42. Desglycinamide-arginine-vasopressin penetrates to the central nervous system and interacts with monoamines in human subjects

1987 ◽  
Vol 89 (2) ◽  
pp. 15
Author(s):  
J. Jolkkonen ◽  
H. Soininen ◽  
M. Lehtinen ◽  
P. Riekkinen
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Arginine Vasopressin ◽  
Human Subjects ◽  
The Central Nervous System

scholarly journals AVP mediates the attenuated febrile response to administration of PGE1 in rats near term of pregnancy

1998 ◽  
Vol 275 (3) ◽  
pp. R691-R696 ◽  
Author(s):  
Heather L. Eliason ◽  
James E. Fewell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Receptor Antagonist ◽  
Core Temperature ◽  
Arginine Vasopressin ◽  
Intracerebroventricular Injection ◽  
Intracerebroventricular Administration ◽  
Febrile Response ◽  
The Central Nervous System ◽  
Near Term

Rats have an attenuated febrile response to intracerebroventricular injection of PGE1 near the term of pregnancy, the mechanism of which is unknown. The present experiments were carried out to test the hypothesis that arginine vasopressin (AVP), functioning as an endogenous antipyretic substance in the central nervous system, mediates this attenuated febrile response. The febrile response to intracerebroventricular injection of 0.2 μg PGE1 was determined in pregnant and nonpregnant rats after an intracerebroventricular injection of either vehicle or a vasopressin V1-receptor antagonist. After intracerebroventricular administration of vehicle, intracerebroventricular administration of 0.2 μg PGE1 produced significant increases in core temperature in both nonpregnant and pregnant animals. The increase in core temperature, however, was attenuated both in magnitude and duration in pregnant compared with nonpregnant animals. After intracerebroventricular administration of a vasopressin V1-receptor antagonist, intracerebroventricular administration of 0.2 μg PGE1 produced significant increases in core temperature that were similar in nonpregnant and pregnant animals. Our data support the hypothesis that a pregnancy-related activation of AVP as an endogenous antipyretic substance in the central nervous system attenuates the febrile response to intracerebroventricular administration of PGE1 near term of pregnancy in rats.

Arginine vasopressin does not mediate the attenuated febrile response to intravenous IL-1β in pregnant rats

1999 ◽  
Vol 276 (2) ◽  
pp. R450-R454 ◽  
Author(s):  
Heather L. Eliason ◽  
James E. Fewell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Receptor Antagonist ◽  
Core Temperature ◽  
Arginine Vasopressin ◽  
Temperature Response ◽  
Endogenous Pyrogen ◽  
Febrile Response ◽  
Pregnant Rats ◽  
The Central Nervous System

Rats have an attenuated febrile response to intravenous endogenous pyrogen [e.g., interleukin-1β (IL-1β)] near the term of pregnancy. The present experiments were carried out on 25 nonpregnant and 32 pregnant rats to test the hypothesis that arginine vasopressin functioning as an endogenous antipyretic substance in the central nervous system mediates this attenuated febrile response. An intravenous injection of recombinant rat IL-1β (rrIL-1β) after intracerebroventricular vehicle produced a significant increase in core temperature in both nonpregnant and pregnant animals, the magnitude and duration of which was greater in the nonpregnant rats. In nonpregnant rats, intravenous rrIL-1β after intracerebroventricular vasopressin V1-receptor antagonist accentuated the core temperature response compared with that observed with intravenous rrIL-1β after intracerebroventricular vehicle. In pregnant animals, however, intravenous rrIL-1β after intracerebroventricular vasopressin V1-receptor antagonist produced a decrease in core temperature rather than an increase in core temperature, which was observed with intravenous rrIL-1β after intracerebroventricular vehicle. Thus our data do not support the hypothesis that a pregnancy-related activation of arginine vasopressin as an endogenous antipyretic substance in the central nervous system attenuates the febrile response to intravenous rrIL-1β near the term of pregnancy in rats.

Body-core temperature decreases during hypoxic hypoxia in Long–Evans and Brattleboro rats

1994 ◽  
Vol 72 (12) ◽  
pp. 1528-1531 ◽  
Author(s):  
Deborah J. Clark ◽  
James E. Fewell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Core Temperature ◽  
Arginine Vasopressin ◽  
Hypoxic Hypoxia ◽  
Body Core Temperature ◽  
Brattleboro Rats ◽  
Body Core ◽  
The Central Nervous System ◽  
Long Evans

In newborn mammals, hypoxic hypoxia produces a regulated decrease in body-core temperature, the mechanism of which is unknown. Since plasma and cerebrospinal fluid levels of arginine vasopressin increase during hypoxemia and intracerebroventricular administration of arginine vasopressin decreases body-core temperature, it has been hypothesized that an increase in central arginine vasopressin may mediate this response. Experiments were therefore carried out to test the hypothesis that the body-core temperature response to hypoxic hypoxia would be different in Brattleboro rats (which lack arginine vasopressin containing cells in the central nervous system) compared with that observed in Long–Evans rats (which have arginine vasopressin containing cells in the central nervous system). Both mild (15% oxygen) and severe (10% oxygen) hypoxic hypoxia decreased body-core temperature in both strains of rats, the decrease actually being accentuated in the Brattleboro rats. Thus, our data do not support the hypothesis that an increase in central arginine vasopressin mediates the regulated decrease in body-core temperature during hypoxic hypoxia in rats.Key words: hypoxic hypoxia, thermoregulation, arginine vasopressin, Brattleboro rats, Long–Evans rats.

scholarly journals Update in the CNS Response to Hypoglycemia

2012 ◽  
Vol 97 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Rory J. McCrimmon
Keyword(s):  
Type 2 Diabetes ◽  
Central Nervous System ◽  
Type 1 Diabetes ◽  
Nervous System ◽  
Animal Studies ◽  
Human Subjects ◽  
Diabetes Research ◽  
The Central Nervous System

Hypoglycemia remains a major clinical issue in the management of people with type 1 and type 2 diabetes. Research in basic science is only beginning to unravel the mechanisms that: 1) underpin the detection of hypoglycemia and initiation of a counterregulatory defense response; and 2) contribute to the development of defective counterregulation in both type 1 and type 2 diabetes, particularly after prior exposure to repeated hypoglycemia. In animal studies, the central nervous system has emerged as key to these processes. However, bench-based research needs to be translated through studies in human subjects as a first step to the future development of clinical intervention. This Update reviews studies published in the last 2 yr that examined the central nervous system effects of hypoglycemia in human subjects, largely through neuroimaging techniques, and compares these data with those obtained from animal studies and the implications for future therapies. Based on these studies, it is increasingly clear that our understanding of how the brain responds and adapts to recurrent hypoglycemia remains very limited. Current therapies have provided little evidence that they can prevent severe hypoglycemia or improve hypoglycemia awareness in type 1 diabetes. There remains an urgent need to increase our understanding of how and why defective counterregulation develops in type 1 diabetes in order for novel therapeutic interventions to be developed and tested.

Effects of Hyperoxia on Lung Utrastructure

1970 ◽  
Vol 28 ◽  
pp. 26-27
Author(s):  
Gladys Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Light Microscopy ◽  
Oxygen Effects ◽  
Age Dependent ◽  
The Central Nervous System ◽  
The Subject ◽  
Space Age ◽  
Alveolar Septa ◽  
Extensive Damage

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.

Emigration of neutrophils in the central nervous system

1983 ◽  
Vol 41 ◽  
pp. 788-789
Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Osmium Tetroxide ◽  
White Blood Cells ◽  
Arterial Perfusion ◽  
E Coli ◽  
Intracisternal Injection ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
Interendothelial Junctions

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.

Mammalian Bone Marrow Acetylcholinesterase

1982 ◽  
Vol 40 ◽  
pp. 44-45
Author(s):  
Ezzatollah Keyhani
Keyword(s):  
Central Nervous System ◽  
Bone Marrow ◽  
Nervous System ◽  
Common Property ◽  
Extracellular Medium ◽  
The Central Nervous System ◽  
The Common ◽  
Mammalian Bone

Acetylcholinesterase (EC 3.1.1.7) (ACHE) has been localized at cholinergic junctions both in the central nervous system and at the periphery and it functions in neurotransmission. ACHE was also found in other tissues without involvement in neurotransmission, but exhibiting the common property of transporting water and ions. This communication describes intracellular ACHE in mammalian bone marrow and its secretion into the extracellular medium.

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