Disease relevance of Inactin

• To examine the role of plasma extravasation in CsA-induced hypovolemia, intravascular plasma volumes (PV), blood volumes, [125I]albumin disappearance, and changes in hematocrit (Hct) were measured in Inactin-anesthetized rats subjected to minimal surgery [1].
• DESIGN: Male Sprague-Dawley rats (n = 15, body weight 350-420 g) were anesthetized with thiobutabarbital sodium (Inactin, 100 mg/kg intraperitoneally) [2].
• The relative importance of endothelial derived relaxing factor (EDRF)/nitric oxide (NO) in maintaining kidney function in normal condition and in acute renal failure (ARF) were evaluated in inactin anesthetized rats [3].
• In Inactin anaesthetized rats, hypothermia at 28 degrees C decreased GFR by 50% but failed to alter efferent renal sympathetic nerve activity (ERSNA) [4].
• Tubular transit time was measured in the conscious state and during inactin anesthesia in control rats as well as in unilaterally nephrectomized rats with compensatory hypertrophy [5].

High impact information on Inactin

• Glandular pressure was measured using microelectrodes, red blood cell velocity (V[RBC]) was measured using a cross-correlation technique, and blood flow was measured using laser Doppler flowmetry in exposed gastric mucosa of thiobutabarbital sodium-anesthetized rats [6].
• Inulin and para-aminohippurate clearances were used to assess GFR and renal plasma flow (RPF) in three groups of male C57Bl/6 mice anesthetized with inactin (100 mg/kg, intraperitoneally) and ketamine (10 mg/kg) [7].
• The effects of DDMS on the mean arterial pressure (MAP) and renal blood flow (RBF) responses to infusion of an NO donor and a synthase inhibitor were also examined in thiobutabarbital-anesthetized, Sprague-Dawley rats [8].
• After 6 to 8 weeks of treatment, with rats under thiobutabarbital anesthesia, direct blood pressure was determined [9].
• At 7-9 weeks of age, the pressure-natriuresis relation was studied while the rats were under Inactin anesthesia 1 week after the right kidney and adrenal gland were removed [10].

Chemical compound and disease context of Inactin

• The ability to excrete a volume of isotonic saline equal to 10% of body weight infused over 60 min, was examined in awake rats and in rats anesthetized with 1 of the 2 agents most commonly used in renal clearance studies, Inactin or Nembutal [11].
• The hemodynamic effects of N(G)-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide (NO) synthase) were examined in thiobutabarbital-anesthetized control-rats and rats with monocrotaline-induced pulmonary hypertension [12].
• Effect of hyperthermia on blood levels of corticosterone and certain metabolites in rats during thiobutabarbital anaesthesia [13].

Biological context of Inactin

• We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats [14].
• Intravenous (i.v.) administration of selegiline and rasagiline (1 mg kg(-1)) to anaesthetized rats (thiobutabarbital, 100 mg kg(-1), i.p.) did not affect mean arterial pressure (MAP), carotid blood flow (CBF) or carotid vascular resistance (CVR) [15].
• To exclude a direct interaction between propofol and endothelin, in thiobutabarbital anesthetized rats, endothelin-induced cerebral vasoconstriction was examined using videomicroscopy, with or without propofol [16].
• Glomerular filtration rates under inactin anesthesia were measured during two 20-minute periods before a 20-minute amino acid infusion and also during three 20-minute periods after the amino acid infusion [17].
• In Sprague-Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1'-methylpropyl)-2-thiobarbiturate) and infused with 0.077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1,D-Arg8]-vasopressin (dDAVP) did not induce natriuresis [18].

Anatomical context of Inactin

• To investigate this question, the luminal pressure in gastric glands was studied after omeprazole treatment in Inactin-anesthetized rats [19].
• The mean arterial pressure (mmHg) was measured in Inactin-anesthetized rats by a PE-50 catheter in the femoral artery [20].
• Rats were anaesthetized (Inactin) and a 12-mm segment of proximal duodenum with an intact blood supply was cannulated in situ [21].
• On the other hand, the increase in secretion of renin produced by inactin anesthesia does not appear to be mediated by the sympathetic nervous system [22].
• Male Sprague-Dawley rats (210-325 g) anesthetized with Inactin were placed on a surgical heating table for a period of about 2 h before blood was collected via puncture of the abdominal aorta [23].

Associations of Inactin with other chemical compounds

• Renal function studies using standard clearance techniques were done in control and rilmenidine-infused (20 micrograms/Kg/min i.v. for 80 min) Wistar rats anesthetized with Inactin [24].
• Experiments were performed in Inactin-anesthetized male Sprague-Dawley rats treated for 7 +/- 1 days with a subcutaneous corticosterone (Cort) pellet or in control rats [25].
• To test this hypothesis, we first measured the VE-induced increase in renal sodium excretion and urine flow with and without blockade of NO, with microinjection of NG-monomethyl-L-arginine (L-NMMA; 200 pmol in 200 nl), within the PVN of Inactin-anesthetized male Sprague-Dawley rats [26].
• In inactin-anesthetized rats, acute administration of cyclosporine A (100 mg/kg i.p.) significantly decreased paraaminohippuric acid (PAH) and inulin clearances [27].
• To determine the mechanism by which immobilization and head-up tilt under inactin anesthesia increase plasma renin activity (PRA), the effect of these stimuli on plasma levels of vasoactive intestinal polypeptide (VIP) were measured and the effect of the beta-adrenergic blocking drug, propranolol on the response of plasma renin activity determined [22].

Gene context of Inactin

• Inhibition of NOS with N(omega)-nitro-l-arginine methyl ester (l-NAME; 50 mg/kg iv) in Inactin-anesthetized WT and nNOS(-/-) mice increased arterial blood pressure by 28-31 mmHg and significantly decreased blood flow in the renal cortex (18-24%) and the renal medulla (13-18%) [28].
• METHODS: AT1A receptor-deficient mice and their wild-type controls were anesthetized with inactin and ketamine, and were prepared to allow intravenous infusions of solutions and measurements of aortic pressure and urine collections [29].
• Administration of endothelin to inactin-anesthetized rats resulted in a significant renal vasoconstriction as evidenced by a reduction in both renal plasma flow and glomerular filtration rate [30].
• Male Munich-Wistar rats, normal Han:SPRD rats, and heterozygous Han:SPRD rats with autosomal-dominant polycystic kidney disease were anesthetized with Inactin and solutions containing SF were administered by constant intravenous infusion [31].
• In male rats anesthetized with Inactin, continuous infusion of OT (125 ng/kg x h) increased plasma OT to about 70 pg/ml; renal Na+ excretion increased 10-fold, and urine volume and K+ excretion also were elevated [32].

Analytical, diagnostic and therapeutic context of Inactin

• METHODS: Glandular pressure and mucous gel thickness were measured with microelectrodes during intravital microscopy in thiobutabarbital sodium-anesthetized rats [33].
• Surface pH (H(+)-selective microelectrodes), permeability (clearance of (51)Cr-EDTA), and mucosal blood flow (laser-Doppler flowmetry) were studied in Inactin-anesthetized rats [34].
• In this investigation, we examined the changes in the levels of these peptides detected by immunohistochemistry in response to cervical vagal stimulation in the inactin-anesthetized male Wistar rat [35].
• 1. The effect of sodium pentobarbital and Inactin anaesthesia on renal haemodynamics in the rat was evaluated with radioactive microspheres 15 micrometer in diameter [36].
• Intravenous injection of TRAP (1 mg/kg) in inactin-anesthetized rats produced a biphasic response in blood pressure characterized by an initial depressor response (-25 +/- 3 mmHg for 15-30 s) followed by a pronounced pressor response (50 +/- 7 mmHg for 2-3 min) [37].

References