Dr. Roman  Plachinta  Md image

Dr. Roman Plachinta Md

1 Pillsbury St Ste 202
Concord NH 03301
603 244-4776
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 13512
NPI: 1114138880
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The protective effect of protein kinase C and adenosine triphosphate-sensitive potassium channel agonists against inflammation in rat endothelium and vascular smooth muscle in vitro and in vivo. - Anesthesia and analgesia
Volatile anesthetic pretreatment protects the vasculature from inflammation-induced injury via mechanisms involving the activation of adenosine triphosphate-sensitive potassium (K(ATP)) channels and/or protein kinase C (PKC). Therefore, we hypothesized that K(ATP) and PKC agonists may mimic the protective effects of volatile anesthetics in vitro and in vivo. In vitro, rat vascular smooth muscle cells (VSM) and aortic endothelial cells (AEC) were used to evaluate whether pretreatment with a K(ATP) agonist, cromakalim (CRK), or a PKC agonist, phorbol 12-myristate 13-acetate (PMA), decreases lipopolysaccharide (LPS)-induced cell injury. Cell survival was determined by trypan blue staining after 6 h. In vivo, rats received systemic LPS or saline with or without pretreatment with PMA or CRK. Mean arterial blood pressure, the response to endothelium-dependent (acetylcholine; ACH) and -independent (sodium nitroprusside) vasodilators, and arterial blood gases were determined after 6 h. Cell survival in VSM and AEC control cultures was more than 90%, which was not altered in the presence of PMA or CRK, whereas LPS significantly decreased cell survival. PMA (0.1-10 microM) significantly attenuated the LPS-induced decrease in cell survival by 28%-37% in VSM and 39%-53% in AEC, and CRK (1 mM) increased cell survival by 24% in VSM and 22% in AEC. In vivo, PMA and CRK pretreatment had no significant effect on measured variables in control rats. LPS decreased mean arterial blood pressure and vasodilation to ACH and sodium nitroprusside and caused hypoglycemia. PMA, but not CRK, increased ACH-dependent vasodilation (46%) at 6 h, but neither agonist altered the other detrimental effects of LPS. In conclusion, PKC and K(ATP) agonists appear to protect AEC and VSM cells against inflammation in vitro, but the systemic administration of PKC and K(ATP) agonists appeared to exert minimal or no protection in our in vivo model.
Isoflurane pretreatment supports hemodynamics and leukocyte rolling velocities in rat mesentery during lipopolysaccharide-induced inflammation. - Anesthesia and analgesia
We hypothesized that the protective effects of isoflurane (ISO) pretreatment on the vasculature may be attributed, in part, to altered leukocyte-endothelial interactions. Rats were anesthetized with pentobarbital and then randomized into four groups: control, ISO-control (pretreatment with 30 min of 1.4% ISO), lipopolysaccharide (LPS; 10 mg/kg IV), and ISO-LPS (ISO pretreatment and then LPS). The mesentery was prepared for intravital videomicroscopy. Mean arterial blood pressure (MAP), along with microcirculatory variables that included postcapillary venular and arteriolar blood flow velocity and leukocyte dynamics (number of rolling and adherent leukocytes and individual rolling leukocyte velocities), were measured hourly (baseline and at 0-4 h). In LPS rats, ISO pretreatment significantly (P < 0.05) attenuated the decrease in MAP at 2 and 4 h after LPS and increased leukocyte rolling velocities after 2-4 h. Four hours after LPS, leukocyte rolling velocities were >200% more rapid (63.7 +/- 27.6 microm/s versus 19.8 +/- 6.4 micro m/s) in ISO-LPS versus LPS rats. In control rats, ISO pretreatment had no effect on MAP or leukocyte rolling velocities but increased the number of rolling leukocytes. ISO pretreatment had no effect on arteriolar and postcapillary venular blood flow velocity in LPS rats or leukocyte adherence in LPS or control rats. In conclusion, ISO pretreatment supported hemodynamics and increased leukocyte rolling velocities but did not alter the number of rolling or adherent leukocytes in the mesenteric microcirculation during LPS-induced inflammation.Isoflurane pretreatment supported hemodynamics and increased leukocyte rolling velocities in the mesenteric microcirculation during lipopolysaccharide-induced inflammation. Faster rolling velocities may reduce the incidence of inflammation by decreasing leukocyte-endothelial interactions and cellular injury.
Isoflurane pretreatment inhibits lipopolysaccharide-induced inflammation in rats. - Anesthesiology
Previous studies have indicated that volatile anesthetic pretreatment protects cells from inflammation; therefore, the authors hypothesized that pretreatment with isoflurane may attenuate the hemodynamic and pathologic changes to the vasculature that are associated with inflammation.Rats received intravenous lipopolysaccharide or saline placebo with and without pretreatment with isoflurane (1.4% for 30 min immediately before lipopolysaccharide). Mean arterial pressure (MAP) and response to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) vasodilators were assessed hourly for 6 h. Tumor necrosis factor-alpha concentrations, arterial blood gases, and vascular histology were also determined.Lipopolysaccharide decreased MAP and vasodilation to acetylcholine and sodium nitroprusside. Lipopolysaccharide also caused acidosis, endothelial swelling, and endothelial detachment from the smooth muscle. Isoflurane pretreatment prevented the decrease in MAP for 5 h and attenuated the decrease at 6 h. Pretreatment increased the vasodilation to acetylcholine in lipopolysaccharide rats to control concentrations but had no effect on sodium nitroprusside. In control rats, isoflurane pretreatment increased the response to acetylcholine and sodium nitroprusside but had no effect on MAP. Isoflurane pretreatment prevented the acidosis and endothelial damage to mesenteric and aortic vessels, and attenuated the increase in tumor necrosis factor-alpha associated with lipopolysaccharide-induced inflammation.Pretreatment with 30 min of isoflurane attenuated the decrease in MAP and endothelium-dependent vasodilation, the acidosis, the increase in tumor necrosis factor-alpha, and the damage to the vascular endothelium associated with lipopolysaccharide-induced inflammation in rats. This study suggests that isoflurane pretreatment may protect the vasculature during inflammation.

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