the heart rate responses of BDI rats increased immediately. The novel use of the female Brattleboro rat in this study provides evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin during the blood pressure recovery phase following haemorrhage, and indicates a possible direct influence of gonadal steroids on the recovery process.

A role for vasopressin in the stress-induced inhibition of gonadotrophin secretion: studies in the brattleboro rat.

Abstract The effects of stress on the secretion of adrenocorticotrophin, corticosterone and luteinizing hormone (LH) in rats congenially lacking hypothalamic vasopressin (Brattleboro rats) and in normal controls of the parent strain (Long Evans) have been compared in an attempt to examine the role of vasopressin in the stress-induced depression of gonadotrophin secretion. In the Long Evans rats, stress (0.6 mg/100g histamine, ip) initiated, within 5 and 20 min respectively, significant (P <0.01, Student's t-test) increases in the plasma adrenocorticotrophin and corticosterone concentrations. It also caused a reduction in the serum LH concentration which was maximal at 5 min. By contrast, in the vasopressin deficient Brattleboro rats, stress had no effect on the serum LH concentration and produced only modest increases in pituitary adrenocortical activity compared with those in Long Evans controls. Pretreatment of both Long Evans and Brattleboro rats with dexamethasone (20mug/100 g ip, daily for 3 days) effectively abolished the pituitary-adrenal response to stress. The steroid treatment also prevented the stress-induced suppression of LH in the Long Evans rats; indeed, these animals, unlike the vehicle-treated controls, exhibited a rise in serum LH concentration within 5 min of exposure to stress. Stress did not affect the serum LH concentrations in steroid-treated Brattleboro rats. The results confirm previous reports that vasopressin is required for the full expression of the pituitary-adrenocortical response stress. They also provide novel evidence which suggests that vasopressin released in stress contributes to the impairment of gonadotrophin secretion.

Desamino-8D-arginine vasopressin treatment of Brattleboro rats: effect on sensitivity to pressor hormones.

The cardiovascular effects of intravenous injections of vasopressin, angiotensin II and noradrenaline were studied in anaesthetized adult male Brattleboro rats with hereditary diabetes insipidus on lifelong treatment with the vasopressin V2 receptor agonist desamino-8D-arginine vasopressin in the drinking fluid, which restored fluid input and output to normal rat values. The pressor response to 20 ng.kg-1 vasopressin was significantly greater (P < 0.005) in the vasopressin V2 receptor agonist-treated rats than in the control animals, but the responses to all higher doses of the peptide were comparable. Doses of noradrenaline from 40 to 160 ng.kg-1 had similar pressor effects in the treated and control rats, while the pressor response to the highest dose of noradrenaline (320 ng.kg-1) was significantly lower (P < 0.01) in the vasopressin V2 receptor agonist-treated rats. Furthermore the pressor responses to all three doses of angiotensin II (40, 80 and 160 ng.kg-1) were significantly attenuated in the treated rats compared to the control group (P < 0.001, P < 0.05 and P < 0.0005 respectively), as were the decreases in heart rate (P < 0.005 at 40 ng.kg-1, P < 0.01 at 80 ng.kg-1). The hypovolaemic stimulus induced by a blood loss of 20 ml.kg-1 resulted in a lower mean arterial blood pressure initially in the treated Brattleboro rats, but subsequent recovery was similar in both treated and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Stability of the vasopressin V2 receptor-adenylyl cyclase system in rat kidney.

In the Brattleboro rat with diabetes insipidus vasopressin V2 receptor mRNA and the mRNA of various adenylyl cyclase (AC) isoforms are moderately reduced compared with those of normal rats. In the present study renal vasopressin V2 receptor mRNA was modestly higher (by 34%), as was expression of AC 5, 6 and 9 mRNAs (up to 22% greater), in BDI rats treated with the vasopressin V2 receptor agonist desamino-[Arg8] vasopressin than in untreated controls. AC 4 mRNA was decreased by 17% following desamino-[Arg8s] vasopressin treatment. While the stimulatory Gsalpha mRNA was little affected by the desamino-[Arg8] vasopressin treatment, two of the inhibitory G proteins were raised (Galphai-2 by 54% and Galphai-3 by 57%). Treatment of Sprague-Dawley rats with a specific vasopressin V2 receptor antagonist (SR 121463A) was not associated with any marked changes in mRNA expression. These results indicate that the vasopressin V2 receptor adenylyl cyclase system mediating the antidiuretic response to vasopressin is relatively stable. The Gi proteins may be involved in the stabilizing mechanism.

Lack of effect of Pitressin on the learning ability of Brattleboro rats with diabetes insipidus using positively reinforced operant conditioning.

Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) received daily subcutaneous injections of vasopressin in the form of Pitressin tannate (0.5 IU/24 hr). They were initially deprived of food and then trained to work for food reward in a Skinner box to a fixed ratio of ten presses for each pellet received. Once this schedule had been learned the rats were given a discrimination task daily for seven days. The performances of these BDI rats were compared with those of rats of the parent Long Evans (LE) strain receiving daily subcutaneous injections of vehicle (arachis oil). Comparisons were also made between these two groups of treated animals and untreated BDI and LE rats studied under similar conditions. In the initial learning trial, both control and Pitressin-treated BDI rats performed significantly better, and manifested less fear initially, than the control or vehicle-injected LE rats when first placed in the Skinner box. Once the initial task had been learned there was no marked difference in the discrimination learning between control or treated BDI and LE animals. These results support the view that vasopressin is not directly involved in all types of learning behaviour, particularly those involving positively reinforced operant conditioning.

Increased aversion to bitter-tasting fluids in the Brattleboro rat.

The large daily water intake of Brattleboro rats with diabetes insipidus (BDI) is believed to be due to the volume of depletion caused by their lack of circulating anti-diuretic hormone. However an increased fluid consumption cannot necessarily be interpreted as an increased behavioural drive to drink. In order to examine these rats' motivation to drink, quinine at various concentrations was given in the drinking water as sole fluid source to BDI rats and rats of the parent Long Evans (LE) strain, and their fluid balance after twenty-four hours was determined. Brattleboro rats reduced their fluid intakes significantly more than the control LE rats at the highest concentration of drug used (100 mg/l), suggesting a decreased motivation to drink. A two bottle preference test for quinine showed that the BDI rats actually have a higher taste threshold for the drug in solution in drinking water than the control LE rats. This suggests that the increased aversion to quinine in solution when it is the sole drinking source cannot be due to the BDI rats tasting the quinine at a lower concentration than the LE animals. Nor are greater toxic effects of quinine in BDI rats likely to account for the different drinking responses when presented with quinine solutions, since intragastric administration of the drug had no effect on water consumption in these animals. When BDI rats were given bitter-tasting sucrose octa-acetate solutions as their sole drinking source, drinking was again drastically reduced. However LE rats actually increased their fluid consumption when given sucrose octa-acetate showing a preference for this substance in solution to tap water.(ABSTRACT TRUNCATED AT 250 WORDS)

The abnormal quinine drinking aversion in the Brattleboro rat with diabetes insipidus is reversed by the vasopressin agonist DDAVP: a possible role for vasopressin in the motivation to drink.

The Brattleboro rat with hypothalamic diabetes insipidus (BDI) has an abnormal aversion to drinking quinine-adulterated water compared with normal rats of the parent Long Evans (LE) strain. This BDI animal tolerates marked hypovolemia and decreased body weight in preference to drinking the quinine-adulterated fluid, indicative of a reduced motivation to drink. Acute or chronic treatment of BDI rats with desamino-8D arginine vasopressin (DDAVP) restored to normal their drinking response to quinine solution. Partial restoration of fluid turnover in BDI rats with hydrochlorothiazide, which has an antidiuretic effect in diabetes insipidus (when vasopressin is absent), failed to abolish the abnormal drinking response to quinine-adulterated solution in 8 out of 12 animals. In contrast, induction of diabetes mellitus in LE rats, which resulted in a marked polydipsia and polyuria even though vasopressin was still present, did not impair the drinking response to quinine solutions. These results suggest that the abnormal drinking response to quinine-adulterated fluid in BDI rats is reversed by treatment with the vasopressin V2-receptor agonist DDAVP but is unlikely to be a consequence of the restoration of fluid turnover to normal levels by a renal action. A possible central action involving vasopressin and the motivation to drink is discussed.

Behavioral variability within the Brattleboro and Long-Evans rat strains.

Samples of genetically diabetes insipidus (DI) and normal (NO) rats were obtained from American suppliers (Rochester (RO)/DI and NO) and from the colony maintained at Charing Cross Hospital in London (Charing Cross (CC)/DI and NO) to test the hypothesis that the behavior of vasopressin-deficient Brattleboro (DI) and possibly normal Long-Evans rats may vary significantly between different colonies. DI rats of both colonies exhibit longer latencies to emerge into an open field than do NO rats. RO/DI and CC/DI rats acquire goal-approach behavior in a straight runway at similar rates. Following shock in the runway goal box, however, RO/DI rats exhibit marked recovery of running behavior relative to CC/DI rats over the ten post-shock sessions. All DI animals show reductions in goal-approach speed on the first post-shock trial, indicating that the aversive experience is remembered. CC/NO rats acquire goal-approach behavior more slowly than RO/NO rats, but neither NO group shows substantial recovery of goal approach behavior following shock. CC/DI rats showed impaired acquisition of a delayed non-match to sample task relative to RO/DI rats. All groups demonstrated the ability to utilize representational memory to solve the delayed non-match to sample problem once the contingency was learned. The results indicate that DI and normal Long-Evans rats from different colonies show marked differences in behavior. Since differences between DI and normal rats on tests indicating memory are not consistent across colonies, it is unlikely that vasopressin deficit is solely responsible for memory deficiencies. However, vasopressin deficiency may result in changes in temperament.

Sweep potential polarography and multiwire surface tissue electrodes.

A multitipped seven barrelled platinum electrode for brain surface oxygen measurements during neurosurgery is described. Its performance has been examined when employed under conditions of sweep potential polarography. Although there is no plateau within the oxygen polarogram, the electrode displays linear performance within the physiological range, gives reproducible results in practice, has an acceptable temperature coefficient and a fast response time.

Effect of hypotension induced by ATP and adenosine on brain surface oxygen tensions in the sheep.

A multitipped oxygen electrode has been used to measure cortical surface oxygen tensions in the sheep. A histogram of the pattern of supply of oxygen to cortical tissue within the microcirculation during normal conditions is presented. Systemic arterial pressure was reduced to a mean of 30 mmHg with either Adenosine or ATP, and further oxygen tension measurements undertaken. The oxygen histogram was shifted to the left in these circumstances, and there was an increase in the frequency of occurrence of very low tissue oxygen tensions. This suggests that the use of these agents to induce profound hypotension may be associated with significant ischaemia within the microcirculation.

Pure tone thresholds for the rhesus monkey.

Auditory thresholds were measured for 18 ears from 13 rhesus monkeys using a simple reaction-time procedure. The threshold contour was a smooth W-shaped function with rises at the extreme frequencies and around 4 kHz and was comparable in shape with previously reported thresholds for this animal. Standard deviations averaged 5.3 dB.