PubMed Health⌕ Search

Biomedical subjects

I T Velasco

Publications and source records attributed to I T Velasco.

At least 19 recordsLinked to original sources
PubMed2004

The role of the vagus nerve in hypertonic resuscitation of hemorrhagic shocked dogs.

Previous studies have suggested a critical role for the vagi during the hypertonic resuscitation of hemorrhagic shocked dogs. Vagal blockade prevented the full hemodynamic and metabolic recovery and increased mortality. This interpretation, however, was challenged on the grounds that the blockade also abolished critical compensatory mechanisms and therefore the animals would die regardless of treatment. To test this hypothesis, 29 dogs were bled (46.0 +/- 6.2 ml/kg, enough to reduce the mean arterial pressure to 40 mmHg) and held hypotensive for 45 min. After 40 min, vagal activity was blocked in a reversible manner (0 masculine C/15 min) and animals were resuscitated with 7.5% NaCl (4 ml/kg), 0.9% NaCl (32 ml/kg), or the total volume of shed blood. In the vagal blocked isotonic saline group, 9 of 9 dogs, and in the vagal blocked replaced blood group, 11 of 11 dogs survived, with full hemodynamic and metabolic recovery. However, in the hypertonic vagal blocked group, 8 of 9 dogs died within 96 h. Survival of shocked dogs which received hypertonic saline solution was dependent on vagal integrity, while animals which received isotonic solution or blood did not need this neural component. Therefore, we conclude that hypertonic resuscitation is dependent on a neural component and not only on the transient plasma volume expansion or direct effects of hyperosmolarity on vascular reactivity or changes in myocardial contraction observed immediately after the beginning of infusion.

Animals↗
PubMed2001

Refeeding procedures after 43 days of total fasting.

Refeeding syndrome encompasses fluid and electrolyte imbalances and metabolic, intestinal, and cardiorespiratory derangements associated with appreciable morbidity and mortality. Although refeeding syndrome has been well documented in concentration-camp subjects, and more recently during parenteral therapy of critically ill patients, little is known about the importance of refeeding syndrome during recovery from a hunger strike. Thus, we studied the response to a four-step dietary replenishment routine in eight hunger strikers who refused food for 43 d. In this retrospective, observational study, we assessed the safety and efficacy of the refeeding procedure and analyzed the clinical and nutritional course of the cohort during both starvation and refeeding, mainly on the basis of clinical as well as a few biochemical determinations. During starvation, average weight loss was about 18% and, with the exception of occasional oral vitamins and electrolytes, the subjects consumed only water. Available body-composition and biochemical profiles showed no clinically significant changes during starvation, but one-half of the group displayed spontaneous diarrhea at some time before refeeding. Stepwise nutritional replenishment lasted for 9 d, after which all patients tolerated a full, unrestricted diet. Only one episode of diarrhea occurred during this phase, and both clinical and biochemical indexes confirmed a favorable clinical course, without any manifestation of refeeding syndrome. In conclusion, we observed the following: 1) Hypophosphatemia and other micronutrient imbalances did not occur, nor was macronutrient intolerance detected. 2) Despite some episodes of diarrhea, nutritional replenishment was not associated with significant enteral dysfunction. 3) There was some fluid retention, but this was mild. 4) Acute-phase markers were abnormally elevated during the refeeding phase, without associated sepsis or inflammation.

Acute-Phase Proteins↗
PubMed2001

Enhanced expression of Fc alpha receptor I on blood phagocytes of patients with gram-negative bacteremia is associated with tyrosine phosphorylation of the FcR-gamma subunit.

Sepsis caused by gram-negative bacteria is a common finding having high incidence and mortality. Fc alpha RI (CD89), a receptor for immunoglobulin A (IgA), has been shown to mediate bacterial phagocytosis, which might play a role in the pathogenesis of sepsis. In this study the expression and function of Fc alpha RI were analyzed on blood monocytes and neutrophils of patients with bacteremia. We found a marked increased in expression of the alpha- and gamma-subunits of the Fc alpha RI on both types of cells in patients with gram-negative bacteremia, but not in patients with gram-positive bacteremia. This increase was independent of serum IgA levels. Fc alpha RI M(r) was lower on cells from gram-negative patients than on cells from controls (50-65 kDa versus 55-75 kDa), despite a similar 32-kDa backbone, indicating altered glycosylation. Increased levels of Fc alpha RI on blood phagocytes correlated with enhanced serum IL-6 levels, but not with IFN gamma or TNF-alpha. FcR-gamma chain associated with Fc alpha RI was phosphorylated in patients neutrophils, indicating functional engagement of this receptor during gram-negative sepsis. Increased expression and activation of Fc alpha RI-gamma 2 complexes following gram-negative infections suggests its involvement in host defense against bacteria.

APACHE↗
PubMed1993

Isochloremic hypertonic solutions for severe hemorrhage.

Two different hypertonic (2400 mOsm/L) isochloremic dextran solutions (sodium acetate, HAD; and sodium lactate, HLD; in 0.9% NaCl + 6% dextran 70) were compared with HSD (2400 mOsm/L NaCl + 6% dextran 70) as initial treatment for severe uninterrupted arterial bleeding. The substitution of dextran 70 for lactated Ringer's solution as the maintenance isotonic infusion fluid was also analyzed. Experiments were performed in pentobarbital-anesthetized dogs. A recently developed model, pressure-driven hemorrhage (PDH), which mimics uninterrupted arterial bleeding, was employed. It was found that (1) the substitution of dextran 70 for lactated Ringer's as isotonic fluid makes no difference in hemodynamic terms; (2) isochloremic hypertonic solutions are similar in their hemodynamic resuscitative effect, representing an improvement over hypertonic NaCl in terms of cardiac output, O2 delivery and O2 consumption; (3) HAD proved superior to HLD in terms of O2 consumption and correction of pH/base excess.

Acetates↗
PubMed1993

[Early hemodynamic effects of the rapid infusion of sodium chloride Dextran-70 hypertonic solution as treatment for hemorrhagic shock in dogs].

PURPOSE: To study the early hemodynamic effects of the rapid infusion of 7.5g/dl NaCl/ 6g/dl dextran-70 solution in dogs submitted to hemorrhagic shock. METHODS: Mongrel dogs were anesthetized with pentobarbital and a electromagnetic flowmeter probe was placed around the ascending aorta or the portal vein. By external bleeding the arterial pressure was lowered to 40mmHg and held for 30min. The animals received a 4ml/kg infusion of the hypertonic solution in 90s. Arterial blood pressure and flow were registered continuously during 3min and the derived hemodynamic variables were calculated at regular time intervals. RESULTS: The total plasma protein concentration decreased and the cardiac output showed a continuous elevation during the infusion. The arterial blood pressure showed two oscillations and then decreased during a short period of time. This moment was coincident with the initial increase of the portal flow and preceded the elevation of the systemic vascular resistance and the arterial pressure. CONCLUSION: The rapid infusion of hypertonic NaCl/dextran solution to dogs in hemorrhagic shock determines immediate and intense hemodynamic effects. During the infusion period there is volemic expansion and the cardiac output increases rapidly. The arterial pressure shows oscillations and decreases as a consequence of visceral arterial dilation before starting its final elevation that occurs as the vascular resistance increases.

Animals↗
PubMed1992

Physical and physiological characteristics of pressure-driven hemorrhage.

Research on hemorrhage has concentrated on its effects rather than the manner of occurrence. A new experimental method in which the rate of bleeding is a function of prevailing arterial pressure is proposed and described. The effects of standard crystalloid volume expansion and of small volume hypertonic treatment on this protocol are demonstrated. In pressure-driven hemorrhage, survival time and the decay of arterial pressure, cardiac output, oxygen consumption, and base excess are functions of the bleeding rate, but plasma proteins and hematocrits are independent. The decay of arterial pressure is also a complex function of blood volume deficit, but this relation is not dependent on the rate of blood removal. Volume expansion induces a recovery of circulatory function despite enhanced blood loss. A comparison between equiosmolar solutions of hypertonic sodium chloride and acetate shows that acetate produces a smaller pressor (hence less blood loss) but larger blood flow (hence higher O2 availability) effect. The possible importance of the isochloremic nature of the response to acetate is highlighted.

Acetates↗
PubMed1992

Acute hemodynamic effects of hypertonic (7.5%) saline infusion in patients with cardiogenic shock due to right ventricular infarction.

The hemodynamic effects, after infusion of 4 ml/kg of hypertonic (7.5%) saline solution (HS), were evaluated in six patients (mean age = 56.6 years) with cardiogenic shock (CS) due to right ventricular infarction (RVI). Basal condition data (mean +/- SEM) were as follows: cardiac index (CI) = 1.9 +/- 0.1 1/min/m2, arterial pressure (AP) = 66.5 +/- 0.9 mmHg, and systemic vascular resistance (SVR) = 31.3 +/- 1.0 mmHg/1/min/m2. Five- and 240-minute post-HS infusion data (respectively) revealed: CI = 3.3 +/- 0.1* and 2.9 +/- 0.1* 1/min/m2, AP = 87.7 +/- 1.6* and 80.7 +/- 2.2* mmHg, and SVR = 22.5 +/- 0.6* and 24.5 +/- 1.1* mmHg/1/min/m2 (*P less than 0.05 compared to baseline values). These data suggest that small-volume infusion of HS induced an important acute and sustained hemodynamic improvement in these patients with CS due to RVI.

Hemodynamics↗
PubMed1992

Pressure-driven hemorrhage: a new experimental design for the study of crystalloid and small-volume hypertonic resuscitation in anesthetized dogs.

Fifty pentobarbital anesthetized dogs were subjected to pressure driven hemorrhage (PDH) in which (a) an initial bleeding rate (25 ml/min) was set, and (b) reset min-to-min in proportion to prevailing mean arterial pressure (MAP). When blood loss reached 40 ml/kg, experimental time was set to zero and dogs were divided into five groups: (1) CTR (untreated controls); (2) HSD (NaCl 7.5%-Dextran70 6%, 6 ml/kg, at zero time); (3) LR (lactated Ringers, 25 ml/min from 0-60 min); (4) HSD-LR (combines HSD and LR); (5) DBL-HSD-LR (as HSD-LR, plus second HSD injection, 4 ml/kg, at 30 min). PDH was continued throughout the postresuscitation period. CTR dogs bled 55.5 +/- 2.1 ml/kg and survived to 34.7 +/- 5.0 min postzero; HSD dogs bled 78.6 +/- 2.0 ml/kg, and survived to 51.2 +/- 2.9 min with transient recovery of MAP, cardiac output (CO), and O2 availability (O2A); LR dogs bled 94.5 +/- 3.4 ml/kg and survived for over 60 min, with sustained, partial recovery of MAP, CO, and O2A. HSD-LR dogs bled 111.5 +/- 3.7 ml/kg and survived for over 60 min with improved hemodynamic and metabolic response. In DBL-HSD-LR dogs, the second HSD produced higher MAP, CO, and O2A, but hematocrit was lowered to a critical level. Thus, standard LR resuscitation is effective in PDH, in spite of increased blood loss; a single HSD lengthens survival when used alone and improves recovery when added to LR.

Anesthesia↗
PubMed1992

Effect of hypertonic sodium chloride (7.5%) on uncontrolled hemorrhage in rats and its interaction with different anesthetic procedures.

Small volumes (4-6 ml/kg) of hypertonic NaCl (7.5%, HS) have been shown to correct the hemodynamic alterations caused by severe blood loss, but it has been claimed that its use is detrimental to rats undergoing uncontrolled arterial bleeding. The interaction between uncontrolled hemorrhage and HS was reexamined in experiments performed on male Wistar rats anesthetized with neurolidol-ketamine (NK), pentobarbital (P), chloralose (C), or urethane (U), (n = 20 in each group), half of them treated with HS (4 ml/kg IV) 15 min after start of bleeding. Uncontrolled hemorrhage was induced by cutting the tail at 12% (T12%) or 50% (T50%) from its tip. NK induced large blood loss (T50%, 32.6 ml/kg; T12%, 16.2 ml/kg) and hypotension (T50%, 70 mmHg drop, T12%; 25 mmHg). Mortality was 3/10 (T50%) and 2/10 (T12%). HS produced a significant transient recovery of mean arterial pressure (MAP) and increased blood loss to 38.9 and 21.8 ml/kg for T50% and T12% respectively, but mortality was not significantly different (T50%, 5/10; T12%, 3/10). The other three anesthetics with a T50% cut produced mild blood loss and slight hypotension, unaffected by HS. Only three of 60 rats died under these anesthetics (two HS, one untreated). In a supplementary P-anesthetized group (P-MIMIC), blood was forcibly removed from a large artery to mimic the loss observed in the NK-T50% group. Hypotension and death rates in P-MIMIC (four HS, one control) were comparable to those observed in NK-T50%. It is concluded that the effects of NK are probably due to its powerful vasodilator effect, apparently sufficient to impede the normal vasoconstrictor response to shock.

Anesthesia↗
PubMed1992

Hypertonic NaCl solution prevents bupivacaine-induced cardiovascular toxicity.

The effects of various hypertonic solutions on the intraventricular conduction disturbances and on the cardiac arrhythmias caused by the intravenous (i.v.) injection of bupivacaine were studied in sodium pentobarbital anesthetized mongrel dogs. Bupivacaine was injected in 2 doses: 3.0 mg/kg and 6.5 mg/kg. Hypertonic solutions, given intravenously 5 minutes before bupivacaine, were 7.5% NaCl, 5.4% LiCl or 50% glucose (2,400 mOsm/l, 5 ml/kg), or 20% mannitol (1,200 mOsm/l, 10 ml/kg). The highest dose of bupivacaine induced severe cardiac arrhythmias and intraventricular conduction disturbances, as reflected by significant increases in QRS complex duration, HV interval and IV interval, as well as a severe hemodynamic impairment. Significant prevention against intraventricular conduction disturbances and ventricular arrhythmias was observed with 7.5% NaCl (QRS complex duration percent increase: 164 +/- 21% in the non pretreated group vs. 75 +/- 14% in the pretreated group, P less than .01; HV interval percent increase: 131 +/- 16% in the non pretreated group vs. 58 +/- 7% in the pretreated group, P less than .01; cardiac index percent decrease: 46 +/- 6% in the non pretreated group vs. 28 +/- 5% in the pretreated group, P less than .025). The three other hypertonic solutions were ineffective. These findings suggest an involvement of sodium ions in the mechanism of hypertonic protection.

Animals↗
PubMed1990

Central angiotensinergic system and hypertonic resuscitation from severe hemorrhage.

Single injections of 4 ml/kg hypertonic NaCl (7.5%) resuscitate dogs from severe blood loss (40-45 ml/kg). Mechanisms involve osmolarity-dependent volume expansion, increased myocardial contractility, and vasodilation. The role of central angiotensinergic pathways in the hemorrhage-hypertonic resuscitation interaction was investigated through experiments performed on male pentobarbital sodium-anesthetized dogs bled to, and held at, 40 mmHg for 30 min. Dogs were treated with 4 ml/kg of 7.5% NaCl or 32 of 0.9% NaCl iv preceded by intracerebroventricular (ICV) injections of 150 micrograms saralasin, 20 micrograms arginine vasopressin inhibitor (AVPI), or 10 micrograms morphine. ICV saralasin and morphine inhibited the full recovery response to hypertonic NaCl, whereas AVPI had no such effect. Saralasin did not inhibit the recovery from hemorrhagic shock produced by large volume isotonic saline reexpansion. These data demonstrate an interaction between the central angiotensin system and small volume hypertonic resuscitation from severe hemorrhagic shock but not between this central system and large volume isotonic reexpansion of circulatory volume. In contrast, the central vasopressinergic system does not appear to be similarly involved.

Angiotensin II↗
PubMed1990

Hypertonic saline resuscitation: saturated salt-dextran solutions are equally effective, but induce hemolysis in dogs.

Hypertonic saline, or saline-dextran resuscitation is normally achieved with an Na+ load of 4.8 to 7.2 mEq/kg given in a small volume (typically 4 to 6 ml/kg NaCl 7.5%). Na+ can also be administered saturated in a smaller volume, e.g., 1 to 1.5 ml/kg NaCl 25%, with similar results. Such reduction in administered volume would be an asset in prehospital trauma management. In the present experiments, severely bled (45 ml/kg) dogs were treated with one of three NaCl/dextran-70 solutions: S1, 25% NaCl + 24% dextran (1.5 ml/kg); S2, 15% NaCl + 14.4% dextran (2.5 ml/kg); S3, 7.5% NaCl + 6% dextran (5 ml/kg). S1, S2, and S3 were pump-infused in 10 min into a peripheral vein; S1 and S2 were also given into the right atrium. S1, S2, or S3 produced a number of similar responses irrespective of the route of administration; arterial pressure, cardiac index, and base excess reverted to near control levels, plasma Na+ was raised to 155-158 mEq/L, and 5-day survival was high and comparable. Plasma volume, and total and mean red cell volumes were similarly affected in all groups; however, peripheral injections of S1 and S2 induced severe hemolysis (plasma Hgb: 53 +/- 6 and 34 +/- 4 mg/dl, respectively), while right atrial S1 and S2 caused mild hemolysis (22 +/- 3 and 14 +/- 3 mg/dl, respectively). In contrast, S3 never induced hemolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Hypertonic and hyperoncotic resuscitation from severe hemorrhagic shock in dogs: a comparative study.

Single bolus injections of hypertonic (7.5%) NaCl (H), hyperoncotic (6%) dextran-70 (D), or of their combination (HD) were given to severely bled (54.2 +/- 1.3 ml/kg) anesthetized dogs. Two shock procedures (30 or 60 min at 35 mm Hg) were tested. Survival was highest (11/12) after HD, lower (9/12) after H, and lowest (7/12) after D; it was higher (15/18 vs. 12/18) after the shorter vs. longer shock procedure. Cardiac index (CI) was restored to 83%-104% of prehemorrhage levels immediately after HD or H; 3 h later it was down to 67%-71% of control; after D, CI was stable at 41% to 50% of control; no differences in the relative performances of the agents tested in the 30 or 60-min shock durations. Arterial pressure recovered to near control levels in all groups; consequently, systemic vascular resistance was reduced after H and HD, but increased after D. Plasma volume recovered to 95% of control after H, 105% of control after HD, but only to 80% after D; however, the response to H was transient. Metabolic acidosis was partially reverted by all solutions. Plasma Na+ was transiently raised by H and HD. Overall differences detected between H vs. HD tend to favor HD as a resuscitative solution.

Animals↗
PubMed1989

Hypertonic saline resuscitation is prevented by intracerebroventricular saralasin but not by captopril.

Hypertonic saline resuscitation (HR, 7.5% NaCl, 4 ml/kg) effectively reverts severe hemorrhage, but a central neural component is probably involved in the survival response. This experiment examines the role of central angiotensinergic pathways in hemorrhage-hypertonic resuscitation interaction. Severely bled (43 +/- 2 ml/kg) pentobarbital-anesthetized dogs with chronically implanted cerebral ventricular cannulae were resuscitated with 4 ml/kg 7.5% NaCl, iv 10 min after intracerebroventricular injection of 0.5 ml normal saline (CT), 150 micrograms saralasin (in 0.5 ml saline, SR), or 10 mg captopril (in 0.5 ml saline, CP). All 10 SR-treated dogs died 2-6 h after HR. Their arterial pressure and cardiac index initially recovered to near pre-hemorrhage levels, but gradually decreased thereafter, base excess remaining at severe metabolic acidosis levels throughout. All CT- and 8/10 CP-treated dogs survived indefinitely, with near normal arterial pressure, cardiac index and base excess levels. It is therefore concluded that the inhibition of central angiotensinergic sites with the competitive antagonist saralasin effectively prevents survival after HR, whereas inhibition of angiotensin converting enzyme by captopril in cerebrospinal fluid is virtually ineffective.

Animals↗
PubMed1989

Hypertonic NaCl antagonizes cardiac arrhythmia induced by bupivacaine.

We studied the effects of pretreatment with hypertonic solutions on the conduction disturbances and cardiac arrhythmias caused by iv injection of bupivacaine in anesthetized mongrel dogs. Bupivacaine was injected in doses of 3 mg/kg and 6.5 mg/kg. The hypertonic solutions used were: 7.5% NaCl, 5.4% LiCl, 50% Glucose (5 ml/kg) and 20% mannitol (10 ml/kg). Bupivacaine induced severe conduction disturbances, as reflected by significant increases in QRS complex duration, HV interval and IV interval, and severe hypotension. The arrhythmias observed were: sinus node dysfunction, nonsustained ventricular tachycardia, sustained ventricular tachycardia and ventricular fibrillation. These effects were dose dependent, and were more evident with the higher dose of bupivacaine. Among all the hypertonic solutions tested, only 7.5% NaCl effectively protected against conduction disturbances and cardiac arrhythmias. These findings suggest an important role for sodium overload in these situations and provide a potentially harmless tool for the treatment of anesthetic accidents with bupivacaine during regional anesthesia.

Animals↗
PubMed1987

Hyperosmotic sodium salts reverse severe hemorrhagic shock: other solutes do not.

Severe hemorrhage in pentobarbital-anesthetized dogs (25 mg/kg) is reversed by intravenous NaCl (4 ml/kg, 2,400 mosmol/l, 98% long-term survival). This paper compares survival rates and hemodynamic and metabolic effects of hypertonic NaCl with sodium salts (acetate, bicarbonate, and nitrate), chlorides [lithium and tris(hydroxymethyl)aminomethane (Tris)], and nonelectrolytes (glucose, mannitol, and urea) after severe hemorrhage (44.5 +/- 2.3 ml/kg blood loss). Sodium salts had higher survival rates (chloride, 100%; acetate, 72%; bicarbonate, 61%; nitrate, 55%) with normal stable arterial pressure after chloride and nitrate; near normal cardiac output after sodium chloride; normal acid-base equilibrium after all sodium salts; and normal mean circulatory filling pressure after chloride, acetate, and bicarbonate. Chlorides and nonelectrolytes produced low survival rates (glucose and lithium, 5%; mannitol, 11%; Tris, 22%; urea, 33%) with low cardiac output, low mean circulatory filling pressure, and severe metabolic acidosis. Plasma sodium, plasma bicarbonate, mean circulatory filling pressure, cardiac output, and arterial pressure correlated significantly with survival; other parameters, including plasma volume expansion or plasma osmolarity, did not. It is proposed that high plasma sodium is essential for survival.

Acetates↗