Disease relevance of Shock

• In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria [1].
• ALT was associated with hemoconcentration, hypotension, and circulatory collapse; however, toxicity could be prevented by platelet-activating factor inhibitor, rat antibody to Fc receptor, or IgM before IgG1 [2].
• Epinephrine improved circulatory collapse and pump dysfunction after brain death, while simultaneously maintaining renal perfusion [3].
• Circulating phospholipase A2 (PLA2) has been recognized as a mediator of circulatory collapse in experimental endotoxic shock [4].
• BACKGROUND AND METHODS: Renal cortical and serum carnitine concentrations were studied in seven anesthetized beagle dogs in which acute circulatory collapse was induced by an iv injection of Escherichia coli endotoxin, 0.5 mg/kg given over 15 mins [5].

High impact information on Shock

• Coronary-artery spasm immediately after myocardial revascularization may cause circulatory collapse and death; although the spasm may be refractory to usual therapy, it may respond to intracoronary nitroglycerin [6].
• Lethal C5a-mediated circulatory collapse in pigs was prevented by pretreatment with F(ab)2-IVIG [7].
• Acting via one or all of these mechanisms, cimetidine may protect against the vascular permeability changes and circulatory collapse that can follow severe thermal injury [8].
• CONCLUSIONS: Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury [9].
• Urotensin II causes fatal circulatory collapse in anesthesized monkeys in vivo: a "vasoconstrictor" with a unique hemodynamic profile [10].

Chemical compound and disease context of Shock

• Similarly, bupivacaine blood concentrations at the onset of respiratory arrest and circulatory collapse were lower in the pregnant group, being 5.2 +/- 0.7 micrograms/ml and 5.5 +/- 0.8 micrograms/ml, respectively, versus 7.5 +/- 1.0 microgram/ml and 8.0 +/- 0.9 micrograms/ml, respectively, in the nonpregnant group (P less than 0.05) [11].
• In pregnant ewes, greater doses of ropivacaine as compared to bupivacaine were required to produce convulsions (7.5 +/- 0.5 vs. 5.0 +/- 0.6 mg.kg-1) and circulatory collapse (12.9 +/- 0.8 vs. 8.5 +/- 1.2 mg.kg-1) [12].
• METHODS: After 120 min of steady state infusion of propofol at a rate of 2 mg x kg(-1) x h(-1), nine instrumented immature swine were studied using a stepwise increasing hemorrhagic model (200 ml of blood every 30 min until 1 h, then additional stepwise bleeding of 100 ml every 30 min thereafter, to the point of circulatory collapse) [13].
• Potential circulatory collapse may ensue when the vasoconstrictor response fails in the splanchnic circulation [14].
• Serum protein binding of mepivacaine was not reduced in pregnancy at the drug concentrations associated with toxic symptoms; at circulatory collapse, it was approximately 22% in NP and P. In contrast, the proportion of bound bupivacaine was 73% in NP and 51% in P, a significant difference [15].

Biological context of Shock

• Following a case of mannitol-induced respiratory and circulatory collapse, the effects of hyperosmolar injections on pulmonary arterial pressure, systemic blood pressure, and cardiac output were studied in dogs [16].
• To evaluate the potential therapeutic value of triiodothyronine (T3) in circulatory collapse, 26 anesthetized, heparinized mongrel dogs were bled rapidly into a reservoir until mean arterial blood pressure (MAP) = 40 mmHg [17].
• Severe, generalized threats such as hypoglycaemia, hypoxia, haemorrhage, circulatory collapse, and fight/flight situations elicit generalized SAMS activation, including cardiac stimulation, splanchnic, cutaneous, and renal vasoconstriction, and usually preserved skeletal muscle blood flow [18].

Anatomical context of Shock

• Observations before death and at autopsy were in accordance with the basic effect of compound 48/80 in rats i.e. the sustained release of mast cell mediators, whose action on the cardiovascular system leads to circulatory collapse [19].

Gene context of Shock

• The use of protamine sulfate in patients has been associated with severe circulatory collapse and myocardial failure [20].
• Fetal circulatory collapse during induction of labor in pregnant patient with epilepsy [21].
• Cardiotoxicity and circulatory collapse have rarely been reported after massive ingestions of diphenhydramine and other H1-receptor-blocking agents, although these substances have local anesthetic properties and have been studied as antiarrhythmics [22].
• A 33-year-old highly parous woman developed severe abdominal pain and signs of circulatory collapse 10 months after tubal sterilisation in the absence of symptoms of pregnancy [23].
• Markedly reduced levels of prekallikrein and high molecular weight kininogen were seen at circulatory collapse and free kallikrein was detected [24].

Analytical, diagnostic and therapeutic context of Shock

• METHODS: Chronically prepared nonpregnant and pregnant sheep were randomized to receive an intravenous infusion of 0.52% levobupivacaine, 0.52% bupivacaine, or 0.50% ropivacaine at a constant rate of 0.1 ml x kg(-1) x min(-1) until circulatory collapse [25].
• OBJECTIVE: To report a case of severe circulatory collapse following an intravenous injection of sodium valproate.CASE SUMMARY: A 5-year-old white girl, who was receiving vasopressor support, developed a severe circulatory collapse following an intravenous injection of valproate 480 mg [26].
• Pretreatment of the animals either with BN 52021 (4 mg.kg-1) or indomethacin (2 mg.kg-1 plus 3 mg.kg-1hr-1) prevented the circulatory collapse and the increase in prostanoid levels during reperfusion [27].
• We hypothesize that thyroidectomy, perhaps by modulating catecholamine metabolism or stimulating liberation of thyrotropin releasing hormone, promotes salutary hemodynamic-metabolic effects during circulatory collapse and enhances survival [28].

References