Biomedical subjects

R Prist

Publications and source records attributed to R Prist.

4 recordsLinked to original sources

PubMed1994

A quantitative analysis of transcapillary refill in severe hemorrhagic hypotension in dogs.

In pressure-driven hemorrhage (PDH), where the rate of bleeding is a function of prevailing arterial pressure, survival time, arterial pressure, cardiac output, oxygen consumption, and base excess are functions of initial bleeding rate. The quantitative rate of transcapillary refill (TR) throughout PDH leading to death was determined in splenectomized dogs, through serial analysis of Cr51-tagged red cell dilution. Mild, moderate, and severe levels of PDH were produced by varying initial bleeding rate (10, 25, and 50 ml/min, respectively). The rate of TR is a function of the severity of PDH, but does not correlate with arterial pressure, cardiac output, or systemic resistance. The volume of transferred fluid represents an ever increasing fraction of total plasma volume, and accounts for more than 75% of plasma volume in preterminal stages of shock. TR sustains a relatively fixed level of plasma volume, equivalent to two-third of the initial plasma volume, irrespective of the rate of bleeding. Hypertonic NaCl (7.5%) enhances TR, while isotonic NaCl reverses it.

Animals↗

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↗

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

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↗