Professor Jan Herget, M.D., Ph.D.

Head,
Department of Physiology
Second Medical School
Charles University
Prague, Czech Republic
Mailing address:
Plzenska 130/221
150 00 Prague 5
Czech Republic
 
Phone +420 2 57310345 or 57310995
Fax +420 2 57310995
e-mail: jan.herget@lfmotol.cuni.cz

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RESEARCH ACTIVITY

MAIN RECENT RESULTS

RESEARCH ACTIVITY

PHYSIOLOGY OF PULMONARY VASCULATURE

(Collaborative team of departments of physiology, biochemistry and pathophysiology funded by grants of Czech grant agencies)

 

Methods available:

  • Isolated perfused rat lungs
  • Measurement of pulmonary artery blood pressure in the rat
  • Small pulmonary vessels myograph
  • Lung mechanics in the rat
  • Lung vessel morphology
  • Biochemical measurement of collagen in peripheral lung vessels (gel and capillary electrophoresis)
  • Biochemistry of oxidant stress of the lung tissue (chemiluminiscence + HPLC)
 

Main recent reviews:

 
Herget J., Hampl V.: Pulmonary circulation. In Biomechanics of the Cardiovascular System. B.B. Sramek, J. Valenta, F. Klime, editors. Faculty of Mechanical Engeneering. Foundation for Biomechanics of Man. Prague, Czech Rep.- Irvine, CA, USA. PP 327 - 336, 1995

Herget J.: Animal models of pulmonary hypertension. Eur Resp. Rev. 559 - 563, 1993.

Herget J., Jezek V.: Pulmonary hypertension in chronic lung disease. Pulmonary Circulation. Advances and Controversies. H. Denolin and C.A. Wavenvoort, editors, Elsevier Science Publishers B.V., Amsterdam, 1989.

 

Main recent papers:

 
Hampl V., Herget J.: Perinatal hypoxia increases hypoxic pulmonary vasoconstriction in adult rats recovering from chronic exposure to hypoxia. Am. Rev. Respir. Dis. 141: 2830 - 2842, 1990. (Click here for abstract)
 
Falus F.,Herget J., J. Hampl V.: Almitrine i low dose potentiates vasoconstrictor responses in isolated rat lung to moderate hypoxia. Eur. resp. J. 4: 689 - 693, 1991. (Click here for abstract)
 
Herget J., Hampl V., Povysilova V., Slavik Z.: Long-term effects pf prenatal indomethacin administration of the pulmonary circulation in the rats. Europ. Resp. J. 8: 209 - 215, 1995. (Click here for abstract)
 
Herget J., Kuklik V.: Perinatal lung injury extends in adults the site of hypoxic pulmonary vasoconstriction upstream. Physiol. Res. 44: 25 - 30, 1995. (Click here for abstract)
 
Wilhelm J., Herget J.: Role of ion fluxes in hydrogen peroxide pulmonary vasoconstriction. Physiol. Res. 44: 31 - 37, 1995. (Click here for abstract)
 
Herget J., Pelouch V., Kolár F., Ostádal B.: The inhibition of angiotensin converting enzyme attenuates the effects of chronic hypoxia on pulmonary blood vessels in the rat. Physiol. Res. 45: 221-226, 1996. (Click here for abstract)
 
Bacáková L., Wilhelm J., Herget J., Novotná J., Eckhart A.: Oxidized collagen stimulates proliferation of vascular smooth muscle cells. Exp. Mol. Pathol. 64: 185-194, 1997. (Click here for abstract)
 
Novotná J, Herget J.: Exposure to chronic hypoxia induces qualitative changes of collagen in the walls of peripheral pulmonary arteries. Life Sci. 62: 1-12, 1998. (Click here for abstract)
Qualitative changes of vascular wall matrix collagens in chronic hypoxic pulmonary hypertension were studied by gel electrophoresis. Male adult rats (n = 12) were exposed to hypoxia (FIO2 = 0.1, 3 wks). Samples of peripheral pulmonary arteries (PPA, diam. 100 - 400 um), main branches of pulmonary artery, and aorta were dissected. Low molecular mass peptides (M. W. approx. 76 and 66 kD) were detected in the gel electrophoretic profile of collagen peptides of PPA of the chronically hypoxic animals and in aorta of both hypoxic and normoxic groups. These peptides were absent in the PPA of normoxic rats. Since the 76 kD peptide bound anticollagen type I antibodies, it appears to be of collagenous nature and it may be the result of collagenolytic activity in PPA isolated from hypoxic lungs. This was confirmed by zymography. We conclude that exposure of rats to chronic hypoxia results in the presence of low molecular mass peptides in the wall matrix of PPA which resemble those found in aorta of normoxic animals.
 

MAIN RECENT RESULTS

PERINATAL HYPOXIA

PERINATAL HYPOXIA INDUCES PERMANENT INCREASE OF HYPOXIC PULMONARY VASOCONSTRICTION WHICH PERSISTS TILL ADULTHOOD

FIGURE 1

Dose response curve to acute hypoxic challenges in the preparation of isolated perfused lungs from rats recovering from the sojourn in isobaric hypoxic chamber (FIO2=0.1)

THE SITE OF HYPOXIC PULMONARY VASOCONSTRICTION IN RATS BORN IN HYPOXIA EXTENDS UPSTREAM.

FIGURE 2 FIGURE 3

Change of peripheral vascular resistance in arterial segment (Ra) and middle segment (Rm) of pulmonary vasculature (double occlusion technique induced by acute hypoxic challenge in control rats (C), rats born in hypoxia and the kept in air (PH), rats born in normoxia and exposed to hypoxia in adulthood (AH).


HYDROGEN PEROXIDE-INDUCED PULMONARY VASOCONSTRICTION

HYDROGEN PEROXIDE PRODUCES PULMONARY VASOCONSTRICTION IN ISOLATED SALINE PERFUSED RAT LUNGS.

FIGURE 4

Arterial bolus injection of 7 mM of H2O2 in the preparation of isolated saline perfused rats lungs.

THE VASOCONSTRICTION BY HYDROGEN PEROXIDE IN RATS EXPOSED FOR 3 DAYS TO CHRONIC HYPOXIA IS INCREASED.

FIGURE 5

Dose pressor response to arterial bolus injections of H2O2 in the preparations of saline perrfused lungs isolated from control rats and rats exposed for 3 days to chronic hypoxia ( FIO2 = 0.1)

ALVEOLAR MACROPHAGES ISOLATED FROM BRONCHOALVEOLAR LAVAGE OF RATS EXPOSED FOR 3 DAYS OF HYPOXIA ( FIO2 = 0.1) PRODUCE MORE H2O2 WHEN STIMULATED. AFTER 3 WEEKS OF HYPOXIA THE PRODUCTION OF H2O2 IS NORMAL.

FIGURE 6 FIGURE 7

Production of H2O2 was measured by luminol-dependent chemiluminescence FMLP = N-formyl-methionyl-leucyl-phenylalanine PMA = phorbol-myristate-acetate

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