Vasopressin Deficiency and Pressor Hypersensitivity In Hemodynamically Unstable Organ Donors

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Jonathan M. Chen ◽  
Suzanne Cullinane ◽  
Talia B. Spanier ◽  
John H. Artrip ◽  
Ranjit John ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diabetes Insipidus ◽  
Low Dose ◽  
Clinical Evidence ◽  
Pressor Response ◽  
Hemodynamic Instability ◽  
Solid Organ ◽  
Organ Donors ◽  
Plasma Vasopressin ◽  
Before And After

Background —Solid organ donors often develop hypotension due to vasodilation, and recently we observed that a variety of vasodilatory states are characterized by vasopressin deficiency and hypersensitivity. Thus, we investigated the prevalence of vasopressin deficiency in hypotensive solid organ donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect of vasopressin replacement in hypotensive donors. Methods and Results —Fifty organ donors were evaluated for hemodynamic instability, (mean arterial pressure [MAP]≤ 70 mm Hg despite the use of catecholamine vasopressors), and in those unstable donors who were not already receiving exogenous vasopressin, low-dose vasopressin was administered as a continuous infusion (0.04 to 0.1 U/min). MAP, catecholamine requirements, serum vasopressin, and serum osmolality were obtained before and after vasopressin administration. Ten patients meeting the enrollment criteria received vasopressin and MAP increased from 72.2±3.5 to 89.8±4.2 mm Hg, ( P <0.05), allowing for complete discontinuation of catecholamine pressors in 4 (40%) patients and a decrement in pressor dose in 4 (40%). Plasma vasopressin levels (2.9±0.8 pg/mL) were low for the degree of hypotension. Conclusions —Hemodynamically unstable organ donors without clinically apparent diabetes insipidus display a defect in the baroreflex-mediated secretion of vasopressin. In these patients, low-dose vasopressin significantly increases blood pressure with a pressor response sufficient to reduce catecholamine administration.

Blood Pressure Responses to Epinephrine in the Etherized Dog, Before and After Baroreceptor Denervation

1956 ◽  
Vol 186 (1) ◽  
pp. 71-73 ◽  
Author(s):  
James G. Hilton ◽  
Robert V. Brown
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Dosage Level ◽  
Control Blood Pressure ◽  
Before And After ◽  
The Difference ◽  
Blood Pressure Responses ◽  
Peak Blood

Experiments were performed on dogs anesthetized with ether to determine the effects of denervation of the baroreceptors upon the blood pressure responses to graded doses of epinephrine. The results of these experiments show that the denervation procedures do not significantly affect the peak blood pressure attained or the duration of the rise in blood pressure resulting from doses of epinephrine. Denervation of the baroreceptors elevated the level of the control blood pressure and reduced the height of the pressor response significantly. At all but the 10.0 µg/kg dosage level the difference in the pressor response could be accounted for by the difference in the control blood pressure.

scholarly journals Low-dose plasmid DNA treatment increases plasma vasopressin and regulates blood pressure in experimental endotoxemia

2012 ◽  
Vol 13 (1) ◽  
pp. 59 ◽  
Author(s):  
Thiago Malardo ◽  
Marcelo E Batalhão ◽  
Ademilson Panunto-Castelo ◽  
Luciana P Almeida ◽  
Everton Padilha ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasmid Dna ◽  
Low Dose ◽  
Experimental Endotoxemia ◽  
Plasma Vasopressin

Pressor responses to vasopressin in pigs and sheep with DOCA hypertension

1989 ◽  
Vol 256 (1) ◽  
pp. H101-H104
Author(s):  
W. D. Ling ◽  
D. P. Brooks ◽  
J. T. Crofton ◽  
L. Share ◽  
D. F. Bohr
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Intake ◽  
Pressor Response ◽  
Dietary Sodium ◽  
Normal Blood Pressure ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Pressor Responses ◽  
Dose Dependent

Pressor responses to vasopressin were determined in pigs and sheep during three experimental periods: 1) before deoxycorticosterone acetate (DOCA) treatment, 2) 21 days after DOCA implantation (100 mg/kg) when a stable hypertension had developed, and 3) after reversal of the hypertension by removing the implant in the sheep or by decreasing the dietary sodium intake in the pigs. The infusion of lysine (LVP) or arginine (AVP) vasopressin into pigs and sheep, respectively, resulted in dose-dependent increases in plasma vasopressin concentration. The levels of plasma LVP or AVP achieved by these infusions were not altered in any of the experimental periods. The administration of vasopressin resulted in dose-dependent increases in mean arterial blood pressure. However, pigs required five times more LVP than sheep required AVP to achieve similar pressor responses. The pressor responsiveness to vasopressin was attenuated when either species was made hypertensive. This effect was reversed when normal blood pressure was restored by reducing sodium intake in the pigs or by removing the DOCA implant from the sheep. These data establish that an increased pressor response to vasopressin does not contribute to DOCA hypertension in pigs or sheep.

Inhibition of plasma vasopressin after drinking in dehydrated humans

1984 ◽  
Vol 247 (6) ◽  
pp. R968-R971 ◽  
Author(s):  
G. Geelen ◽  
L. C. Keil ◽  
S. E. Kravik ◽  
C. E. Wade ◽  
T. N. Thrasher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Volume ◽  
Arginine Vasopressin ◽  
Tap Water ◽  
Renin Activity ◽  
Plasma Vasopressin ◽  
Rapid Fall ◽  
Before And After ◽  
Plasma Arginine

To study the effects of nonosmotic and nonvolumetric factors that may influence secretion of vasopressin, serum Na+, K+, and osmolality (Osm), hemoglobin, hematocrit, plasma arginine vasopressin (AVP), aldosterone (PA), and renin activity (PRA) were measured in five men and three women (26–50 yr, 73 +/- 4 kg) before and after 24 h of mild dehydration (food but no fluid) and seven times during the 1st h after rehydration with 10 ml/kg of tap water (17.5 +/- 0.5 degrees C) consumed in 105 s (range 35-240 s). Dehydration increased mean serum Na+ 3.7 +/- 0.7 meq/l (P less than 0.05), osmolality 9.1 +/- 1.1 mosmol/kg (P less than 0.05), and AVP from a hydrated level of 1.7 +/- 0.2 to 3.3 +/- 0.5 pg/ml (delta = 1.6 pg/ml, P less than 0.05). After rehydration AVP fell to 2.4 +/- 0.3 pg/ml (P less than 0.05) within 3 min and reached the water-replete level of 1.8 +/- 0.3 pg/ml 9 min after drinking started. Serum Na+ and Osm did not change until 30–60 min after drinking. No significant changes occurred in PRA, hemogloblin, hematocrit, or calculated delta in plasma volume, but PA increased from 11.1 +/- 1.5 ng/dl after dehydration to 15.6 +/- 2.6 ng/dl (P less than 0.05) between 30 and 60 min after drinking. The rapid fall in plasma AVP after rehydration took place in the absence of the expected changes in the primary regulators of plasma AVP (i.e., osmolality and plasma volume), with no change in blood pressure. The results suggest that oropharyngeal factors, alone or combined with gastric stimuli, are implicated.

THE FIBRINOLYTIC, FACTOR VIII:C, VON WILLEBRAND FACTOR AND HEMODYNAMIC RESPONSES TO DDAVP IN PATIENTS WITH HEREDITARY NEPHROGENIC DIABETES INSIPIDUS

1987 ◽  
Author(s):  
K BRINK ◽  
F DERKX ◽  
E BROMMER ◽  
J STIBBE ◽  
H KOLSTEE ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Pressor Response ◽  
Receptor Activation ◽  
Plasma Noradrenaline ◽  
Tissue Type ◽  
Hemodynamic Responses ◽  
Calcium Dependent ◽  
V2 Receptor

The pressor response of vasopressin (AVP) is mediated by a calcium-dependent mechanism (VI-receptor), whereas its antidiuretic effect depends on c-ANP (V2-receptor). DDAVP (1-desamino-8-D-arginine vasopressin) is a synthetic V2 analog of AVP. AVP and DDAVP also increase FVIII:C vWF:Ag and tissue-type plasminogen activator (t-PA) in plasma. The mechanism by which AVP and DDAVP elevate these factors is unclear. Patients with X-linked nephrogenic diabetes insipidus (NDI) are resistant to the V2-mediated antidiuretic action of AVP and DDAVP. We therefore have studied the effect of DDAVP (0.4 ug/kg iv infusion in 10 min) in 2 brothers with NDI, their mother and an unrelated patient.In control subjects (n=12) FVIII:C rose 122 (6) % ,mean (SEM), vWF:Ag 104 (4) % and t-PA 115 (7) % over basal levels. This rise was associated with a fall in diascolic blood pressure -11 (3) mmHg and an increase in heart rate from 62 (4) to 91 (5) bpm. Plasma noradrenaline rose from 262 (34) to 590 (84) pg/ml and renin from 16 (3) to 42 (6) uU/ml. Ten out of 12 controls showed facial flusning. The patients with NDI had normal basal FVIII:C, vWF:Ag and t-PA levels. Plasma noradrenaline and renin were within the nor mam range. Tne patients with NDI were also resistant to the stimulatory effect of DDAVP on the release of FVIII:C, vWF:Ag and t-PA. They also showed no change in blood pressure, nearc rate, plasma noradrenaline and renin and had no facial flushing. The carrier had normal responses to DDAVP.Tne increase in FVII:C, vWF:Ag and t-PA and the hemodynamic responses after DDAVP infusion probably appear to depend on extrarenal V2-receptor activation. DDAVP cannot be used in identifying carriers in families at risk.

Effects of Graded Doses of Epinephrine and of Norepinephrine on Blood Pressure Before and After Total Spinal Anesthesia

1956 ◽  
Vol 186 (2) ◽  
pp. 289-293 ◽  
Author(s):  
James G. Hilton ◽  
Shelby C. Reid
Keyword(s):  
Blood Pressure ◽  
Spinal Anesthesia ◽  
Pressor Response ◽  
Procaine Hydrochloride ◽  
Spinal Level ◽  
Response Curves ◽  
Total Spinal Anesthesia ◽  
Before And After ◽  
Higher Doses ◽  
Intraspinal Injection

Experiments have been carried out on dogs anesthetized with pentobarbital sodium to determine the effects of loss of all reflexes at the spinal level upon the responses to graded doses of epinephrine and norepinephrine. Total loss of reflexes was achieved by intraspinal injection of 2% procaine hydrochloride. The results of this study showed that in both the epinephrine and norepinephrine series of animals the maximum to which the blood pressure would rise was significantly lower after total spinal anesthesia than before. The actual rise in blood pressure was significantly greater at the higher doses tested after total spinal anesthesia. At the lower doses tested the differences between responses before and after total spinal anesthesia were slight and not significant. In all cases where there was a pressor response the duration of the pressor response was longer after total spinal anesthesia. In both the epinephrine and norepinephrine series of animals the differences in duration of pressor response reached an approximately constant value at the higher dosage levels. The dose-response curves were derived for each animal and the parameters were compared. The parameter a which has been defined as the theoretical maximum pressor response was significantly greater in both the epinephrine and the norepinephrine animals after spinal anesthesia. This was the only parameter significantly affected by the total spinal anesthesia.

A proposed mechanism for epinephrine potentiation by ganglionic blocking agents

1962 ◽  
Vol 203 (4) ◽  
pp. 753-757 ◽  
Author(s):  
James G. Hilton
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Nervous Activity ◽  
Blocking Agents ◽  
Receptor Sites ◽  
Before And After ◽  
Autonomic Blockade ◽  
Blood Pressures ◽  
Blood Pressure Responses ◽  
Ganglionic Blocking

The blood pressure responses elicited by the injection of 1.0, 5.0, and 10.0 µg/kg of epinephrine were studied before and after blockade of autonomic nervous activity by either ganglionic blocking agents or by total spinal anesthesia. After blockade, blood pressure levels of 100, 130, and 160 mm Hg were maintained by infusion of epinephrine. The results of these studies showed that the pressor responses elicited were inversely related to the level of the maintained blood pressure and that the maximum attained blood pressures did not change markedly with the various maintained blood pressures. In the series of animals treated with ganglionic blocking agents, the maximum blood pressures were approximately the same before and after blockade but in the total spinal anesthetized animals these pressures were approximately 30 mm Hg lower after blockade. It was postulated from these results that autonomic blockade produces an apparent potentiation of epinephrine pressor response not by sensitization of the reacting structures but by lowering the level of catecholamines available to the receptor sites and shifting the dose-response curve to the left.

Effects of angiotensin II on autonomic components of nasopharyngeal stimulation in male conscious rabbits

2005 ◽  
Vol 98 (5) ◽  
pp. 1607-1611 ◽  
Author(s):  
Tarek M. Mousa ◽  
Lie Gao ◽  
Kurtis G. Cornish ◽  
Irving H. Zucker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Cigarette Smoke ◽  
Pressor Response ◽  
Sympathetic Neurons ◽  
Cardiovascular Responses ◽  
Ang Ii ◽  
Before And After ◽  
Conscious Rabbits

Angiotensin II (ANG II) is known to activate central sympathetic neurons. In this study we determined the effects of ANG II on the autonomic components of the cardiovascular responses to stimulation of nasopharyngeal receptors with cigarette smoke. Experiments were carried out in conscious New Zealand White rabbits instrumented to record arterial pressure and heart rate. Rabbits were exposed to 50 ml of cigarette smoke before and after subcutaneous osmotic minipump delivery of ANG II at a dose of 50 ng·kg−1·min−1 for 1 wk in one group and intracerebroventricular (icv) infusion at a dose of 100 pmol/min for 1 h in a second group. The responses were compared before and after heart rate was controlled by pacing. Autonomic components were evaluated by intravenous administration of atropine methyl bromide (0.2 mg/kg) and prazosin (0.5 mg/kg). ANG II given either systemically or icv significantly blunted the pressor response to smoke ( P < 0.05) when the bradycardic response was prevented. This blunted response was not due to an absolute increase in baseline blood pressure after ANG II infusion (71.64 ± 11.6 vs. 92.1 ± 19.8 mmHg; P < 0.05) because normalization of blood pressure with sodium nitroprusside to pre-ANG II levels also resulted in a significantly blunted pressor response to smoke. The effect of smoke was α1-adrenergic receptor-mediated because it was essentially abolished by prazosin in both the pre- and the post-ANG II states ( P < 0.05). These results suggest that elevations in central ANG II reduce the sympathetic response to smoke in conscious rabbits. This effect may be due to an augmentation of baseline sympathetic outflow and a reduction in reflex sensitivity similar to the effect of ANG II on baroreflex function.

scholarly journals Effects of Dexmedetomidine Infusions on Hemodynamic Stability in Patients undergoing Laparoscopic Cholecystectomy

2018 ◽  
Vol 04 (01) ◽  
pp. 010-014
Author(s):  
Himanshu Dodeja ◽  
Vinaya Udaybhaskar ◽  
Amol Singam
Keyword(s):  
Blood Pressure ◽  
Laparoscopic Cholecystectomy ◽  
Cardiovascular System ◽  
Normal Saline ◽  
Pressor Response ◽  
Hemodynamic Instability ◽  
System Stability ◽  
Plasma Catecholamine ◽  
Hemodynamic Stability ◽  
Inhalation Agent

Abstract Objectives: In laparoscopic cholecystectomy, there has been emphasis on maintaining hemodynamic stability by avoiding hypertension, hypotension, or tachycardia. The hemodynamic instability is persistent during the duration of pneumoperitoneum (PNP), namely, CO2 insufflations. This study helps us to find out the efficacy of dexmedetomidine on cardiovascular system stability in patients undergoing laparoscopic cholecystectomy. Materials and methods: Thirty patients were randomized into two groups of 15 members each: group P (placebo group) and group D (dexmedetomidine group). In the former, patients received 0.9% 20 mL normal saline, while in the latter, patients received 0.4 μg/kg/hr of injection dexmedetomidine in 0.9% normal saline. In all patients, age, weight, height, systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded. Results: Dexmedetomidine being a highly selective and potent and specific alpha 2 agonist attenuates the hemodynamic response to tracheal intubation, decreases plasma catecholamine concentration during anesthesia, and decreases perioperative requirements of inhaled anesthetics. We found that dexmedetomidine helped in blunting the pressor response during the intubation, kept the HR and mean arterial pressure stable intraoperatively, and there was faster recovery as the requirement of inhalation agent was decreased intraoperatively. Conclusion: The drug dexmedetomidine maintained cardiovascular stability during laparoscopic cholecystectomy. The inhalational agent (isoflurane) requirement was found to be considerably lower. Also, the mean recovery time as indicated by the ability to vocalize following extubation was found to be significantly less. Hence, it can be recommended in laparoscopic cholecystectomy for maintaining cardiovascular system stability.

Plasma vasopressin in blood pressure homeostasis and in experimental renal hypertension

1980 ◽  
Vol 239 (1) ◽  
pp. H81-H87 ◽  
Author(s):  
P. T. Pullan ◽  
C. I. Johnston ◽  
W. P. Anderson ◽  
P. I. Korner
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Renal Hypertension ◽  
Similar Degree ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Experimental Renal Hypertension

The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension was investigated in the conscious dog. Intravenous infusion of synthetic arginine vasopressin to elevate plasma levels approximately fivefold to 31 pg/ml caused bradycardia in normal dogs, together with suppression of plasma renin activity and angiotensin II. This plasma level of vasopressin also caused elevation of mean arterial blood pressure in dogs with pharmacological total autonomic blockade. A similar degree of elevation of plasma vasopressin concentration was observed following mild nonhypotensive hemorrhage; more severe hemorrhage resulted in an approximate 100-fold increase in plasma vasopressin levels. Severe renal artery constriction in unilaterally nephrectomized dogs caused a marked rise in mean arterial blood pressure, but only a doubling of plasma vasopressin concentration. A suppressor infusion of vasopressin did not potentiate the pressor response to infused angiotensin II. It is concluded that vasopressin may play a role in normal cardiovascular homeostatic responses, but it is unlikely to have a significant direct vasoconstrictor role in the pathogenesis of this form of experimental renal hypertension.

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