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K Anders

Publications and source records attributed to K Anders.

13 recordsLinked to original sources
PubMed1992

Synaptic interaction between medullary respiratory neurones during apneusis induced by NMDA-receptor blockade in cat.

1. Termination of inspiration is an essential component of respiratory rhythm generation and its perturbation can result in apneusis, i.e. significant prolongation of mechanisms, we studied the postsynaptic events in respiratory neurones during apneustic respiratory periods, and compared them to normal respiratory cycles. 2. Experiments were performed in pentobarbitone-anaesthetized, paralysed, thoracotomized cats ventilated with a constant volume or a cycle-triggered constant pressure pump. Apneusis, separated by normal cycles, was induced as follows: the animal was ventilated by a cycle-triggered pump that normally inflated the lungs during the inspiratory burst of phrenic nerve discharge. The NMDA-receptor blocker MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-iminemaleate] (0.3-0.7 mg/kg) was administered intravenously, and, for designated breaths, inflation of the lungs was withheld during neural inspiration. 3. Membrane potential trajectories of forty-one late expiratory (E-2) and eight postinspiratory (PI) neurones of the caudal ventral respiratory group were analysed before and/or after MK-801 administration, during normal and apneustic periods. 4. Before MK-801 administration, withholding lung inflation caused modest (10-20%) lengthening of the inspiratory period; after MK-801 administration, withholding inflation caused apneusis. Provided that the lungs were inflated during the inspiratory phase, the temporal pattern of phrenic nerve, recurrent laryngeal nerve and membrane potential trajectories of E-2 and PI neurones were not significantly altered by MK-801. Apneusis following NMDA-receptor blockade produced consistent changes in the synaptic activation patterns of E-2 neurones. In particular, the slow late inspiratory-related depolarization pattern of E-2 neurones was consistently retarded during apneustic inspiratory phases when compared to normal inspiratory phases. This was due to continuation of Cl(-)-mediated synaptic inhibition of E-2 neurones. Superior laryngeal nerve stimulation stopped apneusis and sustained membrane hyperpolarization of E-2 neurones similar to lung inflation. 5. During the plateau phase of apneusis, correlated 10-20 Hz oscillations could be observed in the integrated phrenic and recurrent laryngeal nerve activities as well as in the membrane potential of E-2 neurones. 6. We conclude that: (i) the prolonged inhibition of E-2 neurones during apneusis is indicative of the process responsible for the prolongation of the inspiratory phase.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

A network model of respiratory rhythmogenesis.

A mathematical model of the three-phase respiratory network proposed by Richter et al. (News Physiol. Sci. 1: 109-112, 1986) is developed and its properties are examined. The model reproduces the experimentally determined trajectories of membrane potential for the five physiologically distinct types of neurons included. Stepwise parameter changes can produce a respiratory rhythm with only two separate electrophysiological phases, result in apnea, or produce more complex patterns of firing. The phase-resetting behavior of the model was obtained with perturbing stimuli and is comparable to experimentally determined phase-resetting data. There is reasonable agreement between model predictions and experimental results. In the model, the properties of the phase singularity make termination of the respiratory rhythm by an appropriately timed perturbation virtually impossible, which is in agreement with experimental observations. The rhythm can be stopped by alterations that simulate the effect of input from the superior laryngeal nerve; the rhythm is locked in the postinspiratory phase. We conclude that our results are consistent with the concept of a network oscillator as the source of the respiratory rhythm.

Animals↗
PubMed1991

The medullary respiratory network in the rat.

1. In urethane or Nembutal anaesthetized and artificially ventilated Wistar rats, respiratory neurones of the ventrolateral medulla oblongata were analysed in extracellular (n = 74) and intracellular (n = 43) recordings. 2. Some respiratory neurones were identified as bulbospinal by their antidromic response to spinal cord stimulation at the C4 level. The neurones examined were not antidromically excited by vagal nerve stimulation. 3. Based on their discharge pattern in relation to efferent phrenic and vagal nerve activity, six types of respiratory neurones were classified: early-inspiratory, throughout-inspiratory, late-inspiratory, post-inspiratory, expiratory, and phase-spanning expiratory-inspiratory neurones. 4. Analysis of postsynaptic activities and IPSP reversal following chloride injection revealed post-inspiratory and expiratory inhibition in inspiratory neurones a pronounced early-inspiratory and a relatively weak expiratory inhibition in post-inspiratory neurones, and an early-inspiratory and post-inspiratory inhibition in expiratory neurones. 5. In phase-spanning expiratory-inspiratory neurones the post-inspiratory inhibition was strong and effectively blocked action potential discharge. Expiratory-inspiratory neurones were quite similar to the group of inspiratory neurones, but seemed to receive tonic excitatory inputs not shunted by weak expiratory inhibition. This pre-inspiratory discharge was readily blocked by weak negative DC injection. 6. Under conditions of experimental hypoxia, or long lasting lung inflation and non-inflation, post-inspiratory neurones displayed a second burst of discharge at the end of the expiratory phase in addition to their longer lasting post-inspiratory discharge. 7. We conclude that in the rat the central respiratory rhythm is organized in three (inspiratory, post-inspiratory, expiratory) phases, and that synaptic interaction within the medullary respiratory network of the rat occurs similarly to that described for the cat.

Action Potentials↗
PubMed1991

Inhibition of caudal medullary expiratory neurones by retrofacial inspiratory neurones in the cat.

1. Comparisons between the spike discharge of inspiratory neurons within the retrofacial area (RFN), and the membrane potential of expiratory neurones within the caudal medulla were made in pentobarbitone-anaesthetized, vagotomized, artificially ventilated cats. Spike-triggered averaging (STA) of synaptic potentials, triggered by the discharge of inspiratory RFN neurones, was utilized to test for synaptic connectivity. 2. Eighty-nine neurons with respiratory-phased discharge patterns were recorded in the vicinity of the RFN. Fifty-four neurones discharged at or slightly before the onset of the inspiratory burst activity of the phrenic nerve and continued firing throughout inspiration. Two continued to fire during post-inspiration. Forty-five of fifty-four inspiratory RFN neurones exhibited incrementing discharge patterns, six discharged with a plateau pattern, while only three neurones had a decrementing discharge pattern. 3. The membrane potential trajectories of caudal expiratory neurones revealed a typical wave of early inspiratory hyperpolarization. Occasionally, a second wave of hyperpolarization occurred during late inspiration, in conjunction with increased phrenic nerve activity. 4. Spike-triggered averaging revealed averaged inhibitory postsynaptic potentials (IPSPs), indicative of inhibitory synaptic connections, between eight and sixty-three pairs of RFN inspiratory and caudal expiratory neurones. 5. Inhibitory postsynaptic potentials detected by STA exhibited a relatively long latency and a slow time course. The IPSPs began, on average, 3.8 ms after an RFN action potential. The rise times, half-widths and durations of IPSPs were longer than expected for a monosynaptic somal input from myelinated axons of inspiratory RFN neurones. It is suggested that an inhibitory relay neurone in the immediate vicinity of the expiratory neurones is activated by a collateral of the RFN inspiratory neurone. 6. Retrofacial inspiratory neurones were antidromically activated only when high-intensity electrical stimulation was applied in the vicinity of caudal expiratory neurones. 7. The averaged IPSPs were preceded by diphasic and triphasic 'spike potentials'. The averaged spike potentials were highly entrained to the action potentials of RFN inspiratory neurones which triggered IPSPs. The spike potentials may be terminal potentials recorded from axons of RFN inspiratory neurones. 8. Evidence for convergence of synaptic inputs was obtained from STA tests in a caudal expiratory neurone receiving IPSPs from four RFN neurones. 9. The functional significance of this observation is discussed. We conclude that RFN inspiratory neurones exert a moderate inhibitory influence and act conjointly with other types of medullary inspiratory neurones.

Animals↗
PubMed1991

Response of the medullary respiratory network of the cat to hypoxia.

1. The effect of systemic hypoxia was tested in anaesthetized, immobilized, thoracotomized and artificially ventilated cats with peripheral chemoreceptor afferents either intact or cut. Extracellular recordings from different types of medullary respiratory neurones and intracellular recordings from stage 2 expiratory neurones were made to determine the hypoxia-induced changes in neuronal discharge patterns and postsynaptic activity as an index for the disturbances of synaptic interaction within the network. 2. The general effect of systemic hypoxia was an initial augmentation of respiratory activity followed by a secondary depression. In chemoreceptor-denervated animals, secondary depression led to central apnoea. 3. The effects of systemic hypoxia were comparable with those of cerebral ischaemia following occlusion of carotid and vertebral arteries. 4. In chemoreceptor-denervated animals, all types of medullary respiratory neurones ceased spontaneous action potential discharge during hypoxia. 5. Reversal of inhibitory postsynaptic potentials (IPSPs) and/or blockade of IPSPs was seen after 2-3 min of hypoxia. 6. During hypoxia, the membrane potential of stage 2 expiratory neurones showed a slight depolarization to -45 to -55 mV and then remained stable. 7. The neurone input resistance increased initially and then decreased significantly during central apnoea. 8. Rhythmogenesis of respiration was greatly disturbed. This was due to blockade of IPSPs and, in some animals, to more complex disturbances of phase switching from inspiration to expiration. 9. Central apnoea occurred while respiratory neurones were still excitable as shown by stimulus-evoked orthodromic and antidromic action potentials. 10. The results indicate that the medullary respiratory network is directly affected by energy depletion. There is indication for a neurohumoral mechanism which blocks synaptic interaction between respiratory neurones in chemoreceptor-intact animals.

Action Potentials↗
PubMed1985

Clinical and pathologic findings of the liver in the acquired immune deficiency syndrome (AIDS).

Clinical data and histologic sections of the liver, including immunohistochemical studies for hepatitis B surface and core antigens, were reviewed in 42 autopsy cases of the acquired immune deficiency syndrome (AIDS). Hepatomegaly, elevation of serum transaminases, and mild elevation of alkaline phosphatase were commonly observed clinical and biochemical abnormalities. Mildly elevated alkaline phosphatase and normal bilirubin levels were present in patients with Mycobacterium avium-intracellulare (MAI) infection, cytomegalovirus (CMV) infection, and Kaposi's sarcoma (KS). Histologic sections demonstrated liver involvement by MAI in eight cases; KS in six cases; cryptococcus in three cases; and CMV in two cases. One case of MAI infection was associated with marked central vein sclerosis, a finding previously unreported. Thirty-two (76%) of 42 cases had serologic or pathologic evidence of hepatitis exposure. Two patients had histologic evidence of chronic active hepatitis. The pathologic processes involving the liver appeared to be secondary to the infections and neoplasms for which this population is susceptible and did not significantly contribute to morbidity or mortality. No findings specific or pathognomic for AIDS were identified in the liver.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Adrenal pathology in the acquired immune deficiency syndrome.

Adrenal pathology was examined in 41 autopsied patients with the acquired immune deficiency syndrome. This represents the largest series and the first study with quantitation of adrenal cortical necrosis. In 32 cases clinical data were analyzed for features of adrenal insufficiency. Common clinical findings included vomiting, diarrhea, fever, hypotension, and hyponatremia. None of the 32 patients showed characteristic skin hyperpigmentation. Two patients were suspected premortem to have adrenal insufficiency. In one of these patients, adrenocorticotrophic hormone (ACTH) stimulation resulted in an adequate rise in plasma cortisol values. In the other patient, the baseline plasma cortisol value was elevated and failed to rise significantly after ACTH stimulation. Pathologic findings included widespread lipid depletion, infection by cryptococcus, and acid-fast organisms consistent with Mycobacterium avium-intracellulare, involvement by Kaposi's sarcoma, and necrotizing adrenalitis due to cytomegalovirus (CMV). A point-counting method was used to quantitate adrenal cortical and medullary necrosis. Necrosis due to CMV was greater in the medulla than the cortex. The maximum amount of adrenal cortical necrosis in any case was 70%. The degree of cortical necrosis was less than that usually associated with adrenal insufficiency.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Chronic active hepatitis of hepatitis B and non-A, non-B etiology. Immunohistochemical localization of hepatitis B core antigen in a series of needle biopsies.

Hepatitis B core antigen (HBcAg) was immunohistochemically demonstrated in 19 of 30 needle liver biopsies (63%) of chronic active hepatitis (CAH) from 15 of 24 patients (63%) whose serum contained hepatitis B surface antigen (HBsAg). The percentage of hepatocytes with nuclear and/or cytoplasmic immunoreactivity was quantified in each biopsy specimen, and these percentages were then compared with the amount of HBsAg and the degree of inflammation within the biopsy specimen. The percentage of HBcAg-positive hepatocytes in a biopsy specimen was greatest in those specimens that contained the most HBsAg, although this finding was not statistically significant. The percentage of HBcAg-positive hepatocytes was greatest in those specimens having the least inflammatory activity, and this was statistically significant (P less than .01). Also, the percentage of biopsy specimens containing HBcAg was increased in those groups with lesser inflammatory activity (P less than .01). By staining for both HBcAg and HBsAg, the detection rate of hepatitis B (HB)-related antigens rose to 27 of 30 biopsies (90%) in 22 of 24 patients (92%).

Biopsy, Needle↗
PubMedDate not supplied

Neuropathologic findings in the acquired immunodeficiency syndrome (AIDS).

The acquired immunodeficiency syndrome (AIDS) is characterized by a severe idiopathic deficiency in T-cell mediated immunity. Homosexuals, intravenous drug abusers and Haitians are predominantly affected, predisposing them to opportunistic infections and neoplasms. In this study, the central nervous system (CNS) was examined at autopsy in 29 AIDS patients. Significant CNS complications occurred in 55%, mainly related to opportunistic infections similar to those seen in patients with other causes of immunosuppression. Progressive multifocal leukoencephalopathy (three cases), cytomegalovirus (CMV) encephalitis (five cases), cryptococcal meningitis (four cases), Mycobacterium avium-intracellulare (three cases), and toxoplasmosis (one case) were found. Widespread microglial nodules were observed in 20 patients, 80% of whom had CMV inclusions elsewhere at autopsy. Primary cerebral lymphoma (one case) and lymphomatoid granulomatosis (one case) were present. Subarachnoid (five cases) and intraparenchymal (three cases) hemorrhage was seen although these were not usually clinically significant. A single case of embolic arterial obstruction with cortical infarction was due to non-bacterial thrombotic endocarditis.

Acquired Immunodeficiency Syndrome↗