Effect of cimetidine on portal hypertension in cirrhotic patients.

Abstract

The dangers of inducing diuresis in patients with pulmonary oedema and normal pulmonary wedge pressures have recently been described." We report a complementary case of acute right heart failure due to right ventricular infarction complicated by hypovolaemia. In this, right ventricular output may provide an insufficient preload for the left ventricle, and there is the apparent paradox of an overloaded right ventricle and an inadequately primed "hypovolaemic" left ventricle. Failure to recognise this may lead to inappropriate diuretic or inotropic treatment and potentially irreversible hypovolaemic shock. Case report A 66-year-old tailor presented with inferior myocardial infarction. He was normotensive and well perfused, with raised jugular venous pressure. Auscultation of the heart was normal and he had no signs of left ventricular failure. Because of the raised jugular venous pressure he underwent diuresis. Over three days he became hypotensive and oliguric. Jugular venous pressure remained raised in the absence of pulmonary congestion, and he developed ankle oedema. Inotropic drugs and diuretics produced no improvement. A Swan-Ganz catheter was inserted (figure). Right atrial pressure was

Verapamil favorably influences hepatic microvascular exchange and function in rats with cirrhosis of the liver.

“…Alternatively, the different effects could be due to different protein binding, antipyrine being much less extensively bound (46) (53). In patients with more advanced liver disease, propranolol has not been effective (54). This could be due to increased hepatic vascular resistance (55) and/or reduced sensitivity to norepinephrine in the splanchnic vascular bed maintaining high flow against an unchanged hepatic resistance (56).…”

Liver Function and Pharmacological Considerations in Pathogenesis and Treatment of Portal Hypertension

“…Antihistamines. Although histamine has been implicated as a mediator of portal hypertension (66) and early reports erroneously assumed that H,-blockers reduced hepatic perfusion (194), it has been shown convincingly that H,-blockers affect neither portal pressure (195,196) nor hepatic perfusion (196)(197)(198). A placebocontrolled trial documented that chronic H,-blockade was unable to prevent repeat bleeding from esophageal varices (199).…”

The Treatment of Oesophageal Varices and Portal Hypertension

“…However, gastric pH, and oesophageal reflux have not been shown to be important in the pathogenesis, and a controlled trial of cimetidine in the prophylaxis of variceal haemorrhage demonstrated no improvement (59). Cimetidine's effect on liver blood flow and portal pressure has subsequently been studied by several groups who have reported a variable effect on liver blood flow and no effect on cWHVP (60). At present therefore we do not have any data to support the use of long-term cimetidine or other H,-receptor antagonist in the treatment of portal hypertension and varices (61-63), or in acute variceal haemorrhage, though cimetidine has been shown to be effective in prevention of haemorrhagic gastritis in patients with fulminant hepatitis (64).…”