Prospective pilot study for evaluation of high-flow oxygen therapy in dyspnoeic dogs: the HOT-DOG study.

OBJECTIVES: To describe the use, effectiveness and tolerance of high-flow oxygen therapy in dyspnoeic dogs. MATERIALS AND METHODS: Prospectively, dogs in acute respiratory distress admitted to an intensive care unit between January and May 2018 that failed to respond to nasal oxygen therapy and medical stabilisation after 30 minutes were transitioned to high-flow oxygen therapy. High-flow oxygen therapy, delivered an inspired oxygen fraction of 100% using an air/oxygen blender, active humidifier, single warmed tube and specific nasal cannula. Respiratory rate, pulse oximetry (SpO2 ), heart rate and a tolerance score were assessed every 15 minutes from T0 (under nasal oxygen) to 1 hour (T60 ), and PaO2 and PaCO2 at T0 and T60 . Complications were recorded for each dog. RESULTS: Eleven dogs were included. At T60 , PaO2 , flow rate and SpO2 were significantly greater than at T0 (171 ± 123 versus 73 ± 24 mmHg; P=0.015; 18 ±12 L/minute versus 3.2 ± 2.0 L/minute, P<0.01; 97.7 ±2.3% versus 91.6 ±7.2%, P=0.03, respectively). There was no significant difference in PaCO2 , respiratory rate or heart rate between T0 and T60 . Tolerance was excellent, and there were no complications. CLINICAL SIGNIFICANCE: High-flow oxygen therapy improves markers of oxygenation in dyspnoeic dogs and is an effective means to deliver oxygen with comfort and minimal complications.

Renal haemodynamic response to amino acids infusion in an experimental porcine model of septic shock.

BACKGROUND: Acute kidney injury (AKI) is common in sepsis. Treatments allowing maintenance of renal blood flow (RBF) could help to prevent AKI associated with renal hypoperfusion. Amino acids (AA) have been associated with an increase of RBF and glomerular filtration rate (GFR) in several species. The aim of this study was to evaluate the effects of an AA infusion on RBF and GFR in a porcine model of septic shock. METHODS: A total of 17 piglets were randomly assigned into three groups: Sham (Sham, n = 5), sepsis without AA (S-NAA, n = 6), sepsis treated with AA (S-AA, n = 6). Piglets preparation included the placement of ultrasonic transit time flow probes around left renal artery for continuous RBF measurement; ureteral catheters for GFR and urine output evaluation; pulmonary artery catheter for cardiac output (CO) and pulmonary arterial pressure measurements. Mean arterial pressure (MAP) and renal vascular resistance (RVR) were also determined. Septic shock was induced with a live Pseudomonas aeruginosa infusion. Crystalloids, colloids and epinephrine infusion were used to maintain and restore MAP > 60 mmHg and CO > 80% from baseline. RESULTS: Renal haemodynamic did not change significantly in the Sham group, whereas RBF increased slightly in the S-NAA group. Conversely, a significant increase in RVR and a decrease in RBF and GFR were observed in the S-AA group. AA infusion was associated with a higher requirement of epinephrine [340.0 (141.2; 542.5) mg vs. 32.5 (3.8; 65.0) mg in the S-NAA group P = 0.044]. CONCLUSION: An infusion of amino acids impaired renal haemodynamics in this experimental model of septic shock.

The effect of intravenous insulin infusion on renal blood flow in conscious sheep is partially mediated by nitric oxide but not by prostaglandins.

To test the effect of insulin on renal perfusion and the participation of NO and PG as mediators of this response, renal blood flow (RBF) was measured in sheep (n = 8) implanted with ultrasonic flow probes around renal arteries and with a systemic arterial pressure (SAP, n = 4) telemetry device. Three protocols were performed: 1) RBF and SAP were recorded (0800 to 1800 h) in fed and fasted sheep, with the latter receiving intravenous (i.v.) infusions (0.5 mL/min) of insulin at 2 or 6 mU/(kg·min); 2) fasted sheep received i.v. infusions of either an inhibitor of NO synthesis (N(G)-nitro-L-arginine methyl ester, L-NAME) alone [0.22 mg/(kg·min), 1000 to 1200 h] or L-NAME (1000 to 1200 h) + insulin during the second hour (6 mU/(kg·min), 1100 to 1200 h); and 3) the same protocol was followed as in protocol 2, substituting L-NAME with ketoprofen [0.2 mg/(kg·min)], a cyclooxygenase inhibitor. In all protocols, plasma insulin and glucose were determined. During insulin administration, euglycemia was maintained and hypokalemia was prevented by infusing glucose and KCl solutions. After the onset of meals, a long-lasting 18% increase in RBF and a 48% insulin increase were observed (P < 0.05), without changes in SAP. Low- and high-dose insulin infusions increased RBF by 19 and 40%, respectively (P < 0.05). As after meals, the increases in RBF lasted longer than the insulin increase (P < 0.05). The L-NAME infusion decreased RBF by 15% (P < 0.05); when insulin was added, RBF increased to preinfusion values. Ketoprofen decreased RBF by 9% (P < 0.05); when insulin was added, RBF increased to 13% above preinfusion values (P < 0.05). In no case was a modification in SAP or glucose noted during the RBF changes. In conclusion, insulin infusion mimics the meal-dependent increase in RBF, independent of SAP, and lasts longer than the blood insulin plateau. The RBF increase induced by insulin was only partially prevented by L-NAME. Ketoprofen failed to prevent the insulin-dependent RBF increase. Both facts suggested that complementary vasodilatatory agents accounted for the insulin effect on sheep renal hemodynamics.

Roles of eating, rumination, and arterial pressure in determination of the circadian rhythm of renal blood flow in sheep.

To assess the roles of feeding behavior (eating and rumination) and systemic arterial pressure (SAP) on determination of the circadian rhythm of renal blood flow (RBF), 20 sheep fitted with ultrasonic flow-metering probes around both renal arteries and a submandibular balloon to monitor jaw movements (6 of them with a telemetry measurement system into the carotid artery for SAP recording), were successively assigned to 6 feeding patterns: once daily in the morning (0900 to 1100 h), afternoon (1700 to 1900 h), or evening (1900 to 2100 h); twice daily at 0900 to 1100 h and 1700 to 1900 h; ad libitum (food renewed each 2 h); and fasting (40 h). All protocols were carried out in autumn-winter, and the fasting pattern was repeated in spring-summer to evaluate the effect of the daylight length on RBF. In the once-daily feeding patterns, a rapid increase in RBF (P < 0.05 vs. 1-h prefeeding mean values) subsequent to the onset of meals was observed, followed by a progressive increase (P < 0.05), reaching a maximum 4 to 6 h after the beginning of eating, and a subsequent gradual decline until the next meal [differences vs. prefeeding values were no longer significant after 11 h (morning pattern), 13 h (afternoon pattern), and 15 h (evening pattern) from the beginning of eating]. In the twice-daily feeding pattern, each meal was also followed by an increase in RBF (P < 0.05 vs. prefeeding values), reaching a maximum 3 to 5 h after the onset of meals, and a posterior decline [differences vs. prefeeding values were no longer significant after 8 h (morning meal) and 5 h (afternoon meal) from the beginning of eating]. In the ad libitum feeding, no apparent rhythm in RBF was found. During fasting, a progressive reduction of RBF was observed from 2 h after the beginning of fasting (P < 0.05 vs. the mean value of the first fasting hour), with a slight rebound (P < 0.05) lasting several hours from approximately 0700 h in autumn-winter and approximately 0500 h in spring-summer. No change in the RBF profile was observed in association with rumination. Except during meals, no correlation was found between RBF and SAP. A detailed description of RBF and SAP recordings is presented. In conclusion, results showed a circadian rhythm of RBF determined by eating behavior, but not by rumination, that was independent of blood pressure and that seemed superimposed on a primary lighting-cycle-dependent RBF rhythm.

Determination of parotid sulfate secretion in sheep by means of ultrasonic flow probes.

The bilateral output of sulfate in parotid saliva, the relationship with its plasma level and with parotid flow, and its variation according to feeding behavior were determined in ad libitum, normal-sulfate (0.28% DM)-fed sheep (n = 6) using a transit time ultrasonic flow meter system to measure salivary flow. Ultrasonic flow meter probes were bilaterally implanted, under general anesthesia, around parotid ducts previously fitted through their oral ends with nonobstructive sampling catheters. Salivary flows were continuously recorded during 24 h, and saliva and blood samples for sulfate determinations were obtained hourly. Jaw movements were monitored with the submandibular balloon technique. The sulfate concentration in parotid saliva (mean of the group = 4.9 +/- 3.7 microg/mL) showed high variability between sheep (individual means from 0.4 +/- 0.3 to 9.3 +/- 5.9 microg/mL) and averaged 12.3% of the more stable plasma level (41.2 +/- 8.1 microg/mL). Pronounced intraindividual variations were also evident (0.1 to 26.3 microg of sulphate/mL of parotid saliva), in strong association with the fluctuations of salivary output. In 4 sheep, a decreasing exponential relationship was observed between parotid sulfate concentration and salivary secretion rate (r2 = 0.36, P < 0.01). This fact and the absence of a relationship between sulfate levels in plasma and in saliva suggest a sulfate secretory process during the passage of primary saliva through the ductal tree of the gland. The greatest rates of bilateral salivary sulfate output were observed during feeding (14.1 +/- 14.0 microg/min) and rumination (12.7 +/- 11.0 microg/min). Nevertheless, 49% of the sulfate output in parotid saliva was present during rest, as a result of the length of the resting times. The contribution of parotid sulfate to the ruminal S pool was highly variable and averaged 13.2 mg/d, representing less than 1% of the S intake. In conclusion, the accurate, reliable, nonobstructive, and bilateral salivary flow monitoring, using a previously characterized ultrasonic flow meter technique, allowed a detailed determination of the secretory dynamics of sulfate in parotid saliva, without disturbing the animal's routine or altering the physiological regulation of salivary output. The results indicated that, in the absence of S deficiency, the recycling of sulfate via saliva seems not to be a major factor in sheep nutrition.

Investigation of the role of aldosterone in hypertension associated with spontaneous pituitary-dependent hyperadrenocorticism in dogs.

The aim of this study was to evaluate the role of aldosterone as an initiating and/or perpetuating factor in hypertension associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Thirteen dogs with PDH and 11 healthy control dogs were used. In all dogs, arterial blood pressure and plasma sodium, potassium, basal aldosterone, post-ACTH aldosterone, basal cortisol and post-ACTH cortisol concentrations were measured. The tests were repeated 10 days and three months after the beginning of o,p'-DDD treatment in PDH dogs. In untreated PDH dogs, plasma aldosterone was significantly decreased, whereas cortisol, sodium and arterial blood pressure were significantly increased compared to healthy dogs. Hypertension remained in most treated PDH dogs despite normalisation of cortisol and persistently low aldosterone levels. These results did not demonstrate that aldosterone is involved in the development and perpetuation of hypertension in PDH. However, glucocorticoids seemed to play a major role as an initiating and perpetuating factor in PDH in dogs.

Comparative study of the cardiovascular effects of losartan in normal and in water- and salt-depleted sheep.

The cardiovascular effects of losartan, a non-peptidic angiotensin II (ANG II) receptor antagonist, were studied in sheep. Eight normotensive, conscious sheep were tested twice: first under normal conditions and second when subjected to water and electrolytic depletion (furosemide 5 mg/kg twice a day for 3 days). Intravenous injection of 30 mg/kg losartan lowered the mean arterial blood pressure (MABP) in both control and water- and electrolyte-depleted sheep alike. The maximal decrease in MABP was significantly greater in diuretic-treated sheep than in controls (20.0 +/- 2.7 vs 9.3 +/- 1.1 mmHg) and occurred earlier (8.0 +/- 3.3 min vs 12.1 +/- 2.9 min). The decrease in blood pressure was associated with tachycardia in both controls and diuretic-treated sheep (+5.5 +/- 1.8 vs +11.3 +/- 3.9 beats/min). The vasopressor response to 0.1 microg/kg ANG II administered 30 min after losartan was completely antagonized. Two hours after losartan administration, MABP was on the increase in all animals and ANG II receptor blockade was partially obliterated in control sheep. The more marked cardiovascular effects recorded in diuretic-treated sheep as compared to control animals were associated with an increased activation of the renin-angiotensin system (plasma renin concentration: 6.51 +/- 1.33 vs 1.42 +/- 0.37 ng angiotensin I/ml/hr).

Extrarenal renin-angiotensin systems are unable to maintain blood pressure in sheep.

1. The present study was designed to assess the participation of extrarenal tissue renin-angiotensin systems (RAS) in pressure homeostasis in sheep. 2. The effect of the administration of an angiotensin II type 1 receptor antagonist (losartan; 30 mg/kg, i.v.) on mean arterial blood pressure (MABP) was investigated in eight intact (controls) and 10 binephrectomized sheep haemodialysed every 2 days for 10 days. 3. In control sheep, losartan decreased blood pressure and this decrease was significantly more marked after furosemide-induced water and salt depletion. After nephrectomy and throughout the anephric period, losartan lost its hypotensive effect, while the plasma renin concentration fell to undetectable levels. Baseline MABP became significantly lower than at the beginning of the anephric period after 7 days. The inability to maintain blood pressure after several volume-depleting haemodialysis sessions proved that an efficient system for blood pressure regulation was lacking after nephrectomy. 4. Renin gene expression measured by reverse transcription-polymerase chain reaction was found in liver, adrenal and arterial wall tissue. Neither nephrectomy nor sodium depletion enhanced this tissue renin gene expression. 5. In conclusion, the present work allows us to exclude an active role of extrarenal RAS in the maintenance of blood pressure. In addition, haemodialysis technology in nephrectomized sheep can be used as a good model for the study of extrarenal control of blood pressure.

Control of diphtheria: guidance for consultants in communicable disease control. World Health Organization.

These guidelines for the control and management of diphtheria are intended for consultants in communicable disease control and regional epidemiologists in England and Wales. They are intended to complement existing guidance from the World Health Organization. The guidelines cover the immediate steps to be taken following identification of a case, what is required to confirm the diagnosis, steps to be taken to minimise the likelihood of further linked cases, and what should be done to disseminate information after a case.

[Pyramidal syndrome. Apropos of 4 cases treated by surgery and review of the literature]. / Le syndrome du pyramidal. A propos de 4 cas traités chirurgicalement et revue de la littérature.

PURPOSE OF THE STUDY: The authors report 4 observations of Piriformis syndrome, defined as a truncked sciatalgy with sciatic nerve and branches located compression at the buttock passing through the subpiriformis canal. MATERIAL: 4 sportive patients, 26 to 41 years old have been treated surgically after an average of one year and a half of evolution and failure of conservative treatments. The surgical procedure consisted in section of the piriformis muscle and neurolysis of the sciatic nerve. METHODS: The follow-up ranged from one year and a half. The observations were confronted with 11 english language publications, representing 20 observations. RESULT: 2 excellent results. One fair. The result of the last patient is uninterpreted due to a post-operative deficiency of the inferior gluteus nerve. But the pre-operative symptomatology has completely disappeared. DISCUSSION: Symptomatology associated a trunked sciatalgy arising during effort and during a long time sitting position, without lumbar pain. Paresthesy and dyspareunia can sometimes added. The specifics clinical signs are pain induced by palpation at the sacrum lateral edge, perception of a tense piriformis ("sausage shaped mass"), pain reproduction by stretching the piriformis (Freiberg) or by its opposite tensing (Pace and Nagle, Beatty). The complementary exams first allow to eliminate all rachidian or discal aetiology. The diagnosis is based on CT, MRI and bone scan which can show modifications of the piriformis muscle and especially the electrommyogram which confirms the syndrome and specifies the compression level. The aetiology is changeable, mainly represented by modification of piriformis (hypertrophy, contracture or micro traumatisms due to sport or after-effects of direct traumatism) and by anatomical modifications of the sciatic nerve, passing completely or in part through the muscle. First, the treatment must be conservative by sport rest, correction of occupational diseases, local injections and especially stretchings. The results are more often favourable. In case of failure and diagnosis certitude, the surgical treatment is the neurolysis of the sciatic nerve and the muscle section at the musculo-tendinous junction. CONCLUSION: This syndrome must be known but, in spite of its proved authenticity now, must stay an exceptional diagnosis and be based on irrefutable criteria.

Disposition of minaprine in animals and in human extensive and limited debrisoquine hydroxylators.

1. The disposition of 14C-minaprine was studied after oral administration of 5 and 20 mg/kg to rats, dogs and macaques, and of 200 mg to human volunteers with a genetic status of either limited or extensive hydroxylation of debrisoquine. 2. The drug was readily absorbed and a large proportion of the administered radioactivity was excreted within 48 h. The total excretion over 5 days ranged from 83% in monkeys to almost 100% in human with a status of extensive hydroxylators. 3. In the two limited hydroxylators Cmax values of total radioactivity in plasma were 4.6 and 3.7 mg equiv/l respectively. Those in the two extensive hydroxylators were 1.9 and 1.6 respectively. The highest value in the animal species was 8.1 in rats at a dose of 20 mg/kg. Plasma Cmax values of minaprine were 4.0 and 1.4 mg/l in limited hydroxylators and 0.35 and 0.23 mg/l in extensive ones. The highest value in the animal species was 2.7 mg/l in dogs treated with 20 mg/kg. 4. In rats and dogs, the ratios of the plasma AUC values for 20 mg/5 mg doses were close to those of the ratios of the doses administered, whereas in the macaque a slower clearance of radioactivity occurred with the higher dose (t 1/2 beta 5.5 h at 5 mg/kg dose versus 25.7 h at 20 mg/kg dose). 5. Marked species differences were observed in the metabolic pathways. The dog and limited hydroxylators showed higher levels of minaprine and its N-oxide (M4) whereas p-hydroxy-minaprine (M3) prevailed in monkey, rat and extensive hydroxylators. 6. In dogs only, seizures appeared within 10-15 min after dosage with minaprine at 20 mg/kg, when the concentrations of minaprine in erythrocytes (6.9 mg/l) and of M4 in plasma (0.40 mg/l) and erythrocytes (0.25 mg/l), were high. 7. The measurements and clinical observations indicate that onset of an adverse behavioural response in humans is unlikely at the dose of 200 mg.

Seed migration and the structure of plant populations : An experimental study on Thymus vulgaris L.

We use chemical typing to compare sub-populations of thyme (Thymus vulgaris L.) growing in the channels of several ravines where seed migration is expected from sub-populations on the plateu to associated basin subpopulations. The results indicate that seed migration does occur. However, there is little effective gene flow between sub-populations. We discuss the implications of restricted gene flow for population dynamics and structure.