Richard D. Rink

Oxidative metabolism in experimental Bacteriodies fragilis bactermia.

Abstract Bacteriodes fragilis has received recent attention as a pathogen in surgical patients. In an effort to assess its pathogenicity, 28 male Sprague-Dawley rats underwent carotid cannulation. With the cannula in the root of the aorta, 14 animals had 1 × 10 10 B. fragilis infused over 30 min with a control receiving only saline. This results in an LD 0 despite the number of bacteria being five times the LD 100 for Escherichia coli . Rats had heart rate, mean arterial pressure, p O 2 , p CO 2 , pH, hematocrit, glucose, and lactate measured very 2 hr. At 6 hr, the hepatic tissue p O 2 was measured with a surface polyelectrode. Paired experimental and control animals were sacrificed at 6 hr, livers were excised and homogenized. Mitochondria were isolated and studied polarographically by measurement of state 3 (ADP-dependent) and state 4 (ADP-independent) respiratory rates. The Respiratory Control Index (RCI) was calculated (state 3/state 4) as a sensitive indicator of mitochondrial oxygen utilization. No hypotension developed in bacteremic rats. Arterial p O 2 , p CO 2 , and pH were essentially unchanged. Blood glucose was unchanged while lactate rose moderately. RCIs of experimental and control mitochondria were similar ( P > 0.05). B. fragilis bacteremia does not produce the changes of mitochondrial respiratory control of E. coli bacteremia or septic peritonitis.

Hepatic oxygen supply in reversible and irreversible hemorrhagic shock.

Abstract Data has been collected in a manner that clarifies the degree to which hepatic oxygen supply is affected during the circumstances of reversible and irreversible hemorrhagic shock. The liver PO2 estimations support the concept that the liver is largely hypoxic during hemorrhagic hypotension. Subsequent nonsurvival is correlated with depressed hepatic reoxygenation and persisting lactic acidosis following retransfusion of all shed blood. By contrast, survivors established significant levels of hepatic PO2 and reversed their acidotic state. We believe the profile of hepatic oxygen supply presented should contribute to the interpretation of alterations of hepatic function reported in other hemorrhagic shock studies.

The acute effects of nicotine, tobacco smoke and carbon monoxide on myocardial oxygen tension in the anaesthetized cat.

1 The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo2) were estimated amperometrically in 33 anaesthetized open‐chest cats with a glass‐insulated 25 gtm platinum cathode within a 22‐gauge needle implanted in the left ventricular wall. 2 MPo2 was 1.6–60 mmHg (mean 23.5 mmHg) when arterial P02 was >80 mmHg. Sequential intravenous infusions of nicotine (2–3 gg/kg every 45 s) or intracheal puffs (3–5 ml) of tobacco smoke commonly produced transitory increases (25–35 mmHg) of arterial pressure and 4–6 mmHg increments of MPo2. Intratracheal puffs (5 ml) of 5% carbon monoxide sufficient to increase carboxyhaemoglobin from 0.8 to 1.5% to 4–7% had no effect on arterial Po2 or blood pressure but typically decreased MPo2 by approximately 1–4 mmHg. Augmentation of MPo2 often succeeded carbon monoxide administration. 3 Arterial hypoxia (arterial Po2 < 60 mmHg) reduced mean MPo2 to 14.4 mmHg but anoxic levels were not observed. Pressor responses to nicotine and tobacco smoke were accompanied by small increases (usually 1–3 mmHg) of MPo2. Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo2 (<10 mmHg) were unaffected as carboxyhaemoglobin was raised to 7–11% during hypoxaemia. 4 It is concluded that nicotine and tobacco smoke cause augmentation of myocardial oxygen supply, even during moderate hypoxaemia. By contrast, smoking dosages of carbon monoxide have the potential of producing a small reduction of MPo2 during normoxia, but the effect is negligible during moderate hypoxaemia.

Plasma albumin repletion after transfusion with polymerized hemoglobin

Pyridoxalated polymerized hemoglobin (PPHG) has promise as a blood substitute for transfusing patients with hemorrhage. Exchange transfusion with PPHG depletes plasma proteins. The purpose of this study was to determine if, during the early repletion of intravascular proteins, albumin was transported from the interstitium of skin or skeletal muscle into the vascular compartment. PPHG was prepared from stroma-free human hemoglobin (100-120 mg/ml). The Hct of anesthetized rats dropped from 42 +/- 4% to 10 +/- 1% after exchange transfusion. Immediately postexchange plasma albumin declined from 24 +/- 2 to 6 +/- 3 mg/ml. Five hours postexchange transfusion plasma albumin had doubled and the skin and skeletal muscle albumin content was 80% of control. These data indicate that a shift of interstitial albumin from skin and skeletal muscle can rapidly replace plasma protein deficits after massive transfusion with PPHG.

Evidence of an Intestinal Factor During Prolonged Hypothermia in the Rat

Three groups of rats surgically treated during the induction of 15 °C total body hypothermia, which was subsequently maintained for 7.5 h. The group whose intestinal circulation had been occluded show