Control of Portal Hypertension

Nusbaum, Moreye; Younis, Mohammed T.; Baum, Stanley; Blakemore, William S.

doi:10.1001/archsurg.1974.01350270072013

Cited by 28 publications

(3 citation statements)

References 14 publications

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“…Administration of a relatively low dose of vasopressin directly into the superior mesen teric artery by continuous infusion (0.1-0.5 U/min) was the initial approach [44], Pre viously, vasopressin had been administered in large, intermittent intravenous boluses (20 U over 20 min). Bolus and continuous intra venous infusion have similar hemodynamic effects [45].…”

Section: Vasoactive Drugsmentioning

confidence: 99%

Clinical Pharmacology of Active Variceal Bleeding

Scarpignato¹

1992

Dig Dis

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Although the mechanism initiating and maintaining variceal hemorrhage is not completely understood, there has been general agreement in recent years on the concept that variceal rupture occurs when the tension on the wall of the varices reaches a critical value (the rupture point) that leads to the leakage of the elastic components of the wall. If this hypothesis is true, the aim of pharmacological treatment should be to reduce variceal wall tension or to prevent any abrupt increase in this parameter. Some vasoconstrictor drugs are currently used in order to achieve these goals and in the attempt to stop the acute bleeding episode. All these agents decrease either portal pressure and azygos blood flow. Vasopressin although effective, has significant cardiac and gastrointestinal adverse effects that discourage its use. Combination with nitroglycerin reduces its adverse effects while maintaining or even enhancing the reduction in portal pressure. Glypressin, which acts as a slow-release preparation of vasopressin, has a longer duration of action and can be administered as single intravenous injections instead of continuous infusion. However, the similarity of effects of these drugs on systemic circulation leads to an overlapping spectrum of untoward effects. Somatostatin and the synthetic octapeptide octreotide display similar pharmacological effects on splanchnic hemodynamics but have a better tolerability profile. Thanks to its longer duration of action and ease of administration, octreotide could become the drug of choice for the early, pre-hospital management of bleeding varices. A different approach to the pharmacological treatment of variceal bleeding may be the use of compounds, like metoclopramide and domperidone, that increase the lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood flow into the submucous venous plexus of the esophagus and hence into the esophageal varices. However, more studies are needed before these compounds be considered a real alternative to the above established drugs.

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Section: Vasoactive Drugsmentioning

confidence: 99%

Clinical Pharmacology of Active Variceal Bleeding

Scarpignato¹

1992

Dig Dis

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“…It cannot be excluded that vasopressin might be beneficial to patients with less severe liver disease. In order to obtain a higher concentration in the splanchnic area with an ensuing stronger vasoconstrictive effect and to reduce the undesirable systemic effects, Nusbaum et al 19 proposed to infuse vasopressin into the superior mesenteric artery. The results of the two controlled studies of superior mesenteric arterial infusion of vasopressin are set out in Table 3.…”

Section: Unite De Recherches De Physiopathologie Hkpatique (Inserm) mentioning

confidence: 99%

Drug Therapy of Portal Hypertension Due to Cirrhosis

Benhamou¹,

Lebrec²

1982

Semin Liver Dis

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“…Likewise, systemic vasopressin is usually only temporarily effective (Shaldon and Sherlock, 1960) and its use is limited by coronary artery constriction leading sometimes to myocardial infarction or serious arrythmia (Beller, Trevino, and Urban, 1971). In 1967, Nusbaum, Baum, Sakiyalek, and Blakemore showed in dogs that the infusion of a small dose of vasopressin into the superior mesenteric artery reduced arterial flow and portal venous pressure without altering systemic arterial pressure or cardiac output and with no evidence of bowel Received for publication 7 November 1972. 59 ischaemia during infusions lasting for up to six hours.…”

mentioning

confidence: 99%

Treatment of bleeding oesophageal varices by infusion of vasopressin into the superior mesenteric artery

Murray‐Lyon¹,

Pugh²,

Nunnerley³

et al. 1973

Gut

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SUMMARY Seventeen patients bleeding from oesophageal varices were treated by continuous infusion of vasopressin through a catheter inserted percutaneously and positioned in the superior mesenteric artery and in two other patients catheterization proved technically impossible. Bleeding was completely controlled on only four out of 18 occasions in the 17 patients treated. In seven patients, bleeding was controlled for two or more days but then recurred although the infusion was continued with an increased dose of vasopressin. There was a high incidence of complications, including bleeding from the site of catheter insertion in the groin and septicaemias. Sengstaken balloon tamponade and oesophageal transection had to be used to control bleeding in some patients but only six out of 17 survived to leave hospital.

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Control of Portal Hypertension

Cited by 28 publications

References 14 publications

Clinical Pharmacology of Active Variceal Bleeding

Clinical Pharmacology of Active Variceal Bleeding

Drug Therapy of Portal Hypertension Due to Cirrhosis

Treatment of bleeding oesophageal varices by infusion of vasopressin into the superior mesenteric artery

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