Result Of Vasodilatation Research Articles

Hemodynamic effects of high dose naloxone in congestive heart failure

In humans, the salutary properties of the opioid agonist morphine in the treatment of acute pulmonary edema and chronic congestive heart failure (CHF) are well known. These are thought to be the result of vasodilatation and concomitant afterload reduction caused by binding with central 1–3 and peripheral 4 opioid receptors. This clinical pharmacologic observation suggests that the endogenous opioid peptides have the potential to contribute favorably to the regulation of the hemodynamic response to acute and chronic CHF. However, contrary to the expectation based on the therapeutic efficacy of morphine, the endogenous opioids may actually exert a deleterious effect on the hemodynamic response to cardiogenic shock and the syndrome of CHF. 5,6 Case reports describe dramatic hemodynamic improvement after the administration of low doses of the narcotic antagonist naloxone to patients suffering cardiogenic shock in the setting of an acute myocardial infarction. 7 The hemodynamic effects of therapeutic (0.02 mg/kg) or maximal (1 mg/kg) doses of naloxone have not been studied in patients with CHF. In normal volunteers naloxone at doses up to 1 mg/kg causes little alteration in blood pressure, heart rate or respiration. 8 If endogenous opioids do play a role in the regulation of the hemodynamic response to chronic myocardial failure, alterations in resting hemodynamics after the administration of an opioid antagonist to patients with CHF should be identified. We report the first study defining the hemodynamic consequences of a graded naloxone infusion in patients with CHF.

The pathology of clubbing: Vascular changes in the nail bed

In this study post-mortem angiograms were prepared from both normal and clubbed hands and attempts were made to estimate the size of the vascular bed in the terminal parts of each finger. Representative cases were also examined histologically. There were no differences between the groups. The increase in blood flow in clubbing is the result of vasodilatation rather than hyperplasia of vessels in the nail bed.

Effects of verapamil and converting enzyme inhibition on bilateral renal function of two-kidney, one-clip hypertensive rats.

Experiments were conducted in two-kidney, one-clip renal vascular hypertensive rats (GHR) to assess the responses of each kidney to acute treatment with the antihypertensive calcium channel blocking agent verapamil in the presence and in the absence of converting enzyme inhibitor (CEI). One group of GHR (0.2 mm inner diam. clip 3 weeks before study) were examined during a control period, and during a second period of infusion of verapamil (600 micrograms h-1 kg-1). A second group of GHR were examined during a control period, during CEI (teprotide, 3 mg h-1 kg-1) infusion and during a third period of verapamil (600 micrograms h-1 kg-1) infusion superimposed on CEI infusion. Although systemic blood pressure (BP) decreased from 175 +/- 4 to 149 +/- 5 mmHg (mean +/- SEM) in response to verapamil alone, renal blood flow for non-clipped kidneys increased from 5.9 +/- 0.4 to 6.5 +/- 0.3 ml/min, indicating a 30% reduction of renal vascular resistance (P values less than or equal to 0.01; n = 9). Glomerular filtration rate (GFR) for non-clipped kidneys (n = 24) increased from 0.91 +/- 0.09 to 1.47 +/- 0.14 ml/min and filtration fraction increased from 0.32 +/- 0.04 to 0.47 +/- 0.03 (P values less than or equal to 0.05). Urine flow rate and absolute and fractional sodium excretion for non-clipped kidneys increased. GFR for clipped kidneys decreased during verapamil. Treatment with CEI alone resulted in nearly identical responses of BP and function of the non-clipped kidney, except filtration fraction was unchanged. The addition of verapamil to ongoing converting enzyme blockade tended to augment the increased GFR of the non-clipped kidney. Plasma renin activity (PRA) increased from 30 +/- 3 to 59 +/- 7 ng of angiotensin (ANG) I h-1 ml-1 with verapamil alone, a significantly larger increment than the increase of PRA from 27 +/- 5 to 39 +/- 9 ng of ANG I h-1 ml-1 in GHR subjected to comparable blood pressure reduction by mechanical aortic constriction. Verapamil resulted in many similar effects on renal function to those observed during blockade of converting enzyme. The increased filtration fraction observed in response to verapamil may be the result of vasodilatation of the afferent arteriole or of an increase in the glomerular ultrafiltration coefficient.

Effect of glycerol on cochlea microcirculation.

Microcirculation in the cochlea of l2 normal anesthetized guinea pigs was investigated after intravenous infusion of 2.4 ml/kg of 40% glycerol. In these experiments endolymphatic PO2, blood pressure, cochlear microphonics, and endocochlear potentials were recorded. Administration of glycerol caused a significant increase in endocochlear PO2 for about 30 minutes. The improvement of hearing in patients with Meniere's disease is thus not only a result of the reduced hydrostatic pressure, as has been demonstrated by others, but may also be the result of vasodilatation, which improves microcirculation in the cochlea with resultant increases in endocochlear PO2.