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Biomedical subjects

R P Menninger

Publications and source records attributed to R P Menninger.

13 recordsLinked to original sources
PubMed1994

Ten years of basic medical physiology in the Mercer problem-based curriculum.

In our curriculum, students learn basic medical physiology and pathophysiology during a 74-week integrated multidisciplinary program. This problem-based program consists of two phases aimed at student acclimation to the educational approach and to coverage of fundamental information, followed by 10 phases devoted to in-depth coverage of the organ systems. Physiological principles are given major emphasis during these latter 10 phases. In this approach, students meet in small groups, identify basic science learning issues (including physiology) from written biomedical cases, research the issues, and discuss these issues in relation to each case. These groups (6-7 students plus a tutor) meet for 3-hour sessions three times each week during each phase. Students receive cases, along with study guides designed to assist in selecting appropriate information sources for each phase. Each student is evaluated on group process skills, oral presentation and defense of a case analysis, and a multiple-choice exam. Internal and external [National Board of Medical Examiners (NBME) Part I] evaluations for the Classes of 1987-1993 indicate that our problem-based approach results in student learning of medical physiology.

Curriculum↗
PubMed1985

Current concepts of volume receptor regulation of vasopressin release.

For 2 decades evidence accumulated that supported the Gauer-Henry hypothesis tying blood volume changes to the control of vasopressin (VP). By the mid 1970's this left atrial hypothesis was generally accepted even though there was a significant body of conflicting data and several definitive questions that had not been answered. In the last decade numerous investigations have addressed these questions and although there are better answers for some, others remain elusive. Pertinent work during the past 10 years is reviewed in the framework of some of these questions. The emphasis is placed on the location of the primary volume receptors, determination of the threshold for effects on VP, the degree of volume-pressure receptor and volume-osmotic receptor interactions, and species differences.

Animals↗
PubMed1981

Right atrial stretch decreases supraoptic neurosecretory activity and plasma vasopressin.

It is generally held that left atrial stretch (LAS) but not right atrial stretch (RAS) reflexly inhibits vasopressin release and results in a diuresis. To reexamine the influence of RAS on the release of vasopressin and on the behavior of antidromically identified supraoptic neurosecretory neurons, RAS and LAS were applied in pentobarbital-anesthetized cats. Weighted 20 or 30 g sutures were placed in the left atrium pulmonary vein junction and at the base of the right atrial appendage. Antidromically identified supraoptic nucleus neurons were inhibited by both RAS and LAS applied independently and together, although fewer neurons were responsive to RAS alone. Simultaneous stretch of both atria resulted in greater inhibition of these neurons than did stretch of either atrium alone. Stretch of the right atrium alone also resulted in a significant decrease in plasma arginine vasopressin measured by radioimmunoassay. Differences between these results and other reports may stem from differences in the method of RAS or the specific right atrial receptors affected.

Animals↗
PubMed1979

Response of supraoptic neurosecretory cells to changes in left atrial distension.

Acute studies were conducted in cats to determine the effects of small changes in left atrial pressure (LAP) on the activity of antidromically identified neurons in the supraoptic nucleus (SON). Inflation of left atrial balloons reproducibly altered the frequency of 15% of the SON neurons. More than half of these increased frequency, probably due to a simultaneous increase in arterial pressure. In a second series, the firing rates of 20% of the SON neurons tested were inversely related to changes in LAP produced by pumping blood into or out of the left atrium. A third series of experiments were conducted in which the left atrium was directly stretched by pulling on a suture placed in the atrial wall in addition to one of the above methods of changing LAP. Directly stretching the left atrium inhibited over 70% of the SON neurons; this included all the neurons that responded to changes in LAP. The results suggest that these SON neurons have differential sensitivities to inputs from left atrial receptors.

Action Potentials↗
PubMed1979

Effects of carotid occlusion and left atrial stretch on supraoptic neurosecretory cells.

Acute experiments were performed on pentobarbital-anesthetized cats to determine whether atrial and carotid baroreceptors affected the same neurosecretory neurons in the supraoptic nucleus (SON) of the hypothalamus. The osmosensitivity of these neurons was also determined. Eighty-two SON neurons were antidromically identified and 63 of these increased their firing rates during complete occlusion of the right carotid artery. Further testing of these 63 neurons demonstrated that 56 were inhibited by directly stretching the left atrium and 61 were excited by intracarotid injection of hypertonic saline. Left atrial stretch greatly reduced the neuronal response to carotid occlusion. These results show that the activity of the majority of the antidromically identified SON neurons is altered by left atrial and carotid artery receptors as well as changes in plasma osmolality. Results are consistent with the known influence of these receptors on plasma vasopressin.

Animals↗
PubMed1976

Hypothalamic and brachial nerve effects on circulation of isolated canine forelimb,.

Canine forelimbs were vascularly isolated and perfused at either constant inflow or constant inflow pressure. A comparison of the effects of electrical stimulation of hypothalamic pressor areas and brachial nerves was made on several vascular parameters. During constant pressure perfusion, forelimb resistance increased and total forelimb volume decreased. Additionally active vascular volumes measured with 131I-labeled albumin and 51Cr-labeled red cells decreased significantly. Capillary diffusion capacity product calculated from extraction of 86RbCl also decreased significantly as did the capillary filtration coefficient (CFC). The only significant differences between hypothalamic and brachial nerve stimulation were noted in the larger decreases in active volumes and CFC during the latter stimulations.

Animals↗
PubMed1976

Forelimb blood flow distribution during hypothalamic dilator response.

An attempt is made to determine whether hypothalamically induced forelimb vascular dilation in the dog affects primarily exchange beds or shunt circuits. Slug injections of [131I] albumin and 86RbCl were used to measure the active vascular volume of the forelimbs and permeability surface area product (PS), respectively. Changes in total vascular volume (TVV), filtration, and capillary filtration coefficient (CFD) were measured by plethysmography. During stimulation, forelimb blood flow increased 25% and TVV increased an average 1.5 ml. There was no plethysmographic evidence of outward capillary filtration. Active vascular volume decreased 11%. PS decreased 11%, and CFC decreased 20%. These results point to a redistribution of blood flow from exchange circuits to faster flow channels. During constant-inflow perfusion, there was evidence from CFC and PS measurements that the capillary surface area was increased while active vascular volume decreased. The results observed with hypothalamic stimulation are different from those obtained with pharmacologic dilators and denervation. It is suggested that the former method has a more selective effect in lowering resistance in the faster shuntlike vessels.

Animals↗
PubMed1976

Skeletal muscle vascular volume changes with increased venous pressure.

Dog gracilis muscles were removed, enclosed in a plethysmograph and perfused at constant inflow pressure or constant inflow. Circulating blood volumes were measured by the constant infusion technique using RBC-51Cr or albumin-131I. Control venous pressure averaged 3 mm Hg and elevations (delta PV) over the range of 5-40 mm Hg were produced. Volume changes were determined during and following delta PV by plethysmography and by changes in total muscle radioactivity. Changes in total (amount of blood in the tissue), active (circulating), and mobilized vascular volumes were calculated. Active vascular volumes and total vascular volumes increased with venous pressure increments up to 25 mm Hg and then plateaued. Active vascular volumes (indicators) increased by amounts significantly greater than the increases in total vascular volume (plethysmography). Volume changes in the constant flow groups were double those in the constant pressure groups. The mobilized active vascular volume (active vascular volume change minus total vascular volume change) consists of a volume of blood contained in vessels unattainable by the indicators during the control period but which were made available to the indicator by the delta PV. Mobilized vascular volume averaged 45% of the active vascular volume change. With venous pressure elevation there was an increase in the RBC-51Cr volume to albumin-131I volume ratio. This suggests a redistribution of red cells with respect to plasma, possibly resulting from reduced plasma skimming.

Animals↗
PubMed1975

Vascular and extravascular volume changes due to elevated venous pressure.

Abrupt elevation of venous pressure causes an initial rapid and a secondary slow increase in total tissue volume (plethysmography). Changes in total tissue volume and blood conductivity from the isovolumetric state were determined to assess what factors determined the two components of the tissue volume change. The initial component of the plethysmograph record would appear to be 90% vascular volume change and 10% extra-vascular volume change. Since the two techniques measured identical amounts of capillary filtration during the second component of the recording there would seem to be no slow component of vascular volume increase following venous pressure elevation. Evidence that elevation of venous pressure causes myogenic closure of precapillary vessels isolating a segment of the microvasculature is presented.

Animals↗