Biomedical subjects
Publications and source records attributed to R C Rogers.
A picoliter pressure ejection system, which is constructed from readily available and inexpensive components, is described. Pressure pulse duration and interpulse interval are controllable by either internal circuitry or by external signals from stimulators or computers. The control features and linearity of ejection volumes are similar to those of more expensive commercial units.
The anaesthetic requirements for tracheal resection include a clear airway, adequate ventilation and good surgical access. Many techniques have been described, none of which is entirely satisfactory. This case reports on the use of high-frequency jet ventilation with 10Fg catheter combined with muscle relaxants and intravenous anaesthesia in a patient with tracheal stenosis.
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Studies were performed to identify the response characteristics of nucleus of the solitary tract neurons receiving afferent projections from the hepatic branch of the vagus nerve. Thirty Sprague-Dawley rats under pentobarbital anesthesia had catheters placed in the ileocolic vein and the inferior vena cava. Neuronal recordings were made in the left medial nucleus of the solitary tract (NST), in the area where hepatic vagal fibers terminate. Sixteen NST cells were identified that responded selectively to the portal infusion of water or hypertonic saline. Two patterns of response were seen: 1) 12 neurons were persistently stimulated by portal hypertonic saline and persistently inhibited by portal water, and 2) four neurons were either transiently excited (n = 3) or transiently inhibited (n = 1) by portal hypertonic saline with no water effect. All units recorded responded to changes of 1% or less in portal blood sodium concentration. Hypertonic mannitol was an ineffective stimulus but choline chloride was as effective as sodium chloride. This suggests that the hepatic receptors utilize an Na+-K+-ATPase electrogenic pump in the transduction process.
In a series of combined electrophysiological and peroxidase histochemical studies, we have established that first-order hepatic and gustatory afferents project to separate regions of the solitary nucleus (NST) and do not converge upon neurons within this structure. Additionally, we have found that hepatic vagal afferent fibers travel in the left cervical vagal trunk and project to the postero-medial division of the left NST. Very small (100-200 micron diameter) iontophoretic injections of horseradish peroxidase (HRP) into physiologically identified zones of the NST reveal that the immediately subjacent parvocellular reticular formation sends efferents to and receives afferents from both the hepatic and gustatory divisions of this nucleus. Further, hepatic and gustatory-NST regions send projections throughout the parabrachial nucleus (PBN). Axons from both the hepatic and gustatory regions of the NST terminate heavily in the posterior dorsomedial part of the PBN. At anterior levels, the gustatory and visceral NST projections are distinctly separate; the medial PBN receives input from gustatory-NST, while the lateral region received input from the hepatic-NST. These results provide anatomical support for our previous findings that single neurons within the PBN can be activated by both gustatory and hepatic afferent activation. Overlapping projections from hepatic (vagal) and gustatory regions of the NST within both the immediately subjacent parvocellular reticular formation as well as the postero-medial PBN may explain in part the decerebrate rat's ability to not only discriminate gustatory stimuli, but also switch its response to a constant stimulus dependent on its nutritive state.
The hepatic branch of the vagus nerve has been implicated as an important source of afferent input controlling both physiological and behavioral homeostasis. In addition, it is clear that parasympathetic efferents to the liver can significantly alter hepatic functions. In order to begin physiological studies on the nature of hepatic afferent and efferent relations, it will be necessary to understand the central anatomical organization of the components of this small visceral nerve. By carefully exposing and dissecting the hepatic branch of the vagus and applying crystalline horseradish peroxidase (HRP) to it, we were able to elucidate a predominant pattern of afferent terminations within the left subnucleus gelatinosus, the medial division of the left solitary nucleus and the left lateral edge of the area postrema. Efferent nuclei were concentrated in the left dorsal motor nucleus of the vagus (DMN) with a few scattered neurons located in the right DMN as well as the left anterior nucleus ambiguous.
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The cell bodies of origin of peripheral nerves, in particular visceral nerves, are often difficult to identify using standard horseradish peroxidase (HRP) methods. The non-ionic surfactant Nonidet-P40, when applied to intact peripheral nerve along with HRP, allows the investigator to examine the neurons of origin of the nerve without cutting the fibers or injecting label into its peripheral terminal field.
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Platelets obtained from some diabetic patients show enhanced in vitro platelet aggregation. This study sought to determine if platelet obtained from insulin-dependent diabetic subjects synthesize increased quantities of the labile aggregating substance, thromboxane A2 (TXA2), and if it may play a role in the enhanced platelet aggregation. Arachidonic acid (1 mM)-stimulated TXA2 synthesis, as determined via radioimmunoassay of its stable metabolite TXB2, was significantly greater (P less than 0.01, N = 12) in platelet-rich plasma obtained from diabetics compared with matched controls. Arachidonic acid-stimulated TXB2 synthesis in the diabetic platelet-rich plasma was positively correlated with the ambient fasting plasma glucose (r = 0.61, P less than 0.02, N = 15). Platelet aggregation induced by arachidonic acid (0.4-0.8 mM) was inhibited significantly less by 13-azaprostanoic acid (P less than 0.04, N = 14), a competitive antagonist of the actions of prostaglandin H2 or TXA2 on platelets, compared with matched controls. The results support the notion that platelets obtained from some insulin-dependent diabetic subjects manifest increased synthesis of TXA2, which may contribute to the enhanced platelet aggregation.
Platelets obtained from some diabetic patients show enhanced in vitro platelet aggregation. These studies were designed to determine if platelets obtained from diabetic subjects manifest increased metabolism of arachidonic acid to labile aggregating substances, such as thromboxane A2 (TXA2), and if they play a role in the enhanced platelet aggregation. Arachidonic acid stimulated TXA2 synthesis, as determined via radioimmunoassay of its stable metabolite TXB2, was significantly greater (p less than 0.01, n = 12) in platelet-rich plasma obtained from diabetic compared to matched controls. Arachidonic acid stimulated TXB2 synthesis in the diabetic platelet-rich plasma was positively correlated with the ambient fasting plasma glucose (r = 0.61, p less than 0.02, n = 15). Platelet aggregation induced by arachidonic acid (0.4-0.8 mM) was inhibited significantly less by 13-azaprostanoic acid (p less than 0.04, n = 14), an antagonist of the actions of prostaglandin H2 or TXA2 on platelets, compared to matched controls. We conclude that platelets obtained from some diabetic subjects manifest increased metabolism of arachidonic acid to labile aggregating substances which may contribute to the enhanced platelet aggregation.
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Platelets obtained from some diabetic patients show enhanced in vitro platelet aggregation. This study sought to determine whether platelets obtained from diabetic subjects synthesize increased quantities of the labile aggregating substance. TXA2, and whether it may play a role in the enhanced platelet aggregation. Arachidonic acid (1 mM)-stimulated TXA2 synthesis, as determined via radioimmunoassay of its stable metabolite TXB2, was significantly greater (p < 0.01, n = 12) in platelet-rich plasma obtained from diabetic patients than in matched controls. Arachidonic acid-stimulated TXB2 synthesis in the diabetic platelet-rich plasma was positively correlated with the ambient fasting plasma glucose (r = 0.61, p < 0.02, n = 15). Platelet aggregation induced by arachidonic acid (0.4 to 0.8 mM) was inhibited significantly less than in matched controls by imidazole, a thromboxane synthetase inhibitor (p < 0.01, n = 11), and 13-azaprostanoic acid, an antagonist of the actions of PGH2 or TXA2 on platelets (p < 0.04, n = 14). We conclude that platelets obtained from some diabetic subjects manifest increased synthesis of TXA2, which may contribute to the enhanced platelet aggregation.
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In 1977 the first case of cholera known to be contracted in Australia during the seventh pandemic occurred in southeastern Queensland. Toxigenic isolates of Vibrio cholerae, biotype eltor, serotype Inaba, phage-type 2, were obtained from the index case, a companion of the patient, the reticulated water supply of their place of residence, and a stretch of the neighbouring river that was being used to supplement fully treated water piped from Brisbane. Treatment of the auxiliary supply consisted solely of chlorination. A section of another river was later shown to contain V. cholerae. No source of pollution was identified for either river. From the persistence of the microorganism in the first river over a two-month period, despite increases in river flow following significant rainfall, it seems that the cholera vibrio can not only survive for a long period but can also grow in the river water. This strongly suggests that certain surface, and possibly subsurface, waters may serve as potential silent foci of V. cholerae. Hence the importance of providing bacteriologically safe water supplies, and the possible need to expand the definition of a 'cholera-receptive area'.
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Previous investigations concerning the function of hepatic sodium and osmoreceptors indicated that the activation of these chemoreceptive structures significantly affected physiological and behavioral mechanisms related to water and electrolyte homeostasis. Though anatomical studies predicted that such information should follow the previously described gustatory afferent pathy, until recently, the precise course taken by higher order hepatic afferents was unknown. The studies described herein verify anatomical predictions with regard to the central course of vagal-visceral afferents, as hepatically activated neurons were localized to two areas known to relay gustatory input. Further, horseradish peroxidase histochemical studies verified that a path between the nucleus of the solitary tract, the parabrachial nucleus and the ventrobasal complex certainly exists. In the light of recent findings regarding projections from the ventrobasal complex to the supraoptic nuclei, from the parabrachial nucleus to the supraoptic nuclei and from the nucleus of the solitary tract to the paraventricular and supraoptic nuclei it seems likely that the viscero-gustatory path which carries hepatic afferent information is the pathway responsible for the physiological and perhaps the behavioral consequences of hepatic sodium or osmotic stimulation.