Disease relevance of Hypovolemia

• Prolonged hypovolemic hypotension or sodium depletion increases renin levels [1].
• Therapeutic effects of dopamine hydrochloride on the peripheral and metabolic defects of shock were investigated in 34 patients with circulatory shock associated with myocardial infarction, bacteremia, or hypovolemia [2].
• In diabetic rats, the glucagon defect appeared to be specific for hypoglycemia, whereas deficient epinephrine secretion also occurred during hypovolemia [3].
• We have studied the water drinking responses, relative to body weight, of Munich Wistar (MW) rats in response to osmotic, hypovolemic, dehydrational, and angiotensin (Ang)-related stimuli as they aged from 3 to 24 months [4].
• In human, autosomal recessive mutations of alpha, beta, or gammaENaC subunits cause pseudohypoaldosteronism type 1 (PHA-1), a renal salt-wasting syndrome characterized by severe hypovolemia, high plasma aldosterone, hyponatremia, life-threatening hyperkaliemia, and metabolic acidosis [5].

Psychiatry related information on Hypovolemia

• Water deprivation for 48 h, leading to extracellular hypertonic hypovolemia with elevated circulating AngII concentrations within the physiological range, caused a significant increase in AoGen-specific hybridization signals in the rostral and medial SFO regions [6].
• Drinking to polyethylene glycol-induced hypovolemia and feeding after food deprivation did not differ between lesioned and sham-lesioned animals [7].

High impact information on Hypovolemia

• Recent evidence indicates that plasma AVP does not increase during progressive hypovolemia until volume loss causes a frank fall in arterial pressure [8].
• We conclude that GC-A-mediated increases in endothelial permeability are critically involved in the hypovolemic, hypotensive actions of ANP [9].
• Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide [9].
• Downregulation of chloride transporters in KD is an early event and can lead to hypochloremia and subsequently hypovolemia and decreased glomerular filtration rate [10].
• Opioid antagonist diprenorphine microinjected into parabrachial nucleus selectively inhibits vasopressin response to hypovolemic stimuli in the rat [11].

Chemical compound and disease context of Hypovolemia

• In edematous and hypovolemic patients, plasma hormonal responses (increases in plasma renin activity and aldosterone and norepinephrine levels) were compatible with baroreceptor-mediated release of vasopressin [12].
• Drinking responses to hypovolemia induced by s.c. injection of colloid (polyethylene glycol) were unchanged in 6- to 15-m.o. rats, then declined precipitously in 18- to 24-m.o. rats [4].
• When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups [13].
• Congestion and hypovolemia are reversible and can be largely prevented by administration of the protective compound N-acetylcysteine (1,200 mg per kg p.o.) 3 hr after acetaminophen [14].
• Much higher levels of ELAM-1 expression and plasma granulocyte-elastase titer in septic shock, as contrasted with traumatic/hypovolemic shock, are consistent with the higher levels of circulating tumor necrosis factor, other cytokines, and LPS in sepsis [15].

Biological context of Hypovolemia

• These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction [16].
• During hypovolemia, vasopressin affects systemic blood pressure independent of the renin-angiotensin system and efferent sympathetic pathways [17].
• This study suggests that although an abundant supply of blood glucose is available as an energy source, glucose uptake in the peripheral tissues is inhibited during hypovolemia by unknown mechanisms and thus homeostasis is curtailed [18].
• Impaired water excretion can be due to a primary defect in the osmoregulation of ADH (inappropriate antidiuresis) or secondary to nonosmotic stimuli like hypovolemia or nausea [19].
• As it is impossible to study this in patients, a rat model was used in which the influence of hypovolemia on the pharmacokinetics and pharmacodynamics of propofol was investigated [20].

Anatomical context of Hypovolemia

• The plasma AVP increase in response to PEG-induced hypovolemia was also attenuated significantly and more potently when NPFF was injected into the cisterna magna so that the given drug could be readily accessible to the dorsal medulla where the nucleus of solitary tract is located (10 micrograms/rat; 2.71 +/- 0.14 pg/ml) [21].
• Our data also suggest a small increase in central nervous system sensitivity for etomidate in hypovolemic animals [22].
• Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group [23].
• In hypovolemic shock, where sympathetic nervous activity is high, the inhibitory effect of dopamine on sympathetic ganglia disappears and its direct vasoconstrictor effect on the vessels dominates [24].
• In the present study, we used subcutaneous polyethylene glycol injections to show that a physiologically relevant stimulus, hypovolemia, will selectively increase the expression of neuropeptide genes in a restricted population of parvicellular corticotropin-releasing hormone-containing neurons in the hypothalamic paraventricular nucleus [25].

Gene context of Hypovolemia

• Although increased endothelin-3 was associated with features suggesting a reduced effective volemia, it is likely that other mechanisms than hypovolemia were mainly responsible for high plasma endothelin levels [26].
• Hypovolemia produced by retro-orbital bleeding also significantly elevated corticosterone in CRH KO mice [27].
• This suggests that AVP has contrasting effects in the inner ear and kidney, which may be physiologically useful for maintaining endolymphatic pressure during severe hypovolemia [28].
• These results indicate that the secretion of PRL is not generally affected by chronic mild hypernatremic hypovolemia in the patients with idiopathic DI [29].
• Together, these changes suggest that the late stimulatory effect of ANP on ACTH/cortisol release reflects an effect secondary to its hypovolemic actions [30].

Analytical, diagnostic and therapeutic context of Hypovolemia

• Subcutaneous injection of the potent, nonselective opioid antagonist diprenorphine inhibits the vasopressin response to acute hypovolemia [11].
• Because changes in extracellular volume during dialysis cause reflex neurohonnonal changes that may influence parathyroid hormone (PTH) release independently of calcium, the influence of isotonic volume depletion (by isolated ultrafiltration) and central hypovolemia (70 degrees tilt) on serum PTH1-84 was studied in 16 hemodialysis patients [31].
• Using lower body negative pressure (LBNP) to simulate central hypovolemia, we previously observed falling mean flow velocities (MFVs) with maintained mean arterial blood pressure (MABP) [32].
• CONCLUSIONS: Patients with CSF hypovolemia frequently have distinct MRI and radioisotope cisternographic abnormalities and often respond favorably to an epidural blood patch [33].
• Imipenem was infused intravenously at a dose of 70 mg . kg(-1) over 30 min, and microdialysis samples were collected for 120 min from hypovolemic (n = 8) and control (n = 8) rats [34].

References