Biomedical subjects
Publications and source records attributed to G Moss.
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Gastric aspiration alone utilizing either a Levin-type nasogastric tube or a gastrostomy tube is inefficient. The esophagus proved to be a more efficient supplemental site for aspiration of a swallowed bolus. For thirty-one patients, esophagogastric aspiration proved to be approximately twelve times as efficient as aspiration via a Levin-type tube for twenty-four patients or a gastrostomy tube in five patients (residual activity, of 3,35, and 42 per cent, respectively). Radiographic studies of a volunteer swallowing barium with each type of nasogastric tube in place showed efficient removal of the contrast agent by esophageal aspiration. With the Levin-type tube, the bolus promptly traversed the stomach and entered the duodenum along parallel channels remote from the x-ray -visualized gastric tube. Efficient postoperative exclusion of swallowed air clinically and experimentally by esophageal aspiration permits more rapid return of gastrointestinal function and full nutrition and perhaps shortened hospitalization.
The paralytic ileus, poor nutritional state, and related complications that often develop following serious serious abdominal surgery have traditionally been accepted as unavoidable. Now, a nasogastric decompression and feeding tube is availabe that usually prevents paralytic ileus and also provides a complete liquid diet starting immedicately after the operation, thus speeding wound healing and recivery.
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Seven beagles were subjected to left pulmonary denervation (autotransplantation) and allowed one to two months for complete recovery. The relative resistances of each dog's pair of lungs were determined by the distribution of 99mTc microspheres delivered intravenously while the subject was awake and then under barbiturate anesthesia. In each case, relative blood flow to the right lung increased at the expense of flow to the left. This is interpreted as a direct decrease in pulmonary vascular resistance on the right under the effects of anesthesia. The implications of such central nervous system control of pulmonary vascular resistance was discussed in relation to the pathophysiology of the respiratory distress syndrome.
Twenty-eight anemic control dogs were subjected to isolated cerebral hypoxemic (PO2,35+/-5 mm Hg) perfusion for 2 hours. All were found to have functional pulmonary impairment. Two hours later, twenty were sacrificed and found to have the bilateral anatomic complex of the respiratory distress syndrome (RDS). All those not sacrificed expired within 20 hours with progressive respiratory distress and at autopsy had the bilateral anatomic complex. Twenty-three beagles with chronic denervation (autotransplantation) of the left lung also were subjected to the 2 hour isolated cerebral arterial hypoxemic perfusion. Minimal pulmonary functional impairment was measurable in all. Ten of sixteen were long-term survivors. The six that succumbed did not appear to suffer respiratory deaths. These six, as well as seven sacrificed 2 hours after perfusion, had the anatomic complex of RDS in the normally innervated right lungs. However, the denervated left lungs were anatomically normal. These findings are offered as additional evidence that RDS has a centrineurogenic etiology. We postulate the following sequence: "shock" causes cerebral (probably hypothalamic) cellular oxygen deprivation and dysfunction; there is autonomically mediated, increased resistance of the pulmonary venules ("postcapillary sphincters"); this leads to capillary hypertension, congestion, hemorrhage, edema, surfactant inactivation, and atelectasis. Pulmonary denervation blocks this sequence and protects the lung.
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For beagles respiring 100 per cent oxygen at ambient pressure, anemia protected against the development of the lung lesions of oxygen toxicity. Similarly, unilateral pulmonary denervation was protective of the affected lung but not of the normally innervated, contralateral lung. This indicates that the lung lesions are triggered by the toxic effect of elevated PO2 at a remote site, most likely the sensitive central nervous system.
Anemic beagles were subjected to 40 mm Hg hemorrhagic shock for 2 hours, which uniformly induced the pulmonary lesions of the "respiratory distress syndrome" (RDS) bilaterally in all six controls. For six subjects with complete denervation of the left lung 2 months previously, the shock regimen induced the lesions in the normally innervated right lungs; all reimplanted, denervated left lungs remained anatomically intact. This is presented as additional evidence for a centrineurogenic etiology for RDS.
Dogs subjected to arterial hemorrhage and infused with 3:1 volumes of lactated Ringer's solution became progressively hypovolemic, to the point of frank shock. Stability and normovolemia were restored only after additional fluid delivery, in a net ratio of 8:1. These were the mathematically predicted values that satisfied Starling's hypothesis.
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Beagles and rats were subjected to hemorrhage regimens that induced the pulmonary complex of the Acute Respiratory Distress Syndrome (ARDS) in 6:6 dogs and 7:8 rats. Pretreatment with diphenylhydantoin (DPH), 5 mg/kg 1-2 hours preceding hemorrhage, resulted in complete prevention of the lung lesions in 8:8 dogs. (P smaller than 0.005). It also provided significant (P smaller than 0.01) protection to 8:11 rats. We offer this as circumstantial evidence that the ARDS has a centrineurogenic etiology.