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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

The rate of flow and electrolyte concentration of parotid saliva were measured before, during and after intravenous and contralateral intracarotid infusion of KCl (0.5 mol.1(-1)) and NaCl (0.5 mol.1(-1)) at 385-625 mumol. min(-1) for 40 min into 5 sheep. In intact conscious sheep contralateral intracarotid infusion of KCl caused marked depression of salivary secretion in all experiments whereas infusion of NaCl had no consistent effect on flow. Intravenous infusion of KCl into the intact conscious sheep caused a slight depression of salivary secretion but minimum flow was significantly higher than that during intracarotid infusion. When the sheep were anaesthetized salivary flow rates were low and contralateral intracarotid infusion of KCl either had no effect on flow or caused an increase in flow. After ipsilateral cervical sympathectomy contralateral intracarotid infusion of KCl into the conscious sheep caused a marked depression of salivary flow similar to that occurring when the sheep were intact. After section of the secretomotor nerve of the gland salivary flow rates were low and contralateral intracarotid infusion of KC1 had no effect on flow. The salivary flow responses of the sheep were consistent, regardless of whether the KCl infusions were given within 24 h or 1-2 weeks after cervical sympathectomy or secretomotor nerve section. Salivary sodium concentration was negatively correlated with salivary flow in all experiments. It was concluded that potassium acted at a site located in the head but by direct action on the salivary gland. The depression of salivary secretion by hyperkalaemia resulted from a decline in neural activity in the parasympathetic secretomotor innervation of the parotid gland.
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PMID:The role of the autonomic nervous system in the depression of parotid salivary secretion during hyperkalaemia in conscious sheep. 24 21

Numerous studies have demonstrated that reticuloendothelial system (RES) depression induced by colloid blockade increases susceptibility to circulatory shock following trauma and sepsis. Recent data have suggested that this may relate to the failure of the RES to clear potentially embolic material derived from activation of the hemostatic system. The present study thus compared the hypotensive response precipitated by trauma or sepsis with that resulting from induction of intravascular coagulation. Mean arterial blood pressure (MABP) was monitored for 120 minutes after sublethal NCD trauma and after intra-aortic injection of live E coli (approximately 10(10) organisms per rat), E coli endotoxin (0.1 mg/100 gm), or bovine thrombin (10 units/100 gm) in 400-500 gm rats 30 minutes after RE blockade (50 mg/100 gm gelatinized lipid colloid) or saline injection. All rats were anesthetized with sodium pentobarbital. No hypotension was observed in blockaded control rats. After trauma, MABP decreased by 20 minutes after injury and recovered to normal levels by 1 hour post-trauma. MABP decreased in blockaded rats after trauma and remained diminished through 2 hours. After live E coli endotoxin or thrombin, both the normal and the blockaded groups underwent an initial hypotension of similar magnitude. A second period of hypotension was much more pronounced in the RE-blockaded animals. Reduced MABP persisted in these animals through 2 hours. These data indicate that RE blockade enhances the hypotensive response to intravascular coagulation and that resulting from trauma or sepsis. This effect was especially apparent during the second phase of hypotension during sepsis and intravascular coagulation. It was suggested that the RES manifests some protective effect against the agents inducing this secondary hypotensive response.
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PMID:Effect of reticuloendothelial blockade on the development of hypotension after trauma, sepsis, and intravascular coagulation. 26 5

Erythrosine and sodium fluorescein, two colors used as a dental plaque disclosing agents, have similar chemical structures differing only in that erythrosine has four iodine atoms in the molecule while sodium fluorescein has no iodine. A comparative toxicological profile was made on both compounds employing oral dose ranges and acute oral toxicity tests in mice and rats. The results show erythrosine to be approximately twice as toxic as sodium fluorescein with LD50 values of 2558 +/- 1.35 mg/kg in mice and 2891 +/- 1.02 mg/kg in rats for erythrosine and 4738 +/- 1.23 mg/kg in mice and 6721 +/- 1.26 mg/kg in rats for sodium fluorescein. The major toxic manifestations of both compounds were those indicative of central nervous system depression.
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PMID:Acute toxicity testing of erythrosine and sodium fluorescein in mice and rats. 26 92

The effect of the intra-arterial injection of 5 to 10 microng of sodium nitroprusside on the caliber of normal and diseased coronary arteries was evaluated in 21 patients during diagnostic cardiac catheterization. In addition, the effect of intra-graft injection of 5 microng of the same agent on the blood flow in aorta-right coronary artery saphenous vein bypass grafts was also evaluated intra-operatively in two patients. The compound induced an increase in the caliber of both normal and stenosed coronary arteries as well as an increase of flow in the grafts. Consistent with measurements of coronary flow response to sodium nitroprusside, angina pectoris which developed in four patients during cardiac catheterization was immediately relieved and the ischemic ST-segment depression significantly reversed after injection of 5 to 10 microng of the drug into the left main coronary artery. Within the dose range used, the drug caused no significant effect on systemic blood pressure or apparently deleterious electrophysiologic changes. No side effects were observed. We conclude that the primary direct action of sodium nitroprusside in the human coronary artery is vasodilatory.
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PMID:Sodium nitroprusside as a coronary vasodilator in man. I. Effect of intracoronary sodium nitroprusside on coronary arteries, angina pectoris, and coronary blood flow. 30 May 57

The rate coefficients and fluxes of sodium across the outside and inside barriers of an in vitro, short-circuited frog skin preparation were determined in the presence of a uremic serum fraction to localize the site of action of an inhibitor of sodium transport. In unpaired studies, the mean depression of short-circuit current (SCC) resulting from the addition of the uremic serum fraction (21.9+/-2.2%) was significantly greater than the decrease in SCC resulting from either frog Ringer's wash or normal serum fractions. Paired studies comparing active and inactive uremic serum fractions indicated that the reduction in net sodium transport, whether calculated from changes in SCC(-0.55+/-0.12muEq/h) or changes in unidirectional Na fluxes (-0.56+/-0.15 muEq/h) was significantly greater in hemi-skins treated with the active fraction. The depression in sodium transport was associated with a significant decrease of sodium movement from the skin to the inside compartment, phi22 (-0.62+/-0.2 muEq/h). The results of these studies suggest that the inhibition of sodium transport ascribed to the uremic serum fraction is due to an inhibition of the active transport mechanism located at the serosal barrier.
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PMID:Site of action of a uremic serum fraction inhibiting sodium transport in frog skin. 31 42

Intramuscularly administered methylprednisolone sodium phosphate (Medrol Stabisol) in single doses of 40, 80, or 160 mg (methylprednisolone equivalents) had a similar effect as the same doses of methylprednisolone sodium succinate (Solu-Medrol) with regard to eosinophil suppression, elevation of glucose, white blood count differential shifts (lympholytic effect), urinary excretion of sodium and potassium, and localized (pain) and systemic side effects. The average plasma methylprednisolone concentration was approximately 20% higher after the intramuscular administration of methylprednisolone sodium phosphate than after methylprednisolone sodium succinate. The differences in plasma methylprednisolone levels produced by the two esters suggest that either hydrolysis of the succinate ester occurs more slowly or the succinate ester distributes more extensively. This difference in plasma level, however, is not reflected in any other pharmacologic evaluation of the two esters, e.g., both eosinophil depression and hyperglycemic response were identical. No clinically significant changes in the vital signs, standard hematology, and clinical chemistry parameters evaluated were noted after 21 successive doses (q.i.d. for five days with one dose in the morning of day 6) of 80 mg methylprednisolone sodium phosphate. An increase was noted in the systolic blood pressure from a pretreatment mean of 113 mm Hg to a posttreatment mean of 123 mm Hg and an increase in the body weight from a pretreatment mean of 177 pounds to a posttreatment mean of 183 pounds. No signs of adrenal suppression were found as judged by plasma cortisol and ACTH levels. Six (6/12) subjects of the methylprednisolone sodium phosphate group, one (1/12) subject of the vehicle group, and one (1/12) subject of the placebo (sterile saline) group reported the following systemic side effects: gas in stomach, headaches, anorectal itching, and dryness of itching of the skin. No trend was observed for any side effect reported. In these double-blind, randomized studies, single (40, 80, and 160 mg) and multiple (80 mg) intramuscular doses of methylprednisolone sodium phosphate were tolerated in healthy volunteers as well as the same doses of methylprednisolone sodium succinate and similar volumes of vehicle or placebo.
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PMID:The clinical pharmacology of methylprednisolone sodium phosphate. I. Intramuscular route of administration. 32 97

Resistance to intravenous (IV) and intraperitoneal (IP) bacterial challenge during periods of reticuloendothelial (RE) depression following trauma as well as the influence of bacteremia on RE phagocytosis were studied. The experimental shock model utilized was the anesthetized (2 mg/100 g sodium pentobarbital) male rat subjected to nonlethal Noble-Collip drum trauma. During post-traumatic RE depression (60 min after injury) rats were challenged IV or IP with Escherichia coli (1.02 X 10(10)). The clearance half-time of the bacterial load injected intravenously in controls was 1.23 +/- 0.10 min. In contrast, the half-time was 3.62 +/- 0.69 min after sublethal trauma (p less than 0.005) and associated with prolonged blood bacterial retention. Pulmonary localization of E. coli administered either IV or IP was elevated in traumatized rats. Comparison of routes of bacterial challenge with respect to blood levels of viable bacteria suggested lower host bacterial resistance to the IP injection as opposed to the IV route of administration. Production of experimental bacteremia in normal rats resulted in a 39% depression (p less than 0.01) of RE test colloid clearance rate accompanied by a 49% increase (p less than 0.01) in pulmonary colloid localization. The data suggest that depressed systemic RE clearance capacity following trauma may decrease systemic resistance to septicemia, and that severe bacteremia may further undermine the functional state of the reticuloendothelial system.
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PMID:Reticuloendothelial phagocytic response to bacterial challenge after traumatic shock. 33 34

The hemodynamic and renal effects of mechanical ventilation with positive end-expiratory pressure (PEEP) were studied with and without continuous dopamine administration in ten patients who had acute pulmonary failure. The application of 20 cm H2O PEEP during mechanical ventilation resulted in improvements in arterial blood oxygen tension, from 63 +/- 6 to 81 +/- 12 torr (mean +/- SE), and intrapulmonary shunt fraction, from 29 +/- 3 to 21 +/- 3 per cent, whereas cardiac output, systemic oxygen transport and renal function were impaired by 20, 19 and 47 per cent, respectively. Dopamine infusion at a rate of 5 +/- 0.05 micrograms/kg/min reversed the deleterious effects of PEEP on cardiovascular and renal function: cardiac output increased from 4.5 +/- 0.3 to 6.0 +/- 0.51, urinary output from 1.0 +/- 0.3 to 1.7 +/- 0.4 ml/min, sodium excretion and creatinine clearance by 50 per cent. Systemic oxygen transport was improved from 680 +/- 44 to 925 +/- ml, arterial oxygen tension from 81 +/- 12 to 102 +/- 14 torr, and total deadspace to tidal volume ratio from 0.49 +/- 0.02 to 0.44 +/- 0.03 with dopamine. The authors conclude that the depression of cardiovascular and renal functions that may occur in patients who need high levels of PEEP for the treatment of acute pulmonary failure can be treated successfully with dopamine infusion. This represents a valuable alternative to expansion of blood volume for the improvement of systemic oxygen transport and arterial blood oxygen tension in critically ill patients.
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PMID:Treatment of cardiac and renal effects of PEEP with dopamine in patients with acute respiratory failure. 37 29

Physiological roles have been suggested for prostacyclin in the cardiovascular system. Prostacyclin was administered by intravenous infusion to unanesthetized rats. Over a 24 hr period, 0.32 mg/kg/day caused only flushing of the ears. Larger doses (0.56 and 1 mg/kg/day) caused hypothermia, behavioral depression, and swelling of the paws. Cumulative dose-response curves for its depressor action were determined in both unanesthetized and anesthetized, vagotomized, ganglion-blocked rats. In unanesthetized rats, the threshold dose was about 0.1 ug/kg/min. Respiratory depression precluded doses larger than 1 ug/kg/min. In anesthetized rats, the threshold dose was about 0.001 ug/kg/min, and the maximally effective dose was about 0.1 micrograms/kg/min. At 0.032 ug/kg/min, blood pressure first fell and then rose slightly. This compensatory rise did not occur in nephrectomized rats, suggesting renin release as the mechanism. Intravenous infusion of 0.1 but not 0.01 ug/kg/min in unanesthetized rats doubled plasma renin activity. In saline-loaded unanesthetized rats, urine volume and urinary sodium excretion were decreased by 0.1 ug/kg/min of prostacyclin.
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PMID:The cardiovascular pharmacology of prostacyclin (PGI2) in the rat. 37 17


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