Direct determination of the contractility of the guinea pig gallbladder: a new in vivo model

1985 ◽  
Vol 63 (9) ◽  
pp. 1038-1042 ◽  
Author(s):  
I. S. Pomeranz ◽  
J. S. Davison ◽  
E. A. Shaffer

In vivo methods to study gallbladder contractility either equate gallbladder emptying with contraction or have relied on changes in gallbladder intravesicular pressure to reflect active transmural tension. We therefore devised an animal model in which the contractile force of the intact gallbladder is measured directly while the blood and neural supply remains uncompromised. Under general anesthesia one pole of the guinea pig gallbladder is anchored to the sternum and the other connected to a force displacement transducer. Any contraction–relaxation between these two points is recorded. This model was validated by measuring gallbladder response to both neuronal and humoral stimulation. Nerve stimulation was accomplished by means of two silver collar electrodes placed in contact with the cystic duct. With nerve stimulation, a frequency (0.5–10 Hz) or amplitude (1–10 V) dependent contraction occurred. Intravenous bethanechol (10 × 104 ng∙kg−1∙h−1) and cholecystokinin (3 × 104 ng∙kg−1∙h−1) both induced dose-dependent gallbladder contraction. This model should prove useful in assessing the physiologic control of gallbladder contraction.

1997 ◽  
Vol 273 (6) ◽  
pp. E1216-E1227 ◽  
Author(s):  
P. C. M. Van Zijl ◽  
D. Davis ◽  
S. M. Eleff ◽  
C. T. W. Moonen ◽  
R. J. Parker ◽  
...  

A new in vivo nuclear magnetic resonance (NMR) spectroscopy method is introduced that dynamically measures cerebral utilization of magnetically labeled [1-13C]glucose from the change in total brain glucose signals on infusion. Kinetic equations are derived using a four-compartment model incorporating glucose transport and phosphorylation. Brain extract data show that the glucose 6-phosphate concentration is negligible relative to glucose, simplifying the kinetics to three compartments and allowing direct determination of the glucose-utilization half-life time [ t ½ = ln2/( k 2 + k 3)] from the time dependence of the NMR signal. Results on isofluorane ( n = 5)- and halothane ( n = 7)- anesthetized cats give a hyperglycemic t ½ = 5.10 ± 0.11 min−1 (SE). Using Michaelis-Menten kinetics and an assumed half-saturation constant Kt = 5 ± 1 mM, we determined a maximal transport rate T max = 0.83 ± 0.19 μmol ⋅ g−1 ⋅ min−1, a cerebral metabolic rate of glucose CMRGlc = 0.22 ± 0.03 μmol ⋅ g−1 ⋅ min−1, and a normoglycemic cerebral influx rate CIRGlc = 0.37 ± 0.05 μmol ⋅ g−1 ⋅ min−1. Possible extension of this approach to positron emission tomography and proton NMR is discussed.


2017 ◽  
Vol 89 (3) ◽  
pp. 1815-1822 ◽  
Author(s):  
Jesus Garoz-Ruiz ◽  
Aranzazu Heras ◽  
Alvaro Colina

1996 ◽  
Vol 104 (2) ◽  
pp. 176-179 ◽  
Author(s):  
J H Graziano ◽  
C B Blum ◽  
N J Lolacono ◽  
V Slavkovich ◽  
W I Manton ◽  
...  

1984 ◽  
Vol 247 (1) ◽  
pp. G105-G111 ◽  
Author(s):  
T. E. Solomon ◽  
T. Yamada ◽  
J. Elashoff ◽  
J. Wood ◽  
C. Beglinger

We determined the relative molar potencies of structural analogues of porcine cholecystokinin (CCK-39, CCK-33, CCK-8, and caerulein). Peptide concentrations delivered in infusates or present in bathing medium were measured by radioimmunoassay. The presence of albumin prevented loss of CCK-39 and CCK-33 from solution to a greater degree than loss of CCK-8 and caerulein from solution. As much as 10-fold differences in CCK-33 and CCK-39 concentrations were seen in albumin-containing versus nonalbumin-containing infusates. The potency estimates calculated from radioimmunoassay-corrected concentrations with CCK-8 as standard (potency 1.00) were canine pancreatic secretion in vivo: CCK-39 4.1, CCK-33 2.2, and caerulein 2.1; rat pancreatic secretion in vivo: CCK-39 2.1, CCK-33 5.4, and caerulein 5.4; rat pancreatic secretion in vitro: CCK-33 1.7, and caerulein 1.2; guinea pig gallbladder contraction in vivo: CCK-33 1.3, and caerulein 0.9; and guinea pig gallbladder contraction in vitro: CCK-33 1.8, and caerulein 5.8. Our data indicate that CCK-8 is not more potent than longer analogues and suggest that larger forms of CCK may be important mediators of the biological actions of CCK.


1988 ◽  
Vol 65 (6) ◽  
pp. 2585-2591 ◽  
Author(s):  
D. J. Dusser ◽  
E. Umeno ◽  
P. D. Graf ◽  
T. Djokic ◽  
D. B. Borson ◽  
...  

To determine whether neutral endopeptidase (NEP), also called enkephalinase (EC 3.4.24.11), modulates the effects of exogenous and endogenous tachykinins in vivo, we studied the effects of aerosolized phosphoramidon, a specific NEP inhibitor, on the responses to aerosolized substance P (SP) and on the atropine-resistant response to vagus nerve stimulation (10 V, 5 ms for 20 s) in guinea pigs. SP alone (10(-7) to 10(-4) M; each concentration, 7 breaths) caused no change in total pulmonary resistance (RL, P greater than 0.5). Phosphoramidon (10(-4) M, 90 breaths) caused no change either in base-line RL (P greater than 0.5) or in the response to aerosolized acetylcholine (P greater than 0.5). However, in the presence of phosphoramidon, SP (7 breaths) produced a concentration-dependent increase in RL at concentrations greater than or equal to 10(-5) M (P less than 0.001). Phosphoramidon (10(-7) to 10(-4) M; each concentration, 90 breaths) induced a concentration-dependent potentiation of SP-induced bronchoconstriction (10(-4) M, 7 breaths; P less than 0.01). Vagus nerve stimulation (0.5-3 Hz), in the presence of atropine, induced a frequency-dependent increase in RL (P less than 0.001). Phosphoramidon potentiated the atropine-resistant responses to vagus nerve stimulation (P less than 0.001) at frequencies greater than 0.5 Hz. The tachykinin antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]-substance P abolished the effects of phosphoramidon on the atropine-resistant response to vagus nerve stimulation (2 Hz, P less than 0.005). NEP-like activity in tracheal homogenates of guinea pig was inhibited by phosphoramidon with a concentration producing 50% inhibition of 5.3 +/- 0.8 nM.(ABSTRACT TRUNCATED AT 250 WORDS)


1973 ◽  
Vol 132 (3) ◽  
pp. 353-359 ◽  
Author(s):  
Isa K. Mushahwar ◽  
Roger E. Koeppe

Determination of the free amino acid and lactate content of testicular tissue in rat, guinea pig, rabbit, cat, gerbil, hamster, chicken and bullfrog indicates a substantial species variation. Insulin hypoglycaemia and ammonium acetate toxicity changes the concentration of several free amino acids of rat testes. 14C radioactivity from labelled acetate and ethanol is rapidly incorporated into some of the free amino acids of rat testes in vivo, whereas incorporation from [14C]glucose is relatively slow. These results have been compared with those obtained from similar studies with rat brain. In contrast to brain, there is no evidence for glutamate compartmentation in testes.


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