[The nature of a microcirculatory change in hypertensive patients during increased blood pressure]

Terapevticheskii Arkhiv
|November 23, 2013
PubMed

Insights

Hypertensive patients exhibit impaired microcirculation (MC) during elevated blood pressure (BP). Compensatory mechanisms are insufficient, leading to nonproductive hemoperfusion and potential target organ damage.

Area of Science:

  • Cardiovascular Physiology
  • Hypertension Research
  • Microcirculation Studies

Background:

  • Hypertension significantly impacts vascular function.
  • Microcirculation plays a critical role in blood pressure regulation and tissue perfusion.
  • Understanding microcirculatory changes in hypertension is crucial for managing the condition.

Purpose of the Study:

  • To investigate alterations in microcirculation (MC) in hypertensive patients experiencing elevated blood pressure (BP).
  • To assess the compensatory mechanisms and endothelial function during hypertensive crises.

Main Methods:

  • Enrolled 66 patients with grades 2-3 hypertension and 57 healthy controls.
  • Temporarily discontinued antihypertensive drugs, categorizing patients by BP levels (< or = 140/90 mm Hg vs. > or = 160/100 mm Hg).
  • Utilized laser Doppler flowmetry to examine microcirculation.

Main Results:

  • Elevated BP in hypertensive patients caused constriction of meta-arterioles and precapillaries, reducing capillary blood flow.
  • Compensatory increases in pulse blood filling led to accelerated flow, decreased vessel diameter, and increased shear stress.
  • Despite stimulating vasodilator release, endothelial reserves were insufficient to normalize BP, resulting in nonproductive hemoperfusion due to shunting and venous congestion.

Conclusions:

  • Severe microcirculation disorders in hypertensive patients with high BP involve incompetent compensatory mechanisms.
  • Reduced endothelial relaxing potential and impaired capillary diffusion contribute to these disorders.
  • These microcirculatory dysfunctions are likely significant factors in target organ damage associated with hypertension.
Abstract

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