Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Splanchnic Circulation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1993

Comparison of the continuously calculated fractional splanchnic extraction of insulin with its fractional disappearance using a new double-tracer technique.

These studies were designed to calculate the fractional disappearance rate (FDR) and splanchnic extraction of insulin in response to an exogenous (intraperitoneal) input of insulin. A double-tracer technique using insulin tritiated on both the A1 and B1 positions was introduced for the measurement of hepatic extraction. The A1 tracer, not previously characterized in vivo, was compared in terms of its kinetics with H3-B1-insulin and unlabeled insulin. The metabolic clearance rates (MCR) of the three insulins were identical, as were the decay curves of the two tracers. To measure splanchnic insulin extraction, one tracer was infused systemically to evaluate the FDR of insulin, and the second was infused into the splanchnic circulation (superior mesenteric artery) and its peripheral appearance was calculated. Splanchnic extraction was determined from the difference between this rate of appearance and the rate of infusion of the mesenteric tracer. After intraperitoneal insulin injection, insulin levels increased to peaks of 549 +/- 93 microU/mL (portal vein) and 473 +/- 99 microU/mL (inferior vena cava) and decreased to basal levels over 3 hours. The FDR decreased from 0.295 +/- 0.051 min-1 to 0.125 +/- 0.026 min-1, and splanchnic extraction decreased from 0.534 +/- 0.06 to 0.232 +/- 0.088. The latter returned to near-basal values more rapidly than did the FDR. In conclusion, the kinetics of insulin both in and out of the steady state have been shown to be nonlinear through physiological insulin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Hepatorenal syndrome.

Hepatorenal syndrome is a common complication in patients with advanced cirrhosis and ascites characterized not only by renal failure but also by marked alterations in systemic hemodynamics and vasoactive systems. Renal failure is due to a marked hypoperfusion of the kidney secondary to renal vasoconstriction. The pathogenesis of hepatorenal syndrome is not completely known but it is thought to be the extreme manifestation of the underfilling of the arterial circulation secondary to an arterial vasodilation, located mainly in the splanchnic circulation. Recently, a new definition and diagnostic criteria of hepatorenal syndrome have been proposed, which has stimulated research in this field. Prognosis of patients with hepatorenal syndrome is very poor. Liver transplantation is the only effective treatment but it is not applicable in all patients due to short survival. New therapies developed during the last few years, such as the use of systemic vasoconstrictors or transjugular intrahepatic portosystemic shunts appear promising, but their usefulness should be evaluated in prospective investigations.

Ascites↗
PubMed2001

Hemodynamic characterization of arterialized and nonarterialized liver transplants in the rat.

Persistent hyperkinetic circulation after liver transplantation has been described in humans, but similar changes have not been well characterized in the rat model. This study aimed to investigate the hemodynamics of the systemic and splanchnic circulations in both arterialized and nonarterialized hepatic allografts. Orthotopic liver transplantation was performed in four groups of Sprague-Dawley rats. Group A comprised sham-operated rats with hepatic artery ligation that did not receive transplants; group B comprised rats that received transplants without arterialization; group C comprised sham-operated rats with intact hepatic artery that did not receive transplants; and group D comprised rats that received transplants with arterialization. Blood flow measurements were performed three weeks after the surgical procedure, using the radioactive microsphere method. The results showed that rats that received transplants exhibited a significantly higher cardiac index and lower systemic vascular resistance than the control rats. Splanchnic hyperemia was also present with increased mesenteric blood flow. However, there was no difference in hemodynamics between rats that received arterialized transplants and those that received nonarterialized transplants. Arterial collateral vessels from adjacent tissues were observed in the nonarterialized grafts; this was confirmed histologically. It is concluded that rats that undergo orthotopic liver transplantation exhibit hyperdynamic circulation, regardless of the arterial reconstruction procedure, possibly due to extensive collateral formation in the hepatosplanchnic circulation.

Animals↗
PubMed2002

Hepatic vascular response to elevated intraperitoneal pressure in the rat.

The rat is increasingly being used to study the physiological response to elevated intra-abdominal pressure (IAP) during laparoscopic surgery. Although decreased portal venous flow associated with the elevated IAP has been reported in large animals, little information is available in rats. Furthermore, the relative blood flow changes in the hepatic artery and portal vein have not been reported. Therefore, this study was performed to elucidate the change in systemic and splanchnic circulation, including hepatic arterial and portal venular flow, during pneumoperitoneum in rats. Sprague-Dawley rats were assigned into either a ventilated or nonventilated group and then subjected to various levels of IAP (0, 5, 10, and 20 mm Hg) using carbon dioxide gas. At each pressure, both cardiac output and splanchnic organ flow were determined using fluorescent microspheres. There was no obvious hemodynamic difference between the ventilated and nonventilated groups. Mean arterial pressure and cardiac index were significantly lower with 20 mm Hg of IAP compared to 0 mm Hg in both groups. Flow to the spleen, stomach, duodenum, total intestine, and portal vein was all decreased by increasing IAP (P < 0.05 at 20 mm Hg compared to 0 mm Hg) and was significantly correlated to the decrease in cardiac index. However, the hepatic arterial flow was relatively preserved throughout all levels of IAP, suggesting activation of the hepatic arterial buffer response. We conclude that the decreased splanchnic flow during pneumoperitoneum largely depends on the decreased cardiac index. Hepatic artery flow, however, is selectively preserved and may provide protection for liver function during sustained elevations in IAP.

Animals↗
PubMed1999

Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high-volume plasmapheresis.

Liver failure represents a major therapeutic challenge, and yet basic pathophysiological questions about hepatic perfusion and oxygenation in this condition have been poorly investigated. In this study, hepatic blood flow (HBF) and splanchnic oxygen delivery (DO2, sp) and oxygen consumption (VO2,sp) were assessed in patients with liver failure defined as hepatic encephalopathy grade II or more. Measurements were repeated after high-volume plasmapheresis (HVP) with exchange of 8 to 10 L of plasma. HBF was estimated by use of constant infusion of D-sorbitol and calculated according to Fick's principle from peripheral artery and hepatic vein concentrations. In 14 patients with acute liver failure (ALF), HBF (1.78 +/- 0.78 L/min) and VO2,sp (3.9 +/- 0.9 mmol/min) were higher than in 11 patients without liver disease (1.07 +/- 0.19 L/min, P <.01) and (2.3 +/- 0.7 mmol/min, P <.001). In 9 patients with acute on chronic liver disease (AOCLD), HBF (1.96 +/- 1.19 L/min) and VO2,sp (3.9 +/- 2.3 mmol/min) were higher than in 18 patients with stable cirrhosis (1.00 +/- 0.36 L/min, P <.005; and 2.0 +/- 0.6 mmol/min, P <.005). During HVP, HBF increased from 1.67 +/- 0.72 to 2.07 +/- 1.11 L/min (n=11) in ALF, and from 1.89 +/- 1.32 to 2.34 +/- 1.54 L/min (n=7) in AOCLD, P <.05 in both cases. In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 +/- 2.5 vs. 6.6 +/- 2.2 L/min, NS) during HVP. Blood flow was redirected to the liver as the systemic vascular resistance index increased (1,587 +/- 650 vs. 2, 020 +/- 806 Dyne. s. cm-5. m2, P <.01) whereas splanchnic vascular resistance was unchanged. In AOCLD, neither systemic nor splanchnic vascular resistance was affected by HVP, but as cardiac output increased from 9.1 +/- 2.8 to 10.1 +/- 2.9 L/min (P <.01) more blood was directed to the splanchnic region. In all liver failure patients treated with HVP (n=18), DO2,sp increased by 15% (P <.05) whereas VO2,sp was unchanged. Endothelin-1 (ET-1) and ET-3 were determined before and after HVP. Changes of ET-1 were positively correlated with changes in HBF (P <.005) and VO2,sp (P <.05), indicating a role for ET-1 in splanchnic circulation and oxygenation. ET-3 was negatively correlated with systemic vascular resistance index before HVP (P <.05) but changes during HVP did not correlate. Our data suggest that liver failure is associated with increased HBF and VO2, sp. HVP further increased HBF and DO2,sp but VO2,sp was unchanged, indicating that splanchnic hypoxia was not present.

Acute Disease↗
PubMed1993

Effects of PEEP on splanchnic hemodynamics and blood volume.

The effects of intermittent positive pressure ventilation with PEEP on splanchnic circulation and hepatic oxygen supply were studied in six beagles. PEEP of 0, 0.5 and 1.0 kPa (0, 5, 10 cmH2O, PEEP0, PEEP5 and PEEP10, respectively) of 30 min duration was applied in a random sequence. Hepatic arterial blood flow and portal venous blood flow were measured by electromagnetic flow meters. Blood volume changes in the splanchnic area were assessed from hepatic and splenic dimensions determined by sonomicrometry. PEEP5 and PEEP10 were associated with proportional decreases in both hepatic blood flow and cardiac output, while mean arterial pressure remained unchanged. Reflecting the decrease in hepatic blood flow, the hepatic oxygen supply decreased with the level of PEEP, and hepatic venous hemoglobin oxygen saturation was significantly less during PEEP10 (55.1 +/- 14.3%) than during PEEP5 (62.6 +/- 17.4%) and PEEP0 (62.3 +/- 11.9%). Hepatic venous and portal venous pressure increased with the level of PEEP. Hepatic dimensions increased by 7-8% and 16-19% during PEEP5 and PEEP10, respectively, but no significant changes in splenic dimension were observed. We conclude that PEEP5 and PEEP10 are accompanied by a decrease in hepatic blood flow and oxygen supply along with hepatic congestion.

Animals↗
PubMed2000

Hepatorenal syndrome.

Hepatorenal syndrome is a functional renal failure that occurs in cirrhotic patients with advanced liver disease and ascites. The diagnostic criteria and clinical types of this syndrome have recently been revised. Hepatorenal syndrome is caused by marked hypoperfusion of the kidney as the result of renal vasoconstriction, which is thought to be the extreme manifestation of an underfilling of the arterial circulation. This circulatory dysfunction is the consequence of arterial vasodilation in the splanchnic circulation. Liver transplantation is the best treatment for HRS, but its applicability is low because of the short survival of these patients. New therapies, such as the use of systemic vasoconstrictors or TIPS, seem promising, but prospective investigations are needed to delineate their role in the management of cirrhotic patients with HRS.

Diagnosis, Differential↗
PubMed1999

Prostaglandin E1 infusion and functional hepatic flow in control subjects and in patients with cirrhosis.

Metabolic effects of prostaglandin E1 have been previously demonstrated in cirrhosis, apparently independent of changes in large splanchnic vessel hemodynamics. The effects of prostaglandin E1 on functional liver blood flow were tested by measuring the extrarenal clearance of D-sorbitol in six controls and eight patients with cirrhosis during systemic superinfusion of saline or prostaglandin E1 (30 microg/hr), in random order. Doppler ultrasonography of systemic and splanchnic circulation was also performed before the test and at the end of the two study periods. Prostaglandin E1 infusion increased femoral blood flow by nearly 60% in controls and over 30% in cirrhosis, without any effect on mean arterial pressure and heart rate. Mesenteric artery and portal blood flow were unchanged, as were Doppler-measured resistance indices in the liver, spleen and kidney. Sorbitol-assessed functional hepatic flow was 30% lower in cirrhosis, and did not change systematically during prostaglandin E1 infusion. We conclude that prostaglandin E1, at doses able to elicit metabolic effects and changes in systemic hemodynamics, does not affect splanchnic blood flow and/or hepatic microcirculation in normal subjects and in portal-hypertensive patients with cirrhosis.

Aged↗
PubMed1999

Effects of desflurane on the pig intestinal circulation during hypotension.

BACKGROUND: The aim of the present study was to analyze the perfusion pressure dependency for the splanchnic vascular effects of desflurane (DES). METHODS: We measured portal blood flow (QPORT, perivascular ultrasound) and jejunal mucosal perfusion (JMP; laser Doppler) in pentobarbital-anesthetized pigs (n=10). Experimentally, decreases in mean arterial pressure (MAP) were produced by pericardial infusions of dextran. The protocol included sets of measurements at incremental doses of DES (1, 2, 4 and 6%) prior to and during pericardial infusions. RESULTS: Although QPORT and JMP decreased significantly during pericardial infusions, DES, irrespective of dose, did not reduce QPORT until MAP had decreased below 65-70 mm Hg. In higher MAP ranges, vasodilation in pre-portal tissues was powerful enough to maintain QPORT in spite of concurrent decreases in driving arterial pressure, as produced by either DES or pericardial infusion, or by a combination of both. We found no effects of DES on JMP even at very low MAP (about 40 mm Hg during pericardial infusion), indicating that the normal physiological response of the small intestine to redistribute blood flow from deeper to more superficial layers during hypotension was unimpaired by DES. CONCLUSIONS: Our data suggest a wide dose-tolerability of DES as regards the splanchnic circulation during hypotensive states.

Anesthetics, Inhalation↗
PubMed1984

Selective and non-selective beta receptor blockade in the reduction of portal pressure in patients with cirrhosis and portal hypertension.

To elucidate the mechanisms by which beta receptor blockade leads to a reduction of portal pressure, 18 patients with cirrhosis and portal hypertension were given comparable doses of propranolol or metoprolol. The fall in portal pressure was more marked with propranolol together with a significant reduction in hepatic blood flow, which was not seen with metoprolol. No correlation between the reduction in cardiac output and the decrease in portal pressure or changes in hepatic blood flow could be elicited in each group, but there was a direct relationship between the decrease in hepatic blood flow and fall in portal pressure in the propranolol treated patients. The difference observed may be related to blockade of beta 2 vasodilator receptors in the splanchnic circulation which will occur only with propranolol and lead to a greater fall in splanchnic blood flow than will be produced by a reduction in cardiac output alone. Metoprolol, by maintaining effective hepatic blood flow, may be preferable to propranolol in patients with severely impaired liver function.

Cardiac Output↗
PubMed2004

Postprandial splanchnic haemodynamic changes in patients with liver cirrhosis and patent paraumbilical vein.

OBJECTIVE: The haemodynamic changes induced by a meal on collateral vessels in portal hypertensive cirrhotic patients are not well characterized. We aimed to study the postprandial modifications of splanchnic circulation in patients with a patent paraumbilical vein (PUV). METHODS: We studied 10 cirrhotic patients with patent PUV and 10 matched cirrhotic patients without PUV, by using echo colour Doppler at baseline and 15, 30 and 45 min after a standard mixed liquid meal (400 ml; 600 kcal). Calibre and blood flow velocities of the superior mesenteric artery, portal vein and PUV were obtained; congestion index of portal vein, portal blood flow, paraumbilical blood flow and effective portal liver perfusion were calculated; intrahepatic and intrasplenic arterial resistance and pulsatility indexes were recorded. RESULTS: We observed a postprandial splanchnic hyperaemia (superior mesenteric artery and portal vein blood flow increased after the meal in both groups; ANOVA P < 0.05), with no changes of hepatic impedance. In PUV patients, PUV constricted significantly postprandially, maximally at 30 min (calibre -17.5 +/- 7.0%; P = 0.003). Intrasplenic impedance, which may reflect portal pressure, increased, maximally at 30 min (pulsatility index +22.6 +/- 27.0%; P = 0.01), and inversely correlated with PUV vasoconstriction (R = 0.75, P = 0.01). In non-PUV patients intrasplenic impedance did not change. Portal liver perfusion increased similarly in both groups. CONCLUSIONS: PUV constricts after the meal, and this vasoconstriction is associated with an increase of splenic impedance which may indicate the postprandial increase of portal pressure observed in cirrhosis. The increase in postprandial portal liver perfusion in the PUV group is allowed by a paradox constriction of the collateral vessel.

Adrenergic beta-Antagonists↗
PubMed2001

The effects of dopamine and epinephrine on hemodynamics and oxygen metabolism in hypoxic anesthetized piglets.

BACKGROUND: The most appropriate inotropic agent for use in the newborn is uncertain. Dopamine and epinephrine are commonly used, but have unknown effects during hypoxia and pulmonary hypertension; the effects on the splanchnic circulation, in particular, are unclear. METHODS: The effects on the systemic, pulmonary, hepatic, and mesenteric circulations of infusions of dopamine and epinephrine (adrenaline) were compared in 17 newborn piglets. Three groups [control (n = 5), dopamine (n = 6) and epinephrine (n = 6)] of fentanyl anesthetized newborn piglets were instrumented to measure cardiac index (CI), hepatic arterial and portal venous blood flow, mean systemic arterial pressure (SAP), mean pulmonary arterial pressure (PAP), and arterial, portal and mixed venous oxygen saturations. Systemic, pulmonary, and mesenteric vascular resistance indices [systemic vascular resistance index (SVRI), pulmonary vascular resistance index (PVRI), mesenteric vascular resistance index (MVRI)], and systemic and splanchnic oxygen extraction and consumption were calculated. Alveolar hypoxia was induced, with arterial oxygen saturation being maintained at 55-65%. After 1 h of stabilization during hypoxia, each animal received either dopamine or epinephrine; randomly administered doses of 2, 10, and 32 microg kg-1 min-1 and 0.2, 1.0, and 3.2 microg kg-1 min-1 respectively were infused for 1 h at each dose. Results were compared with the 1 h hypoxia values by two-way analysis of variance. RESULTS: Epinephrine increased CI at all doses, with no significant effects on SAP and SVRI. Although epinephrine increased PAP at 3.2 microg kg-1min-1, it had no effect on PVRI. Dopamine had no effect on CI, SAP, and SVRI, but increased PAP at all doses and PVRI at 32 microg kg-1min-1. The SAP/PAP ratio was decreased with 32 microg kg-1min-1 dopamine, whereas epinephrine did not affect the ratio. In the mesenteric circulation, dopamine at 32 microg kg-1 min-1 increased portal venous flow and total hepatic blood flow and oxygen delivery, and decreased MVRI; epinephrine had no effect on these variables. Epinephrine increased hepatic arterial flow at 0.2 microg kg-1 min-1; dopamine had no effect on hepatic arterial flow at any dose. Despite these hemodynamic changes, there were no differences in systemic or splanchnic oxygen extraction or consumption at any dose of dopamine or epinephrine. CONCLUSIONS: Epinephrine is more effective than dopamine at increasing cardiac output during hypoxia in this model. Although epinephrine preserves the SAP/PAP ratio, dopamine shows preferential pulmonary vasoconstriction, which might be detrimental if it also occurs during the management of infants with persistent fetal circulation. Dopamine, but not epinephrine, increases portal flow and total hepatic flow during hypoxia.

Animals↗
PubMed2002

Mice with targeted deletion of eNOS develop hyperdynamic circulation associated with portal hypertension.

Systemic vasodilation is the initiating event of the hyperdynamic circulatory state, being most likely triggered by increased levels of vasodilators, primarily nitric oxide (NO). Endothelial NO synthase (eNOS) is responsible for this event. We tested the hypothesis that gene deletion of eNOS and inducible NOS (iNOS) may inhibit the development of the hyperdynamic circulatory state in portal hypertensive animals. To test this hypothesis, we used mice lacking eNOS (eNOS-/-) or eNOS/iNOS (eNOS/iNOS-/-) genes. A partial portal vein ligation (PVL) was used to induce portal hypertension. Sham-operated animals were used as a control. Hemodynamic characteristics were tested 2 wk after surgery. As opposed to our hypothesis, PVL also caused significant reduction in peripheral resistance in eNOS-/- compared with sham animals (0.33 +/- 0.02 vs. 0.41 +/- 0.03 mmHg. min x kg body wt x ml(-1); P = 0.04) and in eNOS/iNOS-/- animals with PVL compared with that of the sham-operated group (0.44 +/- 0.02 vs. 0.54 +/- 0.04; P = 0.03). This demonstrates that, despite gene deletion of eNOS, the knockout mice developed hyperdynamic circulation. Compensatory vasodilator molecule(s) are upregulated in place of NO in the systemic and splanchnic circulation in portal hypertensive animals.

Animals↗
PubMed2000

[Hepatorenal syndrome].

BACKGROUND: The association of renal failure with terminal liver insufficiency is referred to as hepatorenal syndrome (HRS). It is characterized by impaired renal function together with abnormalities in arterial circulation and activity of endogenous vasoactive system. In the pathogenesis of HRS, vasodilatation in the splanchnic circulation plays a major role. This leads to underfilling in arterial circulation in this area with subsequent vasoconstriction in renal arteries leading to lower renal circulation and functional renal failure. One of the most difficult tasks in clinical evaluation of patients with cirrhosis is to diagnose renal functions, because the standard methods used in evaluation of glomerular filtration are not reliable. The most important agents in the treatment of patients with cirrhosis, ascites and HRS are identification, prevention of precipitating factors, correction and treatment of prerenal failure and acute tubular necrosis. Up to now, the only effective treatment of HRS is ortothopic liver transplantation, which cannot be applied in all patients. CONCLUSIONS: HRS is a serious complication of liver diseases with a very bad prognosis qouad vitam and qouad sanationem, which is only rarely reversible. After diagnosing HRS, the renal insufficiency is already mostly progressive, and patients have only a minimal chance to improve their renal functions. The only currently proved treatment modality, which is successful in terms of improving renal functions and long-term survival rate is liver transplantation. (Tab. 2, Fig. 1, Ref. 28.)

Hepatorenal Syndrome↗
PubMed2003

ETA receptors mediate vasoconstriction, whereas ETB receptors clear endothelin-1 in the splanchnic and renal circulation of healthy men.

The contribution of the endothelin (ET) receptors ET(A) and ET(B) to basal vascular tone and ET-1-induced vasoconstriction in the renal and splanchnic vasculature was investigated in six healthy humans. ET-1 was infused alone and in combination with the selective ET(A) receptor antagonist BQ123 or the selective ET(B) receptor antagonist BQ788 on three different occasions. BQ123 did not affect basal arterial blood pressure, splanchnic vascular resistance (SplVR) or renal vascular resistance (RVR), but inhibited the increase in vascular resistance induced by ET-1 [64+/-18 versus -1+/-7% in SplVR ( P <0.05); 36+/-6 versus 12+/-3% in RVR ( P <0.0001)]. BQ788 increased basal SplVR and RVR [38+/-16% ( P =0.01) and 21+/-5% ( P <0.0001) respectively], and potentiated the ET-1-induced vasoconstriction. Plasma ET-1 increased more after ET(B) blockade than under control conditions or after ET(A) blockade. These findings suggest that the ET(A) receptor mediates the splanchnic and renal vasoconstriction induced by ET-1 in healthy humans. The ET(B) receptor seems to function as a clearance receptor and may modulate vascular tone by altering the plasma concentration of ET-1.

Adult↗
PubMed2005

[Long-term pharmacological treatment of portal hypertension].

Portal hypertension is an unavoidable complication of liver cirrhosis, which usually limits the survival (bleeding from esophageal varices, ascites). Increase in portal pressure is not only due to mechanical obstruction of portal circulation, but there is also a dynamic component (endothelial dysfunction of hepatic microcirculation) and increased blood flow through the splanchnic circulation. For the long-term treatment of portal hypertension two groups of medicaments are available at present: non-selective betablockers (vasoconstriction in splanchnic bed) and nitrates (lowering of intrahepatic resistance). Long-term treatment is necessary in these situations: Primary prophylaxis of bleeding from esophageal varices (in patients, who never bled, but with "risk" varices)--non-selective betablockers; secondary prophylaxis (in patients after variceal bleeding)--non-selective betablockers (possibly with nitrates) or endoscopic treatment. It is clearly documented, that this treatment lowers the risk of the first or repeated bleeding from varices and hence lowers the mortality and morbidity due to this complication in patients with liver cirrhosis. Another serious complication of liver cirrhosis is the spontaneous bacterial peritonitis. All patients after that infection have to receive prophylactic treatment with antibiotics. This treatment should be long life, till the disappearance of ascites or till the liver transplantation.

Esophageal and Gastric Varices↗
PubMed1992

Effects of theophylline on hemodynamics and tissue oxygenation in patients with cirrhosis.

Since adenosine may play a role in the hyperdynamic circulation of cirrhosis, we examined the effects of theophylline (an adenosine receptor antagonist) on systemic and splanchnic hemodynamics, tissue oxygenation and sympathoadrenal activity in patients with cirrhosis and liver failure. Theophylline (aminophylline) was administered intravenously for 30 min. Six patients received a dose of 3 mg/kg and eight others a dose of 6 mg/kg. The low dose caused plasma theophylline concentrations of 7.4 +/- 1.8 mg/ml (mean +/- S.E.), and induced a significant increase in heart rate from 84 +/- 5 to 93 +/- 8 beats/min. This dosage did not significantly change other hemodynamic values, oxygen (O2) consumption, or sympathoadrenal activity. The high dose elicited plasma theophylline concentrations of 15.8 +/- 4.0 mg/ml. This dose significantly increased heart rate from 78 +/- 5 to 87 +/- 7 beats/min and significantly decreased right atrial pressure from 2.5 +/- 1.0 to 1.4 +/- 0.8 mmHg, stroke volume from 52 +/- 3 to 47 +/- 5 ml.beat-1.m-2 and systolic arterial pressure from 140 +/- 5 to 129 +/- 6 mmHg. In contrast, O2 consumption, sympathoadrenal activity, and all other hemodynamic values (including azygos blood flow) were not significantly modified. As a result, we conclude that, in patients with cirrhosis, theophylline may cause decreased stroke volume which lowers systolic arterial pressure. In our patients theophylline also had a positive chronotropic effect but no vasoconstrictor effect on systemic and splanchnic circulation. Finally, theophylline did not improve tissue oxygenation in patients with cirrhosis.

Adult↗
PubMed1975

Vascular spider: a cutaneous manifestation of hyperdynamic blood flow in hepatic cirrhosis.

Arteriography and gas analysis of blood aspirated from a vascular spider in a patient with hepatic cirrhosis were done before excision and histologic examination of the lesion. This study supports earlier work suggesting that a spider angioma is a cutaneous manifestation of a generalized hyperdynamic circulation in hepatic cirrhosis. Moreover, based upon a variety of experimental and clinical observations on the splanchnic circulation in cirrhosis, it is suggested that the portal hypertension blood flow encounters the obstacle posed by the scarred liver ("active congestion").

Arm↗