Hepatic circulatory changes following endotoxin shock in the dog

1963 ◽  
Vol 204 (4) ◽  
pp. 641-644 ◽  
Author(s):  
Walter Muller ◽  
Louis L. Smith
Keyword(s):  
Cardiac Output ◽  
Plasma Volume ◽  
Salmonella Enteritidis ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Endotoxin Shock ◽  
Volume Reduction ◽  
Arterial Flow ◽  
Hepatic Arterial Flow ◽  
Endotoxin Administration

Hepatic arterial and portal venous pressure, flow, and resistance changes have been measured in healthy dogs following the administration of intravenous Salmonella enteritidis endotoxin. The hepatic circulatory changes have been compared with those occurring in total body hemodynamics. Intravenous endotoxin caused an immediate fall in blood pressure, cardiac output, and central venous pressure. There was an abrupt rise in the net portal pressure which was associated with a marked fall in hepatic arterial and portal venous flows following endotoxin administration. There was a gradual reduction in the ratio of portal venous to hepatic arterial flow indicating relative maintenance of the hepatic arterial circulation during the period of endotoxin shock. Hepatic arterial flow increased from 7 to 9% of cardiac output, whereas portal venous flow fell from 15 to 11% of cardiac output following endotoxin administration. The hematocrit showed a progressive rise during the period of observation indicating acute plasma volume reduction. This finding suggests that some of the changes observed in hepatic circulation following endotoxin administration may be due to acute plasma volume reduction.

Increased myocardial contractility during endotoxin shock in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H715-H722 ◽  
Author(s):  
P. M. Kober ◽  
J. X. Thomas ◽  
R. M. Raymond
Keyword(s):  
Myocardial Contractility ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Terminal Phase ◽  
Endotoxin Administration ◽  
Before And After ◽  
Anesthetized Dogs

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

The role of hepatic arterial flow on portal venous and hepatic venous wedged pressure in the isolated perfused CCl4-cirrhotic liver

2008 ◽  
Vol 295 (1) ◽  
pp. G197-G202 ◽  
Author(s):  
Alexander Zipprich ◽  
Mauricio R. Loureiro-Silva ◽  
Irita D'Silva ◽  
Roberto J. Groszmann
Keyword(s):  
Liver Perfusion ◽  
Venous Pressure ◽  
Arterial Flow ◽  
Hepatic Arterial Flow ◽  
Drug Induced ◽  
Arterial Perfusion ◽  
Elevated Pressures ◽  
Flow Pressure ◽  
And Control

In cirrhosis, hepatic venous pressure gradient is used to measure portal venous and sinusoidal pressures, as well as drug-induced decreases of elevated pressures. The aim of this study was to investigate the influence of hepatic arterial flow (HAF) changes on portal venous perfusion (PVPP) and wedged hepatic venous pressure (WHVP). Normal and CCl4-cirrhotic rats were subjected to a bivascular liver perfusion with continuous measurements of PVPP, WHVP, and hepatic arterial perfusion pressure. Flow-pressure curves were performed with the use of different flows either through the portal vein (PVF: 20–32 ml/min) or HAF (5–15 ml/min). Increases in HAF lead to significant absolute and relative increases in PVPP ( P = 0.002) and WHVP ( P < 0.001). Absolute changes in HAF correlated to absolute changes in PVPP (cirrhosis: r = 0.64, P < 0.001; control: r = 0.67, P < 0.001) and WHVP (cirrhosis: r = 0.71, P < 0.001; control: r = 0.82, P < 0.001). Changes in PVPP correlated to changes in WHVP due to changes in PVF only in cirrhosis ( r = 0.75, P < 0.001), whereas changes in HAF correlated in both cirrhosis ( r = 0.92, P < 0.001) and control ( r = 0.77, P < 0.001). In conclusion, increases and decreases in HAF lead to respective changes in PVPP and WHVP. This suggests a direct influence of HAF on PVPP and WHVP most likely due to changes in sinusoidal perfusion.

Splanchnic and systemic haemodynamic response to volume changes in patients with cirrhosis and portal hypertension

1999 ◽  
Vol 96 (5) ◽  
pp. 475-481 ◽  
Author(s):  
Panagiotis VLAVIANOS ◽  
Padraik MAC MATHUNA ◽  
Roger WILLIAMS ◽  
David WESTABY
Keyword(s):  
Cardiac Output ◽  
Portal Hypertension ◽  
Systemic Vascular Resistance ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Haemodynamic Response ◽  
Volume Depletion ◽  
Compensated Cirrhosis

We investigated the haemodynamic response to volume depletion and subsequent repletion in patients with cirrhosis and portal hypertension. Twelve patients with compensated cirrhosis and portal hypertension were included in the study. The haemodynamic changes occurring after removal of approx. 15% of the blood volume, and subsequently after isovolume repletion with colloid, were assessed. Baseline haemodynamic measurements showed increased cardiac output and a systemic vascular resistance at the lower limit of normal. The hepatic venous pressure gradient (HVPG) was increased, at 18 mmHg. After depletion, arterial pressure, cardiac output and all right-heart-sided pressures decreased, and systemic vascular resistance increased. HVPG decreased to 16.0 mmHg. All the above changes were statistically significant. After blood volume restitution, the haemodynamic values returned to baseline. In particular, an increase in HVPG was shown in four out of the twelve patients (two with ascites and two without), which was small in three of them. However, HVPG remained the same as or lower than the baseline in the other eight patients. Patients with cirrhosis and portal hypertension exhibit an abnormal haemodynamic response to blood volume depletion. After volume repletion, no increase in the portal pressure was noted in this group of patients as a whole, although four out of the twelve patients did show an increase, possibly due to extensive collateral circulation.

scholarly journals A rare anastomosis between the root of common hepatic artery and proper hepatic artery: implications for pancreaticoduodenectomy

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Takeshi Morinaga ◽  
Katsunori Imai ◽  
Keisuke Morita ◽  
Kenichiro Yamamoto ◽  
Satoshi Ikeshima ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Hepatic Artery ◽  
Pancreatic Head ◽  
Common Hepatic Artery ◽  
Arterial Flow ◽  
Anastomotic Site ◽  
Proper Hepatic Artery ◽  
Arterial Reconstruction ◽  
Hepatic Arterial Flow ◽  
The Common

Abstract Background Hepatic artery anomalies are often observed, and the variations are wide-ranging. We herein report a case of pancreatic cancer involving the common hepatic artery (CHA) that was successfully treated with pancreaticoduodenectomy (PD) without arterial reconstruction, thanks to anastomosis between the root of CHA and proper hepatic artery (PHA), which is a very rare anastomotic site. Case presentation A 78-year-old woman was referred to our department for the examination of a tumor in the pancreatic head. Contrast-enhanced computed tomography (CT) revealed a low-density tumor of 40 mm in diameter located in the pancreatic head. The involvement of the common hepatic artery (CHA), the root of the gastroduodenal artery (GDA), and portal vein was noted. Although such cases would usually require PD with arterial reconstruction of the CHA, it was thought that the hepatic arterial flow would be preserved by the anastomotic site between the root of the CHA and the PHA, even if the CHA was dissected without arterial reconstruction. PD with dissection of the CHA and PHA was safely completed without arterial reconstruction, and sufficient hepatic arterial flow was preserved through the anastomotic site between the CHA and PHA. Conclusion We presented an extremely rare case of an anastomosis between the CHA and PHA in a patient with pancreatic cancer involving the CHA. Thanks to this anastomosis, surgical resection was successfully performed with sufficient hepatic arterial flow without arterial reconstruction.

Lower vascular tone and larger plasma volume in Parkinson's disease with orthostatic hypotension

2011 ◽  
Vol 111 (2) ◽  
pp. 443-448 ◽  
Author(s):  
J. T. Groothuis ◽  
R. A. J. Esselink ◽  
J. P. H. Seeger ◽  
M. J. H. van Aalst ◽  
M. T. E. Hopman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Flow ◽  
Orthostatic Hypotension ◽  
Vascular Resistance ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Dilution Method ◽  
Significant Difference ◽  
Head Up Tilt

The pathophysiology of orthostatic hypotension in Parkinson's disease (PD) is incompletely understood. The primary focus has thus far been on failure of the baroreflex, a central mediated vasoconstrictor mechanism. Here, we test the role of two other possible factors: 1) a reduced peripheral vasoconstriction (which may contribute because PD includes a generalized sympathetic denervation); and 2) an inadequate plasma volume (which may explain why plasma volume expansion can manage orthostatic hypotension in PD). We included 11 PD patients with orthostatic hypotension (PD + OH), 14 PD patients without orthostatic hypotension (PD − OH), and 15 age-matched healthy controls. Leg blood flow was examined using duplex ultrasound during 60° head-up tilt. Leg vascular resistance was calculated as the arterial-venous pressure gradient divided by blood flow. In a subset of 9 PD + OH, 9 PD − OH, and 8 controls, plasma volume was determined by indicator dilution method with radiolabeled albumin (125I-HSA). The basal leg vascular resistance was significantly lower in PD + OH (0.7 ± 0.3 mmHg·ml−1·min) compared with PD − OH (1.3 ± 0.6 mmHg·ml−1·min, P < 0.01) and controls (1.3 ± 0.5 mmHg·ml−1·min, P < 0.01). Leg vascular resistance increased significantly during 60° head-up tilt with no significant difference between the groups. Plasma volume was significantly larger in PD + OH (3,869 ± 265 ml) compared with PD − OH (3,123 ± 377 ml, P < 0.01) and controls (3,204 ± 537 ml, P < 0.01). These results indicate that PD + OH have a lower basal leg vascular resistance in combination with a larger plasma volume compared with PD − OH and controls. Despite the increase in leg vascular resistance during 60° head-up tilt, PD + OH are unable to maintain their blood pressure.

Doppler sonography in the posttransplant patient: use of nifedipine to detect hepatic arterial flow.

1994 ◽  
Vol 163 (4) ◽  
pp. 863-864 ◽  
Author(s):  
K P Moresco ◽  
R S Shapiro ◽  
K P Halton ◽  
M A Sadler ◽  
S Emre ◽  
...  
Keyword(s):  
Doppler Sonography ◽  
Arterial Flow ◽  
Hepatic Arterial Flow ◽  
Patient Use
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