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Biomedical subjects

M H Witte

Publications and source records attributed to M H Witte.

At least 127 records · Page 7Linked to original sources
PubMed1978

Peritoneovenous (LeVeen) shunt. Control of renin-aldosterone system in cirrhotic ascites.

Because of the unusual clinical course of a patient with hepatic cirrhosis, refractory ascites, and hepatorenal syndrome, we were able to examine the complex interrelationships between massive ascites, renin-aldosterone activity, and renal and hepatic function before and after placement of a peritoneojugular vein (LeVeen) shunt. Measurements indicated that when the shunt was functioning, renin-aldosterone production was suppressed, the hepatorenal syndrome was reversed, and ascites remitted. These data suggest that hyperreninemia, hyperaldosteronism, and functional renal abnormalities of this disorder are potentially reversible and arise primarily from the imbalance between formation and drainage of hepatosplanchnic lymph rather than from hepatocellular dysfunction, lowered plasma oncotic pressure, or portal hypertension.

Adult↗
PubMed1978

Effect of glucagon on hepatic lymph (tissue) PO2 after ligation of the hepatic artery: an experimental study.

In 17 greyhound dogs, hepatic oxygenation was examined after hepatic artery ligation (HAL) and subsequent administration of pharmacologic dosages of glucagon during various hemodynamic maneuvers at different per cents of oxygen in the inspired air. Measurements included arterial and portal pressure, PO2 and O2 content of arterial, portal and hepatic venous blood, and hepatic lymph (tissue) PO2. The following were observed: 1) an increase in FIO2 progressively raised hepatic lymph (tissue) PO2; 2) distal HAL decreased hepatic oxygenation; 3) a decrease in portal oxygen delivery by cross-clamping the superior mesenteric artery (X-SMA) aggravated hepatic deoxygenation induced by HAL; 4) with normovolemia and HAL, glucagon increased portal O2 delivery and hepatic venous blood O2 content, but either failed to raise hepatic lymph PO2 (FIO2 of 21% or 40%) or did so transiently (FIO-100%); 5) with an FIO2 of 100%, induced hemorrhage or X-SMA in conjunction with HAL blocked a rise in hepatic lymph PO2 after glucagon. It is concluded that administration of glucagon after HAL increases hepatic O2 delivery via the portal system, but nonetheless has minimal overall effect on hepatic tissue PO2. Accordingly, use of this agent after HAL in patients is probably of limited practical value in raising hepatic tissue PO2.

Animals↗
PubMed1978

Humoral immunity in experimental hyposplenism.

The immune response to an intravenous bolus of sheep erythrocytes, a large particulate antigen, was examined in weanling Sprague-Dawley rats after varying reduction in spleen size by splenic artery ligation (SAL) or partial amputation (pSx), and the results were compared with splenectomized (Sx) and sham-operated controls. Whereas SAL and pSx rats both produced higher 5 day (primary response) hemolysin antibody titers (P less than 0.001) than Sx rats, levels were lower (P less than 0.05) than in sham-operated rats with larger spleens (P less than 0.001). A similar heterophile pattern was seen in SAL rats at 22 days (secondary response). Within each group there was a positive correlation between splenic weight and serum hemolysin titer (r greater than 0.81) (P less than 0.001). Whereas spleen weight of sham-operated rats increased only 58%, splenic remnants in pSx rats enlarged 139% to 412%, with the greatest percentage of growth in the smallest remnants (25 mg) and the least in the largest remnants (200 mg). These data demonstrate a measurable immunologic advantage of splenic remnants (hyposplenism) over asplenism. This difference, although suboptimal as compared with that of a whole spleen (eusplenism), nonetheless may bolster body defenses to certain forms of bacterial sepsis.

Amputation, Surgical↗
PubMed1977

Left sided segmental portal hypertension following mesocaval interposition shunt.

Following a mesocaval interposition shunt in three patients with cirrhosis of the liver, bleeding esophageal varices recurred in two and left sided portal hypertension partially persisted in one patient. Angiographic and pressure studies of the portal system demonstrated effective decompression of the greater splanchnic venous system but continued lesser splanchnic venous hypertension. Recurrent variceal hemorrhage ceased following splenectomy done as an emergency. In contrast to a standard portacaval shunt, it is suggested that after an interposition mesocaval shunt, altered jet streaming of mesenteric blood flow may divert gastrosplenic venous drainage away from the interposition shunt with persistence of lesser splanchnic venous hypertension. Recognition of this entity and of the need for splenectomy is advocated.

Adult↗
PubMed1976

Ischemic therapy in thrombocytopenia from hypersplenism.

Percutaneous transfemoral arterial balloon occlusion or gelatin sponge embolization of the splenic artery or both were carried out in three high-risk patients with hepatic cirrhosis to reduce splenic hyperfunction and improve severe thrombocytopenia. Although this maneuver raised peripheral platelet counts in each patient, in one patient left upper quadrant pain with splinting of the lower chest cage led to hypostatic lower lobe pneumonia, while in another septic splentitis with gas-forming organisms necessitated splecectomy. Transfemoral occlusion of the splenic artery, although an effective, noninvasive approach to control splenic hyperfunction, has at the same time potential dangers that should be viewed with extreme caution in therapeutic application.

Adult↗
PubMed1976

Relationship of splanchnic blood flow and portal venous resistance to elevated portal pressure in the dog.

To determine the relationship of splanchnic blood flow and portal venous resistance to elevated portal pressure, in situ perfusion of the splanchnic circuit was carried out in 12 freshly killed dogs at varying perfusion rates and degrees of acute and chronic portal vein constriction. In six normal dogs before being killed, portal pressure averaged 8-8 +/- 1-2 mmHg and portal flow 658 +/- 81 ml/min. In the absence of portal vein constriction, increasing splanchnic perfusion to 1800 ml/min, minimally raised portal pressure (12-8 +/- 1-5 mmHg). With progressive acute constriction of the portal vein, however, comparable perfusion rates lead to progressively higher portal pressure levels and with greater than 90% constriction, portal pressure was greater than 30 mmHg with minimal elevation in splanchnic flow rate. In six other dogs before being killed but live to nine weeks after placement of an ameroid constrictor on the portal vein, portal pressure averaged 13-6 +/- 1-4 mmHg or slightly higher than in normal dogs (P greater than 0-02). Mesenteric venography and necropsy findings uniformly demonstrated 90% occlusion of the portal vein with extensive portasystemic collateralization. With increased perfusion of the splanchnic bed, portal pressure rose rapidly to approximately 35 mmHg with a flow rate of 1 800 ml/min.. These data suggest that, in disorders where resistance to transhepatic portal flow is marked, a small increment in splanchnic blood flow, which normally exerts little or no influence on portal pressure, promotes profound portal hypertension and may account for spontaneous 'rupture' of oesophageal varices. On the other hand, where resistance to transhepatic portal flow is mild but splanchnic blood flow is markedly hyperdynamic, reducing inflow may be sufficient to ameliorate extreme portal hypertension and its sequelae.

Animals↗
PubMed1976

Splenic artery ligation in selected patients with hepatic cirrhosis and in Sprague-Dawley rats.

The effects of splenic artery ligation were studied in Sprague-Dawley rats and in eight selected symptomatic patients with hepatic cirrhosis. In rats, this maneuver induced splenic infarction, reduced functional splenic mass, transiently raised platelet and reticulocyte counts and was without local complications. In seven selected patients with cirrhosis and prominent splenomegaly, the splenic artery was markedly enlarged, splenic arterial flow was greatly increased and splenic artery ligation partially lowered portal pressure. In three patients with varying cytopenias secondary to hypersplenism splenic artery ligation uniformly improved peripheral blood elements, although varying degrees of hypersplenism later recurred necessitating splenectomy in one. In five other patients, splenic artery ligation in conjunction with coronary vein ligation in four was performed for bleeding esophageal varices. Two patients later required portacaval shunting, and one other in whom operation was undertaken in desperation died of hepatic failure. Celiac-mesenteric arterioportography, operative portography, hemodynamic measurements and examination of peripheral blood elements in these eight patients suggests that splenic artery ligation in conjunction, where appropriate, with coronary vein ligation has several potentially beneficial effects. Hypersplenism may be sufficiently controlled to alleviate clinical symptoms. Arterial inflow into the portal system is reduced tending to lower portal pressure. Transheptic portal flow from the mesenteric bed is preserved. Venous anastomotic channels still functioning around the splenic pedicle and no longer draining a hyperdynamic splenic circuit may be converted into an escape route for mesenteric venous blood entering the portal system under high pressure. Nonetheless, each of these effects and their interrelationships require further study before this operation assumes a larger role in the treatment of complications of portal hypertension.

Animals↗
PubMed1976

Splenic artery ligation in experimental hypersplenism.

The effects of splenic artery ligation (SAL) were examined in Sprague-Dawley rats with methyl-cellulose-induced hypersplenism. When performed close to the splenic hilium, SAL effectively reduced functioning splenic mass and raised peripheral counts of leukocytes and platelets, a response similar to that following total splenectomy. In hypersplenism, therefore, a satisfactory hematologic response may not necessary require total ablation of the spleen but merely substantial reduction of functioning splenic tissue.

Animals↗
PubMed1975

Protein content of liver lymph in patients with portal hypertension secondary to hepatic cirrhosis.

Protein content of liver lymph was measured in 14 patients with portal hypertension secondary to advanced hepatic cirrhosis. An abnormally low concentration was found in each patient, averaging 52% of plasma levels. This finding reflects a decreased sinusoidal permeability to protein, the possible effect of "capillarization of the sinusoid" and may bear on development of portal congestion.

Adult↗