Adrenal catecholamines in E. coli endotoxin shock

1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
Endotoxin Shock ◽  
Mean Blood Pressure ◽  
E Coli ◽  
Arterial Blood ◽  
Splanchnic Nerves

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960

Effect of vasopressors on organ blood flow during endotoxin shock in pigs

1987 ◽  
Vol 252 (2) ◽  
pp. H291-H300 ◽  
Author(s):  
M. J. Breslow ◽  
C. F. Miller ◽  
S. D. Parker ◽  
A. T. Walman ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Left Ventricle ◽  
Arterial Blood Pressure ◽  
Endotoxin Shock ◽  
Organ Blood Flow ◽  
Shock Model ◽  
Blood Pressure Elevation ◽  
Arterial Blood

A volume-resuscitated porcine endotoxin shock model was used to evaluate the effect on organ blood flow of increasing systemic arterial blood pressure with vasopressors. Administration of 0.05–0.2 mg/kg of Escherichia coli endotoxin (E) reduced mean arterial blood pressure (MAP) to 50 mmHg, decreased systemic vascular resistance to 50% of control, and did not change cardiac output or heart rate. Blood flow to brain, kidney, spleen, and skeletal muscle was reduced during endotoxin shock, but blood flow to left ventricle, small and large intestine, and stomach remained at pre-endotoxin levels throughout the study period. Four groups of animals were used to evaluate the effect of vasopressor therapy. A control group received E and no vasopressor, whereas the other three groups received either norepinephrine, dopamine, or phenylephrine. Vasopressors were administered starting 60 min after E exposure, and the dose of each was titrated to increase MAP to 75 mmHg. Despite the increase in MAP, brain blood flow did not increase in any group. Norepinephrine alone increased blood flow to the left ventricle. Kidney, splanchnic, and skeletal muscle blood flow did not change with vasopressor administration. The dose of norepinephrine required to increase MAP by 20–25 mmHg during E shock was 30 times the dose required for a similar increase in MAP in animals not receiving E. We conclude that hypotension in the fluid resuscitated porcine E shock model is primarily the result of peripheral vasodilatation, that the vascular response to vasoconstrictors in this model is markedly attenuated following E administration, that blood pressure elevation with norepinephrine, dopamine, and phenylephrine neither decreases blood flow to any organ nor increases blood flow to organs with reduced flow, and that norepinephrine, dopamine, and phenylephrine affect regional blood flow similarly in this model.

Peripheral Resistance Changes and Blood Pooling After Endotoxin in Eviscerated Dogs

1958 ◽  
Vol 195 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert P. Gilbert ◽  
Hiroshi Kuida ◽  
Maurice B. Visscher
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Endotoxin Shock ◽  
E Coli ◽  
Arterial Blood ◽  
Later Phase

Studies were performed on eviscerated dogs maintained with a constant cardiac inflow with and without injections of lethal amounts of E. coli endotoxin. Continuous recordings of mean arterial blood pressure and total venous return permitted determination of changes in total peripheral resistance and extent of vascular pooling. A significant fall in mean arterial blood pressure occurs within 30 minutes after endotoxin in the eviscerated dog with constant cardiac inflow. There is therefore a decrease in total peripheral resistance. There is also a small but significant increase in vascular pooling exceeding that seen without endotoxin but much reduced from that observed in noneviscerated animals given endotoxin. It is concluded that a decrease in vascular tone occurs after endotoxin and that it probably plays a significant role in the later phase of endotoxin shock in the dog.

PROSTACYCLIN (PGI2) FORMATION IN RELATION TO ANAPHYLATOXIN C5a GENERATION DURING RABBIT ENDOTOXIN SHOCK

1987 ◽  
Author(s):  
M Rampart ◽  
H Bult ◽  
A G Herman ◽  
P J Jose ◽  
T J Williams
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Endotoxin Shock ◽  
Rabbit Serum ◽  
Classical Pathway ◽  
E Coli ◽  
Arterial Blood ◽  
Anaphylatoxin C5a

Injection of endotoxin (LPS) in animals, a model for gram-negative septic shock, leads to intravascular activation of the complement system, and is one of the few conditions in which 6-oxo-PGF]CX and thromboxane (TX) B2 (non-enzymic metabolites of PGI2 and TXA2) can be detected in arterial blood. Previously we reported associations between complement activation, PGI2 biosynthesis and LPS-induced hypotension in rabbits. As C5a and C5adesArg trigger endothelial PGI2 formation in vitro, we have now measured the plasma levels of immunoreactive (ir) C5a in relation to generation of PGI2 and changes in arterial blood pressure in LPS shock. Pentobarbitone anaesthethized rabbits received LPS (E. coli 0111:B4, 0.5 mg/kg) or saline via the marginal ear vein. A catheter in the left carotid artery was used to collect blood and to monitor mean arterial blood pressure (MABP). Platelet and leukocyte numbers, haemolytic complement titre (CH50), and plasma ir6-oxo-PGFioc , irTXB2 and irC5a were measured 15 min before and at different times after saline or LPS injection. LPS caused a dose- and time-dependent formation of irC5a in rabbit serum in vitro, predominantly via the classical pathway. LPS also activated complement in vivo, as indicated by about 20 % reduction of CH50 titre (measured after 3h) and a marked increase of arterial irC5a (20-120 ng/ml) in the first 2 to 5 min. After 30 min, irC5a had returned to baseline levels (< 2-5 ng/ml) and remained so up to 3h after injection of LPS. This irC5a peak correlated with a shortlasting initiation of PGI2 release (from < 20 pg/ml up to 550 pg/ml) and a drop in MABP (from about 95 mmHg to 50 mmHg) 2-5 min after LPS. None of these changes occurred after saline injection.In conclusion, LPS activates complement in vivo with concomitant formation of C5a. This peptide may trigger -either directly or after phagocyte activation - endothelial PGI2 biosynthesis, leading to arterial hypotension. This is supported by the suppression of the initial rise of arterial ir6-oxo-PGF1α and hypotension in complement-depleted rabbits. Inhibition of C5a formation or activity may prove to be a meaningful approach to the treatment of septic circulatory shock.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

Forearm and finger blood flow responses to passive body tilts

1979 ◽  
Vol 46 (2) ◽  
pp. 288-292 ◽  
Author(s):  
Y. A. Mengesha ◽  
G. H. Bell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Pulse Rate ◽  
Forearm Blood Flow ◽  
Body Tilt ◽  
Finger Blood Flow ◽  
Arterial Blood ◽  
Forearm Vascular Resistance

Ten to fifteen healthy subjects, ages 18--30 yr, were used to assess the correlation of forearm blood flow with graded passive body tilts and vascular resistance and also to discern the relative effects of body tilts on finger blood flow. In the head-up tilts forearm blood flow and arterial blood pressure fell progressively, whereas forearm vascular resistance and pulse rate increased. In the head-down tilts the forearm blood flow and the arterial blood pressure increased, whereas the forearm vascular resistance and pulse rate decreased. These changes were found to be significantly correlated with the different tilt angles and with one another. In a preliminary study it was found that infrared heating of the carpometacarpal region produced finger vasodilatation similar to the forearm vasodilatation observed by Crockford and Hellon (6). However, unlike forearm blood flow, finger blood flow showed no appreciable response to either the head-up or head-down tilts. This indicates that the sympathetic tone and the volume of blood in the finger are not appreciably altered by this test procedure at least 1 min after the body tilt is assumed.

Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Combined Therapy ◽  
Arterial Blood

Objective To assess the effect of the angiotensin-converting enzyme inhibitor ceronapril on cerebral blood flow (CBF) in patients with moderate hypertension. Design Patients received chlorthalidone 25 mg for 4 weeks, and if diastolic blood pressure remained in the range of 100–115 mm Hg, they were given titrated doses of ceronapril (10–40 mg/d based on blood pressure response) in addition to chlorthalidone for 9 weeks. Setting Outpatient research clinic. Subjects Eligible patients had moderate essential hypertension (diastolic blood pressure 100–115 mm Hg) assessed when the patients were receiving no medications. Thirteen patients were entered into the study; 1 withdrew for reasons unrelated to the study drug. Twelve patients (11 men, 1 woman; mean age 52 y) completed the study. Intervention Ceronapril, given with chlorthalidone. Main Outcome Measures CBF measurements were taken at the start and end of ceronapril therapy using intravenous 133Xe; blood pressures were determined weekly. Results Mean arterial blood pressure decreased from 130 ± 4 to 120 ±7 mm Hg after 4 weeks of chlorthalidone administration, and fell further to 108 ± 8 mm Hg after an additional 9 weeks of combined chlorthalidone-ceronapril therapy (p < 0.05). CBF fell from 44 ± 15 to 34 ± 5 mL/min/100 g during the 9 weeks of combined therapy (p = 0.05). No adverse effects consistent with decreased CBF were observed. The decrease in CBF was not linearly correlated with the change in systemic blood pressure, but was strongly correlated (r = –0.937; p < 0.001) with the initial CBF. Conclusions The decrease in mean arterial blood pressure was not associated with a decrease in CBF. Patients with high CBF may be predisposed to a decrease in CBF when treated with ceronapril and chlorthalidone.

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