scholarly journals BLOOD PH CHANGES AND VENTRICULAR FIBRILLATION IN DEEP HYPOTHERMIA

1962 ◽  
Vol 43 (4) ◽  
pp. 453-458
Author(s):  
B. Malamos ◽  
S. Moulopoulos ◽  
K. Konstandinidis ◽  
E. Panayotopoulos ◽  
E. Paraschou
Keyword(s):  
Ventricular Fibrillation ◽  
Deep Hypothermia ◽  
Ph Changes ◽  
Blood Ph

Effects of blood pH changes on potassium excretion in the dog

1962 ◽  
Vol 202 (4) ◽  
pp. 768-772 ◽  
Author(s):  
Charles Toussaint ◽  
Pierre Vereerstraeten
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Distal Tubule ◽  
Potassium Excretion ◽  
Ph Changes ◽  
Blood Ph ◽  
Ph Level

K+ excretion rate was measured at normal as well as at rising plasma K+ concentration in intact, in K-depleted, and in acetazolamide-treated dogs submitted to acute blood pH changes. The results indicate that, for any given value of glomerular filtration rate, K+ excretion rate is determined by at least three factors: 1) plasma K+ concentration, 2) blood pH level, and 3) presumably, the H+ gradient across the luminal border of the distal tubule. The data further suggest that most of the filtered K+ is reabsorbed by the proximal tubule, even in conditions of high filtered loads.

Responses of trout gill ion transport systems to acute acidosis

1976 ◽  
Vol 64 (2) ◽  
pp. 511-515
Author(s):  
T. H. Kerstetter ◽  
R. Mize
Keyword(s):  
Lactic Acid ◽  
Rainbow Trout ◽  
Ion Transport ◽  
Ion Uptake ◽  
Transport Systems ◽  
Ph Changes ◽  
Blood Ph ◽  
Slow Infusion ◽  
Trout Gill

The response of rainbow trout Na+ and Cl- uptake systems to acute acidosis was tested by slow infusion of lactic acid into anaesthetized animals. Depression of blood pH by 0–4 pH unit had no effect on influx rates for either ion, and we conclude that gill ion uptake systems do not respond rapidly to blood pH changes.

Deep hypothermia in the cat

1959 ◽  
Vol 196 (2) ◽  
pp. 354-356 ◽  
Author(s):  
Arthur F. Battista
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Body Temperature ◽  
Deep Hypothermia ◽  
Critical Parameters ◽  
Large Animal ◽  
Carbon Dioxide Concentrations ◽  
Adult Cats ◽  
Body Cooling

Sixteen adult cats were cooled, using the method of hypercapnia and hypoxia. Seven cats died during the cooling or warming period due to irreversible ventricular fibrillation or cardiac arrest. Nine cats survived and the lowest body temperature obtained was 12.5°C. The rate of body cooling and the oxygen and carbon dioxide concentrations were critical parameters difficult to control in a large animal such as the cat.

An iridium-iridium oxide electrode forin vivomonitoring of blood pH changes

1981 ◽  
Vol 5 (2) ◽  
pp. 86-87 ◽  
Author(s):  
G. Papeschi ◽  
S. Bordi ◽  
M. Carlà ◽  
L. Criscione ◽  
F. Ledda
Keyword(s):  
Iridium Oxide ◽  
Oxide Electrode ◽  
Ph Changes ◽  
Blood Ph

Adverse postresuscitation myocardial effects elicited by buffer-induced alkalemia ameliorated by NHE-1 inhibition in a rat model of ventricular fibrillation

2016 ◽  
Vol 121 (5) ◽  
pp. 1160-1168 ◽  
Author(s):  
Lorissa Lamoureux ◽  
Jeejabai Radhakrishnan ◽  
Thomas G. Mason ◽  
Jeffrey A. Kraut ◽  
Raúl J. Gazmuri
Keyword(s):  
Ventricular Fibrillation ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Spontaneous Circulation ◽  
Male Rats ◽  
Intracellular Acidosis ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Return Of Spontaneous Circulation ◽  
Blood Ph

Major myocardial abnormalities occur during cardiac arrest and resuscitation including intracellular acidosis—partly caused by CO2 accumulation—and activation of the Na+-H+ exchanger isoform-1 (NHE-1). We hypothesized that a favorable interaction may result from NHE-1 inhibition during cardiac resuscitation followed by administration of a CO2-consuming buffer upon return of spontaneous circulation (ROSC). Ventricular fibrillation was electrically induced in 24 male rats and left untreated for 8 min followed by defibrillation after 8 min of cardiopulmonary resuscitation (CPR). Rats were randomized 1:1:1 to the NHE-1 inhibitor zoniporide or vehicle during CPR and disodium carbonate/sodium bicarbonate buffer or normal saline (30 ml/kg) after ROSC. Survival at 240 min declined from 100% with Zoniporide/Saline to 50% with Zoniporide/Buffer and 25% with Vehicle/Buffer ( P = 0.004), explained by worsening postresuscitation myocardial dysfunction. Marked alkalemia occurred after buffer administration along with lactatemia that was maximal after Vehicle/Buffer, attenuated by Zoniporide/Buffer, and minimal with Zoniporide/Saline [13.3 ± 4.8 (SD), 9.2 ± 4.6, and 2.7 ± 1.0 mmol/l; P ≤ 0.001]. We attributed the intense postresuscitation lactatemia to enhanced glycolysis consequent to severe buffer-induced alkalemia transmitted intracellularly by an active NHE-1. We attributed the worsened postresuscitation myocardial dysfunction also to severe alkalemia intensifying Na+ entry via NHE-1 with consequent Ca2+ overload injuring mitochondria, evidenced by increased plasma cytochrome c. Both buffer-induced effects were ameliorated by zoniporide. Accordingly, buffer-induced alkalemia after ROSC worsened myocardial function and survival, likely through enhancing NHE-1 activity. Zoniporide attenuated these effects and uncovered a complex postresuscitation acid-base physiology whereby blood pH drives NHE-1 activity and compromises mitochondrial function and integrity along with myocardial function and survival.

Effect of temperature and hydric conditions on blood pH in embryonic snapping turtles (Chelydra serpentina)

1990 ◽  
Vol 68 (1) ◽  
pp. 190-193 ◽  
Author(s):  
Geoffrey F. Birchard ◽  
Mary J. Packard ◽  
Gary C. Packard
Keyword(s):  
Partial Pressure ◽  
Water Potential ◽  
Pure Water ◽  
Effect Of Temperature ◽  
Chelydra Serpentina ◽  
Blood Samples ◽  
Ph Changes ◽  
Blood Ph ◽  
Snapping Turtles ◽  
Increasing Temperature

The effect of temperature on blood pH in embryonic snapping turtles (Chelydra serpentina) was examined to determine whether the blood pH changes in the same manner as the neutral pH of pure water. Eggs were incubated on moistened vermiculite (water potential of −150 or −950 kPa) at 26 or 27 °C. On day 59 of incubation, eggs were placed in individual containers and assigned to incubators set at temperatures between 18.5 and 30 °C. Blood samples were taken on day 60 of incubation. Blood pH of the embryos varied in a manner similar to that observed in adults of this species: blood pH declined with increasing temperature, with a slope of −0.021 pH/°C. The decrease of blood pH with increasing temperature may be accomplished passively, with blood CO2 partial pressure increasing as a result of greater metabolic production of CO2 while the diffusive excretion of this gas remains relatively constant. No effect of substrate water potential on blood pH was observed.

Plasma and erythrocyte Na, K, Cl and water in hypothermic and hyperthermic dogs

1959 ◽  
Vol 197 (3) ◽  
pp. 648-652 ◽  
Author(s):  
G. B. Spurr ◽  
George Barlow
Keyword(s):  
Body Temperature ◽  
Water Content ◽  
Extracellular Fluid ◽  
Red Cells ◽  
Red Cell ◽  
Cell Water ◽  
Ph Changes ◽  
Blood Ph

Plasma and erythrocyte Na, K, Cl and water have been determined in hyperventilated dogs cooled to 25°C for periods up to 4 hours, in animals heated to either 41.5°C or 42.5°C for 1 hour and in hyperventilated-normothermic dogs. The induced respiratory alkalemia in both normothermic and hypothermic animals appeared to result in a shift of Na from plasma into red cells. Plasma K was reduced in both normothermic and hypothermic dogs, whereas a K elevation in erythrocytes occurred only in the normothermic animals following hyperventilation. Erythrocyte K remained unchanged in hypothermia. It seems, therefore, that the fall in plasma K which occurs in alkalemic normothermic dogs is due partially to a movement of K into red cells whereas, in hypothermia the K leaving extracellular fluid enters cells other than erythrocytes. The plasma and red cell electrolyte changes observed in the two hyperthermic groups of dogs were all in the direction of an increase. It is concluded that these changes were primarily the result of the increased body temperature and of consequent reductions in plasma and red cell water content, rather than the result of the blood pH changes associated with hyperthermia.

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