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Biomedical subjects

V Hossmann

Publications and source records attributed to V Hossmann.

48 records · Page 3Linked to original sources
PubMedDate not supplied

Influence of hospitalization and placebo therapy on blood pressure and sympathetic function in essential hypertension.

The decline in blood pressure (BP) in essential hypertensives following hospitalization may result from: 1) regression toward the mean; 2) reduction of anxiety as patients habituate to a new environment; 3) the placebo effect of medication; and 4) an independent effect of hospitalization itself. A randomized crossover study of 12 essential hypertensives demonstrated a fall in supine blood pressure from 165.0/97.9 +/- 2.3/1.1 mm Hg to 154.3/89.6 +/- 2.7/1.1 mm Hg (p less than 0.005) due to hospitalization. A similar reduction in BP from 164.9/99.5 +/- 8.4/4.1 mm Hg to 151.9/93.4 +/- 4.5/1.9 mm Hg (p less than 0.005) resulted from regression toward the mean and habituation during the study period. Urinary catecholamines fell from 68.7 +/- 5.0 to 55.1 +/- 4.3 micrograms/g creatinine/24 hours (p less than 0.05) due to hospitalization and from 56.1 +/- 5.4 to 49.7 +/- 4.3 micrograms/g creatinine/24 hours (p less than 0.05) with time. Although placebo therapy tended to reduce BP, it failed to do so significantly. When expressed as a percentage of the individual's overall mean, urinary catecholamine excretion fell from 110.5% +/- 3.7% to 89.5% +/- 3.7% (p less than 0.001) during hospitalization and from 105.8% +/- 3.9% to 94.2% +/- 3.9% (p less than 0.05) during the outpatient period. Blood pressure and sympathetic activity rapidly returned to prehospitalization values on discharge. These factors may confound the analysis of drug effects on BP and sympathetic activity in essential hypertensives following admission to hospital.

Adult↗
PubMedDate not supplied

No effect of prostacyclin on blood flow, regulation of blood flow and blood coagulation following global cerebral ischemia.

In normothermic cats under light barbiturate anesthesia, cerebral blood flow was arrested for one hour by intrathoracal occlusion of the innominate, the left subclavian, and both mammary arteries. Recirculation of the brain after ischemia resulted in reactive hyperemia, followed by a decrease of blood flow to about 70% of control (post-ischemic hypoperfusion). During postischemic hypoperfusion, CO2-reactivity was completely abolished. Intravenous infusion of prostacyclin 2 hours after ischemia (1.8 micrograms/kg/min) decreased systemic arterial blood pressure and reduced platelet aggregability but did not improve cerebral blood flow, did not restore CO2-reactivity, and did not influence postischemic changes of blood coagulation. It is concluded that prostacyclin deficiency is not or not the only reason for the development of post-ischemic hypoperfusion and the associated disturbance of flow regulation.

Animals↗
PubMedDate not supplied

Coagulopathy following experimental cerebral ischemia.

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.

Animals↗