Capillary Flow and Capillary Transport in Dog Skeletal Muscle in an Experimental Shock Model (Laparatomy and Exteriorisation of the Small Intestine)

CDKN1C and NAP1L4 in human CDKN1C/KCNQ1OT1 imprinted domain are two key candidate genes responsible for BWS (Beckwith-Wiedemann syndrome) and cancer. In order to increase understanding of these genes in pigs, their cDNAs are characterized in this paper. By the IMpRH panel, porcine CDKN1C and NAP1L4 genes were assigned to porcine chromosome 2, closely linked with IMpRH06175 and with LOD of 15.78 and 17.94, respectively. By real-time quantitative RT-PCR and polymorphism-based method, tissue and allelic expression of both genes were determined using F1 pigs of Rongchang and Landrace reciprocal crosses. The transcription levels of porcine CDKN1C and NAP1L4 were significantly higher in placenta than in other neonatal tissues (P<0.01) although both genes showed the highest expression levels in the lung and kidney of one-month pigs (P<0.01). Imprinting analysis demonstrated that in pigs, CDKN1C was maternally expressed in neonatal heart, tongue, bladder, ovary, spleen, liver, skeletal muscle, stomach, small intestine, and placenta and biallelically expressed in lung and kidney, while NAP1L4 was biallelically expressed in the 12 neonatal tissues examined. It is concluded that imprinting of CDKN1C is conservative in mammals but has tissue specificity in pigs, and imprinting of NAP1L4 is controversial in mammalian species.

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Retention and Subcellular Distribution of 67Ga in Normal Organs

Nuklearmedizin ◽

10.1055/s-0038-1624318 ◽

1986 ◽

Vol 25 (02) ◽

pp. 45-49 ◽

Cited By ~ 2

Author(s):

I. Ando ◽

T. Hiraki ◽

K. Hisada ◽

K. Nitta ◽

H. Ogawa ◽

...

Keyword(s):

Skeletal Muscle ◽

Spinal Cord ◽

Small Intestine ◽

Large Intestine ◽

Subcellular Distribution ◽

Heart Muscle ◽

Subcellular Fractionation ◽

67Ga Citrate

Using normal rats, retention values and subcellular distribution of 67Ga in each organ were investigated. At 10 min after administration of 67Ga-citrate the retention value of 67Ga in blood was 6.77% dose/g, and this value decreased with time. The values for skeletal muscle, lung, pancreas, adrenal, heart muscle, brain, small intestine, large intestine and spinal cord were the highest at 10 min after administration, and they decreased with time. Conversely, this value in bone increased until 10 days after injection. But in the liver, kidney, and stomach, these values increased with time after administration and were highest 24 h or 48 h after injection. After that, they decreased with time. The value in spleen reached a plateau 48 h after administration, and hardly varied for 10 days. From the results of subcellular fractionation, it was deduced that lysosome plays quite an important role in the concentration of 67Ga in small intestine, stomach, lung, kidney and pancreas; a lesser role in its concentration in heart muscle, and hardly any role in the 67Ga accumulation in skeletal muscle. In spleen, the contents in nuclear, mitochondrial, microsomal, and supernatant fractions all contributed to the accumulation of 67Ga.

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Effect of intestinal resection and arginine-free diet on rat physiology

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1995.269.2.g313 ◽

1995 ◽

Vol 269 (2) ◽

pp. G313-G318 ◽

Cited By ~ 10

Author(s):

Y. Wakabayashi ◽

E. Yamada ◽

T. Yoshida ◽

N. Takahashi

Keyword(s):

Skeletal Muscle ◽

Small Intestine ◽

Nitrogen Balance ◽

Control Diet ◽

Intestinal Resection ◽

Dependent Manner ◽

Deficient Diet

The small intestine has been presumed to release citrulline as a precursor for the endogenous arginine synthesis. We studied the effect of intestinal resection and arginine-free diet on rat physiology. We maintained rats with massively resected small intestine (R rats) and those with transected intestines (T rats) on either control or an arginine-free diet. After 4 wk, R rats fed deficient diet [R(-)] lost weight by a mean of 46 g, whereas R rats fed control diet [R(+)] and T rats fed control [T(+)] and deficient diet [T(-)] gained 30-96 g. Average nitrogen balance was 150, 60, 110, and -33 mg/day for T(+), T(-), R(+), and R(-), respectively. The concentrations of arginine in skeletal muscle were 654, 163, 230, and 84 nmol/g, respectively, and those in plasma were 133, 50, 103, and 54 microM, respectively. The concentrations of citrulline in R rats were halved compared with T rats irrespective of diet. We conclude that arginine is synthesized in a small intestine-dependent manner in the rat.

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Effect of vasopressors on organ blood flow during endotoxin shock in pigs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.2.h291 ◽

1987 ◽

Vol 252 (2) ◽

pp. H291-H300 ◽

Cited By ~ 7

Author(s):

M. J. Breslow ◽

C. F. Miller ◽

S. D. Parker ◽

A. T. Walman ◽

R. J. Traystman

Keyword(s):

Blood Pressure ◽

Skeletal Muscle ◽

Blood Flow ◽

Left Ventricle ◽

Arterial Blood Pressure ◽

Endotoxin Shock ◽

Organ Blood Flow ◽

Shock Model ◽

Blood Pressure Elevation ◽

Arterial Blood

A volume-resuscitated porcine endotoxin shock model was used to evaluate the effect on organ blood flow of increasing systemic arterial blood pressure with vasopressors. Administration of 0.05–0.2 mg/kg of Escherichia coli endotoxin (E) reduced mean arterial blood pressure (MAP) to 50 mmHg, decreased systemic vascular resistance to 50% of control, and did not change cardiac output or heart rate. Blood flow to brain, kidney, spleen, and skeletal muscle was reduced during endotoxin shock, but blood flow to left ventricle, small and large intestine, and stomach remained at pre-endotoxin levels throughout the study period. Four groups of animals were used to evaluate the effect of vasopressor therapy. A control group received E and no vasopressor, whereas the other three groups received either norepinephrine, dopamine, or phenylephrine. Vasopressors were administered starting 60 min after E exposure, and the dose of each was titrated to increase MAP to 75 mmHg. Despite the increase in MAP, brain blood flow did not increase in any group. Norepinephrine alone increased blood flow to the left ventricle. Kidney, splanchnic, and skeletal muscle blood flow did not change with vasopressor administration. The dose of norepinephrine required to increase MAP by 20–25 mmHg during E shock was 30 times the dose required for a similar increase in MAP in animals not receiving E. We conclude that hypotension in the fluid resuscitated porcine E shock model is primarily the result of peripheral vasodilatation, that the vascular response to vasoconstrictors in this model is markedly attenuated following E administration, that blood pressure elevation with norepinephrine, dopamine, and phenylephrine neither decreases blood flow to any organ nor increases blood flow to organs with reduced flow, and that norepinephrine, dopamine, and phenylephrine affect regional blood flow similarly in this model.

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