Abiotrophia species as a cause of endophthalmitis following cataract extraction.

Microorganisms of the genus Abiotrophia, members of the oral flora, are known as important causes of bacterial endocarditis. In this study, we report two individual cases of acute vitreous infection caused by Abiotrophia adiacens and Abiotrophia defectiva approximately a week after cataract extraction. Abiotrophia isolates were recovered by cultivation of vitreous humor on chocolate agar and identified via conventional and API 20 Strep identification systems. An 83-year-old male patient (A) and an 80-year-old female patient (B) demonstrated almost identical symptoms of infectious endophthalmitis manifested as hypopyon and opaque media. The vision of both patients was reduced to detection of hand motion in the left and the right eyes, respectively. An emergency pars plana core vitrectomy was performed, and intraocular antibiotics were administered to each patient, who presented 8 months apart in two different institutions. Patients A and B were treated with an intravitreal injection of vancomycin-amikacin and vancomycin-ceftazidime, respectively, which resulted in complete recovery.

Contribution of the liver to thoracic duct lymph flow in a motionless subject.

To ascertain the contribution of the liver to thoracic duct lymph (TDL) flow in a resting subject, afferent hepatic blood flow was temporarily interrupted in dogs by placing an atraumatic clamp across the hepatoduodenal ligament containing the hepatic artery, portal vein and 80% of hepatic lymphatic drainage. To circumvent extrahepatic splanchnic venous sequestration, a side-to-side portacaval shunt (S-S-PCS) was constructed prior to interrupting blood flow. Portal venous pressure, cervical TDL flow, and total protein content were serially monitored. TDL and total protein after S-S-PCS was comparable to that recorded in dogs without celiotomy (0.60 +/- 0.17 ml/min and 3.4 +/- 0.5g/dl, respectively). Interruption of hepatic blood flow was associated with a fall in TDL flow (0.38 +/- 0.8ml; p less than 0.001) and protein content (2.8 +/- 0.7g/dl; p less than 0.01) and TDL/plasma protein ratio (0.58 +/- 0.7 to 0.48 +/- 0.05; p less than 0.01). These data suggest that in the absence of supplemental fluid administration or other exogenous stimulation, hepatic lymph contributes one-third of resting TDL flow.

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.

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.