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Biomedical subjects

C L Witte

Publications and source records attributed to C L Witte.

At least 109 records · Page 6Linked to original sources
PubMed1982

Synergism between the spleen and serum complement in experimental pneumococcemia.

To examine the interplay between the spleen and complement activation in host defense against pneumococcemia, serial colony counts in blood and survival rates were studied after high-dose (10(5)) and low-dose (10(2)) intravenous challenge with growth-phase Streptococcus pneumoniae type 3 in rats with splenic remnants of varying size (partial, total, or no splenic resection) and with or without complement depletion (by pretreatment with cobra venom factor [CVF]). After high-dose challenge, the combination of total splenectomy and CVF produced greater pneumococcemia and higher mortality than either factor alone. After low-dose challenge, survival was uniform except when CVF was coupled with total splenectomy or splenic remnants less than one third of normal size, combinations which resulted in extremely high early mortality. This synergistic interaction between total splenectomy and CVF reveals a serious postsplenectomy immune defect and provides a highly sensitive assay of residual protective function in the spleen.

Animals↗
PubMed1981

Thoracic duct cannulation via a transjugular vascular endoscope (lymphoscope) in the dog.

We describe the feasibility of transjugular endovascular visualization and cannulation of the canine cervical thoracic duct using a flexible cholangioscope modified for lymphoscopy. The lymphoscope is composed of a prismatic side-view optic with a catheter guide channel attached by a metal cap to the terminal end. The technique has clinical applicability to the study of neoplastic diseases, examination and depletion of lymphocyte subpopulations in immunologic disorders, and perhaps the overcoming of increased resistance to lymph flow at the cervical lympho-venous junction in edematous conditions characterized by excessive lymph formation.

Animals↗
PubMed1980

Circulatory control of splenic hyperfunction in children with peripheral blood dyscrasia.

Ligation of the splenic artery was performed upon six children with a variety of peripheral cytopenias associated with hypersplenism to decrease splenic hyperfunction while preserving some splenic tissue. While this procedure initially improved the peripheral blood values in five patients--two patients with hereditary spherocytosis, one patient with idiopathic thrombocytopenic purpura, one patient with pyruvate-kinase hemolytic anemia and one patient with posthepatitic cirrhosis and splenomegaly--the hematologic derangement gradually recurred in four, necessitating eventual splenectomy in two. The sixth patient, an infant with histiocytosis-x, died soon after ligation of the splenic artery. Scintiscans of the spleen corroborated regrowth of the splenic remnant, principally the lower pole to which the vascular supply in the splenocolic ligament was not interrupted. Although ligation of the splenic artery is safe and promptly reduces splenic overreactivity, this operation can only be viewed as temporizing and not as definitive treatment of hypersplenism. On the other hand, in view of the protective function of the spleen against certain bacteria and protozoa, particularly in children with blood dyscrasia, the idea of achieving eusplenism or mild hyposplenism rather than asplenism by a graded reduction in the functional splenic mass through ischemic treatment of hypersplenism seems sound. Alternative methods of circulatory control, for instance, embolization of the splenic artery, of splenic function should be cautiously pursued.

Blood Cell Count↗
PubMed1980

Lymph imbalance in the genesis and perpetuation of the ascites syndrome in hepatic cirrhosis.

Despite extensive study, the pathogenesis of cirrhotic ascites and its relationship to salt and water retention and the hepatorenal syndrome remain unclear. This article reexamines the underlying disturbance in microcirculatory exchange of fluid and protein in the liver and digestive tract and specifically stresses that, in keeping with current interpretation of the Starling hypothesis, ascites appears when the driving force of elevated portal pressure overwhelms the "safety factors" of widened transmural colloid asmotic pressure gradient and accelerated regional lymph flow. In light of recent findings that enhancement of ascitic fluid returned to the bloodstream produces a natriuresis, diuresis, and amelioration of ascites, a "lymph imbalance" theory distinct from the "classic" and "overflow" theories is advanced. This theory proposes that a circulatory imbalance between the rate of fluid leaving and returning to the bloodstream (i.e., the relative rates of lymph formation and lymph absorption) is responsible for a maldistribution of extracellular fluid, which, in turn, stimulates renal salt and water retention, progression of ascites, and finally, the hepatorenal syndrome. Should compensatory factors suffice to prevent or reverse this lymph imbalance, the full cycle is not activated or, if already operating, is deactivated. Thus, portacaval shunt (by reducing the rate of lymph formation) or peritoneovenous shunt (by acting as a megalymphatic collateral to accelerate resorption as well as prevent sequestration of peritoneal fluid), both tend to restore the lymph balance and thereby suppress salt and water retention, correct functional oliguria, and ameliorate ascites.

Acute Kidney Injury↗
PubMed1979

Oxygen exchange in the mesenteric microcirculation of the dog.

The relationships of O2 tension in mesenteric lymph (PmlO2) and mesenteric venous blood (PmvO2) to intestinal O2 delivery/O2 consumption (DO2/VO2) were examined after graded hemorrhage (10 dogs), stepwise increments in FIO2 (4 dogs), and regional infusion of papaverine (2 mg/min or IV glucagon (25 microgram/kg) (4 dogs). Measurements included superior mesenteric arterial flow (SMA-Q), PaO2, PmlO2, and arterial and mesenteric venous blood O2 content (CaO2, CmvO2). Intestinal DO2 was calculated as the product of SMA-Q and CaO2, and VO2 was calculated from the Fick equation [SMA-Q X (CaO2 - CmvO2)]. Graded hemorrhage lowered SMA-Q, DO2 and DO2/VO2 and increased splanchnic O2 extraction (CaO2 - CmvO2). Elevation of FIO2 increased PaO2, PmvO2, and PmlO2. Both PmlO2 and PmvO2 varied directly with DO2/VO2 and PaO2, but PmlO2 showed greater sensitivity to PaO2. Papaverine and glucagon both increased SMA-Q, DO2, CmvO2, and PmvO2, BUT PmlO2 rose after papaverine, indicating greater capillary perfusion, and fell after glucagon, suggesting diversion of mesenteric blood flow through arteriovenous shunts. Thus, either PmvO2 or PmlO2 is ordinarily an accurate measure of intestinal tissue oxygenation, but the disparate response after glucagon suggests that PmlO2 is a more reliable indicator.

Animals↗
PubMed1979

Weight gain and edema on methadone maintenance therapy.

Methadone HCl is currently legally dispensed to approximately 80,000 heroin addicts in the United States. It is widely heralded as being virtually free from other than narcotic side effects. This report describes in detail three patients with massive fluid gain in a population of 420 addicts treated at the Hope Center methadone program in Tucson, Arizona. In no patient was there a prior history of edema, and an intensive search failed to reveal a cause for the swelling. Weight gain uniformly began 3 to 6 months after initiation of methadone or a sharp increase in the dosage, and in all three patients during periods when they sharply reduced or discontinued methadone, edema was resolved associated with a concomitant loss of weight.

Adult↗
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↗