Previous studies have shown that a shift in blood flow away from edematous regions does not occur until the alveoli contain liquid. The present experiments were designed to examine the separate effect of air space liquid, air space plus interstitial liquid, and reduced lung volume on blood flow. We found that reduced lung volume was not associated with significant changes in blood flow and that no systematic change in blood flow occurred when alveoli were filled with isosmotic liquid (autologous plasma). However, when hyposmotic liquid (dilute plasma) was instilled so that both the air space and the alveolar wall interstitial space were filled, blood flow was systematically reduced. This suggested that interstitial liquid was responsible raising vascular resistance in these experiments and that it might also be important in raising local vascular resistance in pulmonary edema. This latter hypothesis was tested in isolated perfused lobes where rapid freezing and quantitative histology showed that the number of open capillaries was significantly reduced in the liquid-filled alveoli (P less than 0.001). These observations suggest that interstitial pressure rises in pulmonary edema with the result that the transmural pressure of the alveolar vessels falls and vascular resistance is increased.
An experimental technique to study the local utero-ovarian circulation in fifteen ewes is described. It involves specific cannulation of the anterior uterine vein, the utero-ovarian vein and the ovarian artery. Experiments to test for direct passage between the uterine vein and ovarian artery were performed, using a highly diffusible gas (133Xe) and a large molecule radioiodinated human serum albumin (131RISA). The ovary was either left attached to or disconnected from its ligaments. Labelled RISA failed repeatedly to cross, indicating no direct shunt; 133Xe crossed with an appearance time of about 20 sec, indicating passive diffusion. Anatomical casts were also prepared using coloured latex injections. Dissection failed to show any direct communications between venous and arterial vessels. These findings fail to support the concept of a local veno-arterial passage of a presumptive uterine luteolysin.
A tracer dose of the presumptive uterine luteolytic factor (PGF2\g=a\) was introduced into the anterior uterine vein of twelve ewes, either as a bolus or as a 40to 60-min infusion (0\m=.\2\g=m\Ci/min). The ipsilateral ovary was left attached to or disconnected from its ligaments. Neither a bolus nor an infusion of [9-3H]PGF2\g=a\ led to any transfer of radioactivity in the ovarian artery under controlled experimental conditions. These results show conclusively that diffusion, filtration, counter-current exchanges and active transport do not occur between the anterior uterine vein, the utero-ovarian vein and the ovarian artery. A direct and local luteolytic action of PGF2\g=a\ is therefore questionable.
The effects of 5 mg/kg acebutolol given intravenously were investigated in anaesthetized dogs after (a) ligation of the left anterior descending coronary artery and (b) coronary reperfusion following 60 min of ligation of the left anterior descending coronary artery. Coronary artery ligation produced, after 4 to 6 h, persistent multiple ventricular ectopic beats and abnormalities of R and T waves and of the S‐T segment. Administration of acebutolol, after the development of persistent ventricular arrhythmias, restored normal sinus rhythm within 5 min of injection. Electrocardiographic abnormalities were also reduced. Coronary artery reperfusion (following 60 min of ligation) resulted in multiple ventricular ectopic beats, ventricular tachycardia and/or ventricular fibrillation. Pretreatment with acebutolol, 15 min before starting reperfusion, markedly reduced the arrhythmias. Acebutolol did not affect peak inspiratory airway pressure. Acebutolol produced significant bradycardia and slight, transient, hypotension. It was without effect on left ventricular systolic pressure, left ventricular end‐diastolic pressure, cardiac output or pulmonary arterial pressure. These results suggest beneficial effects of acebutolol in myocardial ischaemia and coronary reperfusion, without any significant risk of cardiodepression or bronchospasm.
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