Significance of the callicrein-callidinogen-callidin system in shock

1959 ◽  
Vol 197 (2) ◽  
pp. 406-412 ◽  
Author(s):  
Marion E. Webster ◽  
William R. Clark
Keyword(s):  
Synergistic Effect ◽  
Hemorrhagic Shock ◽  
Intravenous Infusion ◽  
Hypotensive Effect ◽  
Enzymatic Action ◽  
Normal Plasma ◽  
Fractionation Procedure ◽  
The Many

Previous investigators have shown that intravenous infusion of partially purified urinary callicrein would reproduce the many features of the shock syndrome. However, infusion of either pancreatic or urinary callicrein prepared by an ethanolic fractionation procedure failed to kill the dogs even when it was given in amounts nine times that previously reported to be toxic. Investigations directed towards the identification of the toxin as measured by earlier studies suggested that a combination of endotoxin and callicrein may have been responsible for the reported lethality. Callicrein is presumed to exert its hypotensive effect by enzymatic action on callidinogen, present in normal plasma, by effecting the release of a polypeptide called callidin. Measurement of the callidinogen content of plasma of dogs killed with endotoxin or by irreversible hemorrhagic shock indicated that small amounts of callicrein may have been released and that these quantities might thus contribute to the death of the animal. The possible synergistic effect and relationship between endotoxin, callicrein and plasmin are discussed.

Plasma K plus and insulin: changes during KCl infusion in normal and nephrectomized dogs

1975 ◽  
Vol 228 (1) ◽  
pp. 107-109 ◽  
Author(s):  
GW Pettit ◽  
RL Vick ◽  
AM Swander
Keyword(s):  
Potassium Chloride ◽  
Intravenous Infusion ◽  
Plasma Insulin ◽  
Simultaneous Measurements ◽  
Normal Plasma ◽  
Arterial Plasma ◽  
Homeostatic Response

Potassium chloride was administered by constant, intravenous infusion in splenectomized, but otherwise normal, dogs. The concentration of potassium, [K+], and of insulin, [insulin], in the arterial plasma was measured at frequent intervals. To assess the relative contributions of extrarenal and renal mechanisms toward the maintenance of normal plasma [K+], the results were compared with data obtained previously in splenectomized, nephrectomized dogs. During the infusion, plasma [K+] increased in the dogs with kidneys intact at a mean rate slightly less than that in the nephrectomized dogs. After the infusion was stopped, plasma [K+] declined to about 0.75 meq/liter above control values in both groups of animals. The results indicate the operation of both renal and extrarenal homoeostatic mechanisms. The renal mechanisms contributed measurably during the infusion of KCl, but not immediately after the infusion was stopped. Simultaneous measurements of plasma [K+] and plasma [insulin] indicate that insulin may be involved in the extrarenal homeostatic response.

THE EFFECT OF NORADRENALINE ON THE SURVIVAL OF RATS SUBJECTED TO HEMORRHAGIC SHOCK

1957 ◽  
Vol 35 (1) ◽  
pp. 93-101 ◽  
Author(s):  
A. M. Lansing ◽  
J. A. F. Stevenson ◽  
C. W. Gowdey
Keyword(s):  
Survival Rate ◽  
Hemorrhagic Shock ◽  
Survival Time ◽  
Intravenous Infusion ◽  
Survival Rates ◽  
Distilled Water ◽  
Sprague Dawley ◽  
Chi Square ◽  
Sprague Dawley Rats ◽  
Chi Square Test

Reports of the efficacy of l-noradrenaline in the treatment of clinical shock stimulated an investigation of its effect in controlled hemorrhagic hypotension. Seventy-three 350-g. male Sprague–Dawley rats were subjected to a standardized hemorrhagic shock procedure. Of 15 control animals that received no treatment, only one survived for 48 hours; none survived of the five controls that received a constant intravenous infusion, after the shock procedure, of 5% glucose in distilled water until death or for 36 hours. The treated animals received, after the shock procedure, an infusion of l-noradrenaline (0.5–2.0 μg./min.) in 5% glucose in distilled water. The survival rates for the treated animals were: treatment for 1 hour, 1/8; treatment for 4 hours, 4/15; treatment until death or for 36 hours, 8/15. Fifteen animals received, in addition to noradrenaline for 36 hours, hydrocortisone administered intravenously (0.7 μg./min.) or intramuscularly (2.5 mg. every 6 hours); seven of these animals survived.Analysis of variance showed that there was no difference in the shock procedure undergone by the controls and by the treated survivors. The Chi square test on the survival rates revealed that the infusion of noradrenaline for 1 hour or 4 hours did not improve survival, but infusion for 36 hours produced a very significant increase in survival time and in total survival rate. The addition of hydrocortisone neither enhanced nor impaired this improvement.

Effects of blockade of brain angiotensin II receptors in conscious, sodium-deprived dogs

1983 ◽  
Vol 245 (6) ◽  
pp. R881-R887 ◽  
Author(s):  
V. L. Brooks ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Intravenous Infusion ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Similar Degree ◽  
Central Action ◽  
Ang Ii ◽  
Sodium Deficiency ◽  
Low Sodium Diet

The present studies were designed to evaluate the physiological significance of the actions of angiotensin II (ANG II) on the brain. The effects of blockade of brain ANG II receptors by intracarotid or intravertebral infusions of saralasin were studied in conscious dogs with high circulating ANG II levels (142 +/- 16 pg/ml) due to a low-sodium diet. Three doses of saralasin were infused into each pair of arteries and intravenously: 0.1, 0.3, and 1.0 micrograms X kg-1 X min-1. Saralasin produced dose-related decreases in arterial pressure during infusion into the carotid or vertebral arteries, confirming that ANG II maintains arterial pressure during sodium deficiency. However, intravenous saralasin administration decreased pressure to a similar degree, suggesting that the hypotensive effect was due to recirculation of saralasin, rather than to blockade of a central action of circulating ANG II. Heart rate was not altered by infusion of saralasin by any route. Saralasin administration also caused a dose-dependent increase in plasma renin activity and plasma ANG II concentration. However, because the increases produced by intracarotid or intravertebral saralasin did not differ from the increase produced by intravenous infusion, these results do not provide evidence that renin release is modulated by a central action of ANG II during sodium deficiency. Plasma corticosteroid levels were reduced (2.4 +/- 0.5 to 1.4 +/- 0.2 micrograms/dl, P less than 0.05) by intravenous infusion of the highest dose of saralasin, but neither intracarotid nor intravertebral saralasin infusion altered plasma corticosteroid concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral blood epinephrine levels in dogs during intravenous infusion

1958 ◽  
Vol 196 (1) ◽  
pp. 145-148 ◽  
Author(s):  
T. R. Poole ◽  
D. T. Watts
Keyword(s):  
Hemorrhagic Shock ◽  
Blood Level ◽  
Peripheral Blood ◽  
Intravenous Infusion ◽  
Maximum Concentration ◽  
Infusion Rate ◽  
Venous Blood ◽  
Blood Levels ◽  
Arterial Blood ◽  
Epinephrine Concentration

Femoral arterial and venous blood epinephrine levels were followed in dogs during the infusion of l-epinephrine at rates of 1.25–10 µg (as the base)/kg/min. for periods of 37–197 minutes. The epinephrine concentration in arterial blood rose from control values of less than 1 µg/l., the lowest concentration that could be estimated, to levels of 8.5, 19, 75 and 201 µg/l. at infusion rates of 1.25, 2.5, 5 and 10 µg/kg/min., respectively. For these same infusion rates, the simultaneously determined venous blood levels were 7.8, 10, 27 and 70 µg/l., respectively. By extrapolation, these data show that at an infusion rate of 3.4 µg/kg/min., the lowest rate known to produce shock in dogs, the arterial blood level was 39 µg/l. This is approximately twice the maximum concentration of 20.6 µg/l. of endogenously released epinephrine observed during hemorrhagic shock in dogs.

Combining Laser Resurfacing and Facial Rejuvenation Surgery

2021 ◽  
Vol 37 (02) ◽  
pp. 233-239
Author(s):  
Jill L. Hessler ◽  
Oscar Trujillo
Keyword(s):  
Synergistic Effect ◽  
Clinical Results ◽  
Facial Rejuvenation ◽  
Candidate Selection ◽  
Volume Loss ◽  
Facial Aging ◽  
Laser Resurfacing ◽  
Skin Laxity ◽  
Surgical Interventions ◽  
The Many

AbstractFacial aging is a multifactorial process involving skin laxity, volume loss, facial rhytids and solar elastosis. Surgical interventions can address the laxity of the skin and restore volume loss but do not fully correct the texture of the skin. Historically, there were concerns over the safety of combining laser resurfacing with facelifting procedures, but now there is much evidence to support the safe use of this combination treatment. When done appropriately, the combination of laser resurfacing with facial rejuvenation surgery can provide a synergistic effect for optimal clinical results. Here, we review the many laser options available and how they may be combined safely with surgical facial rejuvenation. We also review clinical contexts and candidate selection to provide safe, reliable results and minimize complications.

The Development of Total Parenteral Nutrition

2017 ◽  
Vol 83 (1) ◽  
pp. 36-38 ◽  
Author(s):  
Don K. Nakayama
Keyword(s):  
Small Bowel ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Intravenous Infusion ◽  
Circulatory System ◽  
The Body ◽  
University Of Pennsylvania ◽  
Glucose Plasma ◽  
The Many ◽  
Infant Girl

The first patient to receive complete nourishment of a patient by intravenous infusion independent of the alimentary tract was an infant girl born with near-total small bowel atresia. Total parenteral nutrition, the intravenous infusion of nutrients, has been attempted since Harvey's description of the circulatory system in the early 17th century. The modern era of parenteral nutrition began in the early 20th century, when infusions of glucose, plasma, and emulsified fat into humans proved feasible. Robert Elman, working in the 1930s and 1940s, demonstrated that carefully prepared protein hydrolysates could be safely infused intravenously and incorporated by the body. Stanley Dudrick and Douglas Wilmore, surgeon researchers at the University of Pennsylvania, worked through the many details of preparation, administration, and clinical monitoring in beagle puppies before testing them on adult patients malnourished from a variety of surgical complications and gastrointestinal conditions. They applied their techniques and formulations on a newborn wasting away from congenital absence of the small bowel, the baby growing and developing for several months while being nourished completely by total parenteral nutrition. Their techniques, inspired by patients with progressive malnutrition from devastating intestinal conditions and malformations, form the basis of the practice of intravenous nutrition practiced today.

Treatment of Hemorrhagic Shock with Intraosseous or Intravenous Infusion of Hypertonic Saline Dextran Solution

1991 ◽  
Vol 23 (2) ◽  
pp. 123-129 ◽  
Author(s):  
A.C. Chávez-Negrete ◽  
Majluf Cruz ◽  
Frati Munari ◽  
A. Perches ◽  
R. Argüero
Keyword(s):  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Intravenous Infusion ◽  
Dextran Solution

THE EFFECT OF NORADRENALINE ON THE SURVIVAL OF RATS SUBJECTED TO HEMORRHAGIC SHOCK

1957 ◽  
Vol 35 (1) ◽  
pp. 93-101 ◽  
Author(s):  
A. M. Lansing ◽  
J. A. F. Stevenson ◽  
C. W. Gowdey
Keyword(s):  
Survival Rate ◽  
Hemorrhagic Shock ◽  
Survival Time ◽  
Intravenous Infusion ◽  
Survival Rates ◽  
Distilled Water ◽  
Sprague Dawley ◽  
Chi Square ◽  
Sprague Dawley Rats ◽  
Chi Square Test

Reports of the efficacy of l-noradrenaline in the treatment of clinical shock stimulated an investigation of its effect in controlled hemorrhagic hypotension. Seventy-three 350-g. male Sprague–Dawley rats were subjected to a standardized hemorrhagic shock procedure. Of 15 control animals that received no treatment, only one survived for 48 hours; none survived of the five controls that received a constant intravenous infusion, after the shock procedure, of 5% glucose in distilled water until death or for 36 hours. The treated animals received, after the shock procedure, an infusion of l-noradrenaline (0.5–2.0 μg./min.) in 5% glucose in distilled water. The survival rates for the treated animals were: treatment for 1 hour, 1/8; treatment for 4 hours, 4/15; treatment until death or for 36 hours, 8/15. Fifteen animals received, in addition to noradrenaline for 36 hours, hydrocortisone administered intravenously (0.7 μg./min.) or intramuscularly (2.5 mg. every 6 hours); seven of these animals survived.Analysis of variance showed that there was no difference in the shock procedure undergone by the controls and by the treated survivors. The Chi square test on the survival rates revealed that the infusion of noradrenaline for 1 hour or 4 hours did not improve survival, but infusion for 36 hours produced a very significant increase in survival time and in total survival rate. The addition of hydrocortisone neither enhanced nor impaired this improvement.

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